Epigallocatechin-3-gallate (EGCG)

experimental_model

Mature amyloid-beta and alpha-synuclein fibril preparations.

limitations

This does not show removal of deposits from a human brain.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG changed pre-existing aggregates in a laboratory experiment.

primary_references

EGCG remodels mature alpha-synuclein and amyloid-beta fibrils and reduces cellular toxicity. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20385841/ · DOI 10.1073/pnas.0910723107

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 356–362

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mature amyloid-beta and alpha-synuclein fibril preparations. · source_derived_draft · unverified_draft

## egcg-ab-remodel EGCG changed pre-existing aggregates in a laboratory experiment. EGCG bound mature fibrils and remodeled them into smaller amorphous aggregates without measured release of monomers or small diffusible oligomers. Model: Mature amyloid-beta and alpha-synuclein fibril preparations. Limitations: This does not show removal of deposits from a human brain. Evidence access: primary abstract. EGCG remodels mature alpha-synuclein and amyloid-beta fibrils and reduces cellular toxicity. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20385841/ · DOI 10.1073/pnas.0910723107

experimental_model

Cell toxicity comparison of treated versus untreated fibrils.

limitations

Assay result, not clinical cognitive improvement.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The remodeled material was less harmful in that assay.

primary_references

EGCG remodels mature alpha-synuclein and amyloid-beta fibrils and reduces cellular toxicity. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20385841/ · DOI 10.1073/pnas.0910723107

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 372–378

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cell toxicity comparison of treated versus untreated fibrils. · source_derived_draft · unverified_draft

## egcg-aggregate-toxicity The remodeled material was less harmful in that assay. Remodeled aggregates had lower toxicity in the tested cell assay. Model: Cell toxicity comparison of treated versus untreated fibrils. Limitations: Assay result, not clinical cognitive improvement. Evidence access: primary abstract. EGCG remodels mature alpha-synuclein and amyloid-beta fibrils and reduces cellular toxicity. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20385841/ · DOI 10.1073/pnas.0910723107

experimental_model

MDA-MB-231 and A549 cells.

limitations

A pathway readout does not establish a unique causal target or human anticancer efficacy.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Downstream growth signaling changed in the cell experiments.

primary_references

Epigallocatechin gallate (EGCG), a major component of green tea, is a dual phosphoinositide-3-kinase/mTOR inhibitor. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21300025/ · DOI 10.1016/j.bbrc.2011.02.010

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 228–234

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · MDA-MB-231 and A549 cells. · source_derived_draft · unverified_draft

## egcg-akt Downstream growth signaling changed in the cell experiments. EGCG reduced AKT Ser473 phosphorylation alongside proliferation in the tested cancer cells. Model: MDA-MB-231 and A549 cells. Limitations: A pathway readout does not establish a unique causal target or human anticancer efficacy. Evidence access: primary abstract. Epigallocatechin gallate (EGCG), a major component of green tea, is a dual phosphoinositide-3-kinase/mTOR inhibitor. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21300025/ · DOI 10.1016/j.bbrc.2011.02.010

experimental_model

Biophysical and cell-based aggregation experiments.

limitations

Not evidence of preventing or treating human neurodegenerative disease.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG changed how these proteins assembled.

primary_references

EGCG redirects amyloidogenic polypeptides into unstructured, off-pathway oligomers. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18511942/ · DOI 10.1038/nsmb.1437

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 348–354

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Biophysical and cell-based aggregation experiments. · source_derived_draft · unverified_draft

## egcg-amyloid-initiation EGCG changed how these proteins assembled. EGCG bound unfolded amyloid-beta and alpha-synuclein and redirected assembly toward unstructured, relatively nontoxic oligomers in the experimental system. Model: Biophysical and cell-based aggregation experiments. Limitations: Not evidence of preventing or treating human neurodegenerative disease. Evidence access: primary abstract. EGCG redirects amyloidogenic polypeptides into unstructured, off-pathway oligomers. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18511942/ · DOI 10.1038/nsmb.1437

experimental_model

Mature amyloid-beta and alpha-synuclein fibril preparations.

limitations

This does not show removal of deposits from a human brain.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG changed pre-existing aggregates in a laboratory experiment.

primary_references

EGCG remodels mature alpha-synuclein and amyloid-beta fibrils and reduces cellular toxicity. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20385841/ · DOI 10.1073/pnas.0910723107

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 364–370

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mature amyloid-beta and alpha-synuclein fibril preparations. · source_derived_draft · unverified_draft

## egcg-as-remodel EGCG changed pre-existing aggregates in a laboratory experiment. EGCG bound mature fibrils and remodeled them into smaller amorphous aggregates without measured release of monomers or small diffusible oligomers. Model: Mature amyloid-beta and alpha-synuclein fibril preparations. Limitations: This does not show removal of deposits from a human brain. Evidence access: primary abstract. EGCG remodels mature alpha-synuclein and amyloid-beta fibrils and reduces cellular toxicity. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20385841/ · DOI 10.1073/pnas.0910723107

experimental_model

Chemical characterization and cell assays.

limitations

A boronic-acid drug is not interchangeable with dietary boron.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The chemical interaction has evidence beyond a pathway diagram.

primary_references

Molecular characterization of the boron adducts of the proteasome inhibitor bortezomib with epigallocatechin-3-gallate and related polyphenols. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25669488/ · DOI 10.1039/c4ob02512a

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 412–418

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Chemical characterization and cell assays. · source_derived_draft · unverified_draft

## egcg-boronate The chemical interaction has evidence beyond a pathway diagram. NMR and cell experiments characterized boronate and borate EGCG–bortezomib derivatives; adduct stability depended on structural features. Model: Chemical characterization and cell assays. Limitations: A boronic-acid drug is not interchangeable with dietary boron. Evidence access: primary abstract. Molecular characterization of the boron adducts of the proteasome inhibitor bortezomib with epigallocatechin-3-gallate and related polyphenols. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25669488/ · DOI 10.1039/c4ob02512a

experimental_model

Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study.

limitations

Preclinical findings; no human coadministration outcome trial. Chemical form and simultaneous concentrations matter.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

One research group found that EGCG weakened this cancer drug.

primary_references

Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19190249/ · DOI 10.1182/blood-2008-07-171389

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 396–402

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study. · source_derived_draft · unverified_draft

## egcg-bortezomib-antagonism One research group found that EGCG weakened this cancer drug. EGCG blocked bortezomib-mediated anticancer effects in the reported models. Model: Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study. Limitations: Preclinical findings; no human coadministration outcome trial. Chemical form and simultaneous concentrations matter. Evidence access: primary abstract. Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19190249/ · DOI 10.1182/blood-2008-07-171389

experimental_model

Immunocompromised mice; bortezomib 0.8 mg/kg IV twice weekly.

limitations

Concentration-specific animal findings do not establish a human safety threshold.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

A follow-up found antagonism at very high simultaneous exposure.

primary_references

Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21400028/ · DOI 10.1007/s00280-011-1591-2

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 428–434

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Immunocompromised mice; bortezomib 0.8 mg/kg IV twice weekly. · source_derived_draft · unverified_draft

## egcg-bortezomib-high A follow-up found antagonism at very high simultaneous exposure. In CWR22 xenografts, EGCG above 200 micromolar at bortezomib administration abolished measured antitumor activity. Model: Immunocompromised mice; bortezomib 0.8 mg/kg IV twice weekly. Limitations: Concentration-specific animal findings do not establish a human safety threshold. Evidence access: primary abstract. Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21400028/ · DOI 10.1007/s00280-011-1591-2

experimental_model

CWR22 xenograft exposure comparison.

limitations

Not proof of clinical synergy or unrestricted safe coadministration.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The drug interaction was not identical at every concentration.

primary_references

Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21400028/ · DOI 10.1007/s00280-011-1591-2

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 436–442

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CWR22 xenograft exposure comparison. · source_derived_draft · unverified_draft

## egcg-bortezomib-lower The drug interaction was not identical at every concentration. At EGCG 11–16 micromolar, the same model showed no antagonism; tumor-growth inhibition was 63.5% versus 53.9–58.9% with bortezomib alone. Model: CWR22 xenograft exposure comparison. Limitations: Not proof of clinical synergy or unrestricted safe coadministration. Evidence access: primary abstract. Preclinical evaluation of the antitumor activity of bortezomib in combination with vitamin C or with epigallocatechin gallate, a component of green tea. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21400028/ · DOI 10.1007/s00280-011-1591-2

experimental_model

Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study.

limitations

Preclinical findings; no human coadministration outcome trial. Chemical form and simultaneous concentrations matter.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The proposed interference starts with drug chemistry.

primary_references

Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19190249/ · DOI 10.1182/blood-2008-07-171389

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 404–410

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study. · source_derived_draft · unverified_draft

## egcg-bortezomib-proteasome The proposed interference starts with drug chemistry. Direct EGCG–bortezomib reaction prevented proteasome inhibition and downstream stress/death responses; tested nonboronic inhibitors did not show the same antagonism. Model: Myeloma/glioblastoma cell experiments and animal models in the 2009 Blood study. Limitations: Preclinical findings; no human coadministration outcome trial. Chemical form and simultaneous concentrations matter. Evidence access: primary abstract. Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19190249/ · DOI 10.1182/blood-2008-07-171389

experimental_model

KM3 myeloma cells; associated NF-kappaB/caspase pathway readouts.

limitations

Dose, timing and model were not harmonized with the antagonism study; no universal direction can be assigned.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Another study reported a stronger combination effect.

primary_references

Potentiation of (-)-epigallocatechin-3-gallate-induced apoptosis by bortezomib in multiple myeloma cells. · 2009 · https://pubmed.ncbi.nlm.nih.gov/20011976/ · DOI 10.1093/abbs/gmp094

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 420–426

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · KM3 myeloma cells; associated NF-kappaB/caspase pathway readouts. · source_derived_draft · unverified_draft

## egcg-bortezomib-synergy Another study reported a stronger combination effect. A separate 2009 KM3 myeloma-cell study reported synergistic apoptosis with EGCG plus bortezomib. Model: KM3 myeloma cells; associated NF-kappaB/caspase pathway readouts. Limitations: Dose, timing and model were not harmonized with the antagonism study; no universal direction can be assigned. Evidence access: primary abstract. Potentiation of (-)-epigallocatechin-3-gallate-induced apoptosis by bortezomib in multiple myeloma cells. · 2009 · https://pubmed.ncbi.nlm.nih.gov/20011976/ · DOI 10.1093/abbs/gmp094

experimental_model

Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally.

limitations

Do not relabel the purified enzymes as human DHFR or infer that normal tea intake causes folate deficiency.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG inhibited a folate-processing enzyme in a purified animal preparation.

primary_references

The antifolate activity of tea catechins. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15781612/ · DOI 10.1158/0008-5472.can-04-3469

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 124–130

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally. · source_derived_draft · unverified_draft

## egcg-bovine-dhfr EGCG inhibited a folate-processing enzyme in a purified animal preparation. EGCG inhibited bovine DHFR with slow tight binding, Ki 0.109 micromolar. Model: Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally. Limitations: Do not relabel the purified enzymes as human DHFR or infer that normal tea intake causes folate deficiency. Evidence access: primary abstract. The antifolate activity of tea catechins. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15781612/ · DOI 10.1158/0008-5472.can-04-3469

experimental_model

Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally.

limitations

Do not relabel the purified enzymes as human DHFR or infer that normal tea intake causes folate deficiency.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Even enzyme preparations from different species behaved differently.

primary_references

The antifolate activity of tea catechins. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15781612/ · DOI 10.1158/0008-5472.can-04-3469

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 132–138

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally. · source_derived_draft · unverified_draft

## egcg-chicken-dhfr Even enzyme preparations from different species behaved differently. Chicken DHFR showed reversible competitive inhibition, Ki 10.3 micromolar. Model: Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally. Limitations: Do not relabel the purified enzymes as human DHFR or infer that normal tea intake causes folate deficiency. Evidence access: primary abstract. The antifolate activity of tea catechins. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15781612/ · DOI 10.1158/0008-5472.can-04-3469

experimental_model

Single exposure; 14 women and 10 men; COMT genotype assessment.

limitations

Red-cell activity at one time point is not a measurement of brain or liver COMT. No general catecholamine or fat-burning claim follows.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The measured human red-cell result did not match a simple inhibition prediction.

primary_references

The activity of catechol-O-methyltransferase (COMT) is not impaired by high doses of epigallocatechin-3-gallate (EGCG) in vivo. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24972245/ · DOI 10.1016/j.ejphar.2014.06.014

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 180–186

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Single exposure; 14 women and 10 men; COMT genotype assessment. · source_derived_draft · unverified_draft

## egcg-comt-human The measured human red-cell result did not match a simple inhibition prediction. After 750 mg EGCG in 24 volunteers, erythrocyte COMT activity increased by 24% at two hours rather than decreasing. Model: Single exposure; 14 women and 10 men; COMT genotype assessment. Limitations: Red-cell activity at one time point is not a measurement of brain or liver COMT. No general catecholamine or fat-burning claim follows. Evidence access: primary abstract. The activity of catechol-O-methyltransferase (COMT) is not impaired by high doses of epigallocatechin-3-gallate (EGCG) in vivo. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24972245/ · DOI 10.1016/j.ejphar.2014.06.014

experimental_model

Human liver cytosol and metabolite comparisons.

limitations

Assay potency does not establish brain, liver or whole-body inhibition after ingestion.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

A liver preparation showed inhibition of a methyl-transfer enzyme.

primary_references

Inhibition of human liver catechol-O-methyltransferase by tea catechins and their metabolites: structure-activity relationship and molecular-modeling studies. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15857617/ · DOI 10.1016/j.bcp.2005.01.024

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 164–170

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver cytosol and metabolite comparisons. · source_derived_draft · unverified_draft

## egcg-comt-invitro A liver preparation showed inhibition of a methyl-transfer enzyme. EGCG inhibited human liver cytosolic COMT-mediated catechol-estrogen methylation, IC50 0.07 micromolar, with mixed inhibition. Model: Human liver cytosol and metabolite comparisons. Limitations: Assay potency does not establish brain, liver or whole-body inhibition after ingestion. Evidence access: primary abstract. Inhibition of human liver catechol-O-methyltransferase by tea catechins and their metabolites: structure-activity relationship and molecular-modeling studies. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15857617/ · DOI 10.1016/j.bcp.2005.01.024

experimental_model

Human esophageal cancer cells; PCR methylation assays.

limitations

Not a universal epigenome reset or evidence that demethylation is always beneficial.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Some silenced cancer-cell genes showed changes in promoter methylation.

primary_references

Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. · 2003 · https://pubmed.ncbi.nlm.nih.gov/14633667/

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 260–266

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human esophageal cancer cells; PCR methylation assays. · source_derived_draft · unverified_draft

## egcg-cpg Some silenced cancer-cell genes showed changes in promoter methylation. At 5–50 micromolar for 12–144 hours, EGCG reduced methylation-specific signals at p16, RARbeta, MGMT and hMLH1 promoters in KYSE 510 cells. Model: Human esophageal cancer cells; PCR methylation assays. Limitations: Not a universal epigenome reset or evidence that demethylation is always beneficial. Evidence access: primary abstract. Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. · 2003 · https://pubmed.ncbi.nlm.nih.gov/14633667/

experimental_model

Nuclear-extract enzyme assay; molecular docking was also reported.

limitations

The extract assay is not purified DNMT1-specific proof; modeled binding contacts remain predictions.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG affected a DNA-methylation assay.

primary_references

Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. · 2003 · https://pubmed.ncbi.nlm.nih.gov/14633667/

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 252–258

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Nuclear-extract enzyme assay; molecular docking was also reported. · source_derived_draft · unverified_draft

## egcg-dnmt EGCG affected a DNA-methylation assay. EGCG competitively inhibited DNMT activity in nuclear extracts, Ki 6.89 micromolar. Model: Nuclear-extract enzyme assay; molecular docking was also reported. Limitations: The extract assay is not purified DNMT1-specific proof; modeled binding contacts remain predictions. Evidence access: primary abstract. Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. · 2003 · https://pubmed.ncbi.nlm.nih.gov/14633667/

experimental_model

Panel of 28 protein kinases.

limitations

Two inhibited kinases in this panel do not establish selectivity across the entire kinome.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

A kinase-panel experiment identified another target.

primary_references

The specificities of protein kinase inhibitors: an update. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12534346/ · DOI 10.1042/bj20021535

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 236–242

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Panel of 28 protein kinases. · source_derived_draft · unverified_draft

## egcg-dyrk A kinase-panel experiment identified another target. The kinase panel reported EGCG inhibition with IC50 0.33 micromolar. Model: Panel of 28 protein kinases. Limitations: Two inhibited kinases in this panel do not establish selectivity across the entire kinome. Evidence access: primary abstract. The specificities of protein kinase inhibitors: an update. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12534346/ · DOI 10.1042/bj20021535

experimental_model

Chicken liver FAS; biochemical kinetics.

limitations

Not a human weight-loss trial or a direct measurement of human FASN.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG acted on a lipid-synthesis enzyme in a purified preparation.

primary_references

Green tea epigallocatechin gallate: a natural inhibitor of fatty-acid synthase. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11700039/ · DOI 10.1006/bbrc.2001.5923

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 196–202

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Chicken liver FAS; biochemical kinetics. · source_derived_draft · unverified_draft

## egcg-fasn EGCG acted on a lipid-synthesis enzyme in a purified preparation. EGCG inhibited chicken liver FAS through rapid reversible and slower irreversible components; rapid 50% inhibition occurred at 52 micromolar. Model: Chicken liver FAS; biochemical kinetics. Limitations: Not a human weight-loss trial or a direct measurement of human FASN. Evidence access: primary abstract. Green tea epigallocatechin gallate: a natural inhibitor of fatty-acid synthase. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11700039/ · DOI 10.1006/bbrc.2001.5923

experimental_model

Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14.

limitations

Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The study measured a transporter-expression change.

primary_references

Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 524–530

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. · source_derived_draft · unverified_draft

## egcg-hepatic-oct The study measured a transporter-expression change. EGCG pretreatment reduced the specified transporter mRNA by a reported 2.66-fold. Model: Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. Limitations: Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size. Evidence access: primary abstract. Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

experimental_model

Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14.

limitations

Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The study measured a transporter-expression change.

primary_references

Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 532–538

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. · source_derived_draft · unverified_draft

## egcg-hepatic-pgp The study measured a transporter-expression change. EGCG pretreatment reduced the specified transporter mRNA by a reported 2.61-fold. Model: Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. Limitations: Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size. Evidence access: primary abstract. Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

experimental_model

Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14.

limitations

Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The study measured a transporter-expression change.

primary_references

Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 500–506

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. · source_derived_draft · unverified_draft

## egcg-ileal-oatp The study measured a transporter-expression change. EGCG pretreatment reduced the specified transporter mRNA by a reported 4.03-fold. Model: Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. Limitations: Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size. Evidence access: primary abstract. Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

experimental_model

Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14.

limitations

Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The study measured a transporter-expression change.

primary_references

Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 508–514

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. · source_derived_draft · unverified_draft

## egcg-ileal-oct The study measured a transporter-expression change. EGCG pretreatment reduced the specified transporter mRNA by a reported 4.03-fold. Model: Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. Limitations: Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size. Evidence access: primary abstract. Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

experimental_model

Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14.

limitations

Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The study measured a transporter-expression change.

primary_references

Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 516–522

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. · source_derived_draft · unverified_draft

## egcg-ileal-pgp The study measured a transporter-expression change. EGCG pretreatment reduced the specified transporter mRNA by a reported 8.01-fold. Model: Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. Limitations: Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size. Evidence access: primary abstract. Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

experimental_model

Randomized double-blind three-period crossover; eight days per period; stable iron isotopes.

limitations

The reassuring paper title does not negate its significant high-dose result. Low-dose impact in healthy iron-replete people was an author extrapolation, not the studied population.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG reduced iron absorption at the higher tested dose.

primary_references

Epigallocatechin gallate (EGCG) (TEAVIGO) does not impair nonhaem-iron absorption in man. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16008116/ · DOI 10.1016/j.phymed.2004.07.001

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 188–194

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Randomized double-blind three-period crossover; eight days per period; stable iron isotopes. · source_derived_draft · unverified_draft

## egcg-iron EGCG reduced iron absorption at the higher tested dose. In 30 women with low iron stores, 150 and 300 mg EGCG reduced relative nonheme-iron absorption by 14% and 27%; the 300 mg comparison with placebo was significant. Model: Randomized double-blind three-period crossover; eight days per period; stable iron isotopes. Limitations: The reassuring paper title does not negate its significant high-dose result. Low-dose impact in healthy iron-replete people was an author extrapolation, not the studied population. Evidence access: primary abstract. Epigallocatechin gallate (EGCG) (TEAVIGO) does not impair nonhaem-iron absorption in man. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16008116/ · DOI 10.1016/j.phymed.2004.07.001

experimental_model

In-vitro human gut-community fermentation and UHPLC-Q-Orbitrap-MS.

limitations

Metabolite detection in fermentation does not demonstrate systemic human exposure or benefit.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Gut microbes can turn EGCG into chemically different compounds.

primary_references

Reciprocal Interactions between Epigallocatechin-3-gallate (EGCG) and Human Gut Microbiota In Vitro. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32808768/ · DOI 10.1021/acs.jafc.0c03587

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 316–322

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · In-vitro human gut-community fermentation and UHPLC-Q-Orbitrap-MS. · source_derived_draft · unverified_draft

## egcg-microbial-conversion Gut microbes can turn EGCG into chemically different compounds. Human fecal fermentation converted EGCG through ester hydrolysis, ring opening/fission and subsequent reactions to phenolic acids, including 4-phenylbutyric and hydroxyphenylpropionic acids. Model: In-vitro human gut-community fermentation and UHPLC-Q-Orbitrap-MS. Limitations: Metabolite detection in fermentation does not demonstrate systemic human exposure or benefit. Evidence access: primary abstract. Reciprocal Interactions between Epigallocatechin-3-gallate (EGCG) and Human Gut Microbiota In Vitro. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32808768/ · DOI 10.1021/acs.jafc.0c03587

experimental_model

In-vitro fermentation with microbiome profiling.

limitations

Taxon shifts and metabolite correlations do not establish a universally beneficial microbiome in humans.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG also changed the experimental microbial community.

primary_references

Reciprocal Interactions between Epigallocatechin-3-gallate (EGCG) and Human Gut Microbiota In Vitro. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32808768/ · DOI 10.1021/acs.jafc.0c03587

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 324–330

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · In-vitro fermentation with microbiome profiling. · source_derived_draft · unverified_draft

## egcg-microbiome EGCG also changed the experimental microbial community. EGCG-exposed fermentations showed increases in Bacteroides, Christensenellaceae and Bifidobacterium and decreases in selected other taxa. Model: In-vitro fermentation with microbiome profiling. Limitations: Taxon shifts and metabolite correlations do not establish a universally beneficial microbiome in humans. Evidence access: primary abstract. Reciprocal Interactions between Epigallocatechin-3-gallate (EGCG) and Human Gut Microbiota In Vitro. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32808768/ · DOI 10.1021/acs.jafc.0c03587

experimental_model

Biochemical kinase assays plus MDA-MB-231 and A549 cell experiments.

limitations

PI3K isoform is not assigned from abstract; docking is a model, not a solved ligand structure.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG competed with the enzyme’s energy substrate.

primary_references

Epigallocatechin gallate (EGCG), a major component of green tea, is a dual phosphoinositide-3-kinase/mTOR inhibitor. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21300025/ · DOI 10.1016/j.bbrc.2011.02.010

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 220–226

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Biochemical kinase assays plus MDA-MB-231 and A549 cell experiments. · source_derived_draft · unverified_draft

## egcg-mtor EGCG competed with the enzyme’s energy substrate. EGCG showed ATP-competitive inhibition with Ki 320 nanomolar in the reported enzyme assay. Model: Biochemical kinase assays plus MDA-MB-231 and A549 cell experiments. Limitations: PI3K isoform is not assigned from abstract; docking is a model, not a solved ligand structure. Evidence access: primary abstract. Epigallocatechin gallate (EGCG), a major component of green tea, is a dual phosphoinositide-3-kinase/mTOR inhibitor. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21300025/ · DOI 10.1016/j.bbrc.2011.02.010

experimental_model

Genetic screen, cell signaling and experimental tumor-growth models.

limitations

Pathway dependency in these models does not establish human cancer treatment or a dietary threshold.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG removed an inhibitory phosphorylation mark in this pathway.

primary_references

Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 36–42

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Genetic screen, cell signaling and experimental tumor-growth models. · source_derived_draft · unverified_draft

## egcg-mypt EGCG removed an inhibitory phosphorylation mark in this pathway. EGCG dephosphorylated MYPT1 Thr696 through 67LR and eEF1A. Model: Genetic screen, cell signaling and experimental tumor-growth models. Limitations: Pathway dependency in these models does not establish human cancer treatment or a dietary threshold. Evidence access: primary abstract. Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200

experimental_model

Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14.

limitations

Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Purified EGCG also changed nadolol exposure in an animal study.

primary_references

Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 492–498

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. · source_derived_draft · unverified_draft

## egcg-nadolol-rat Purified EGCG also changed nadolol exposure in an animal study. EGCG pretreatment reduced rat nadolol Cmax by 53% and AUC by 51%, with weaker blood-pressure control. Model: Male spontaneously hypertensive rats; EGCG 10 mg/kg/day for 14 days and nadolol 10 mg/kg on day 14. Limitations: Rat transcription/exposure results; mRNA changes do not establish transporter protein activity or a human effect size. Evidence access: primary abstract. Oral epigallocatechin gallate reduces intestinal nadolol absorption via modulation of Oatp1a5 and Oct1 transcriptional levels in spontaneously hypertensive rats. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34303263/ · DOI 10.1016/j.phymed.2021.153623

experimental_model

CHO cells and cell-culture medium comparisons.

limitations

Culture autooxidation cannot be generalized to all tissues or used to dismiss every cell experiment.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG can generate peroxide under some laboratory conditions.

primary_references

Different cytotoxic and clastogenic effects of epigallocatechin gallate in various cell-culture media due to variable rates of its oxidation in the culture medium. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17851114/ · DOI 10.1016/j.mrgentox.2007.07.009

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 332–338

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CHO cells and cell-culture medium comparisons. · source_derived_draft · unverified_draft

## egcg-peroxide EGCG can generate peroxide under some laboratory conditions. EGCG-associated peroxide formation and CHO cytotoxicity differed substantially among seven culture media. Model: CHO cells and cell-culture medium comparisons. Limitations: Culture autooxidation cannot be generalized to all tissues or used to dismiss every cell experiment. Evidence access: primary abstract. Different cytotoxic and clastogenic effects of epigallocatechin gallate in various cell-culture media due to variable rates of its oxidation in the culture medium. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17851114/ · DOI 10.1016/j.mrgentox.2007.07.009

experimental_model

Genetic screen, cell signaling and experimental tumor-growth models.

limitations

Pathway dependency in these models does not establish human cancer treatment or a dietary threshold.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Changing MYPT1 changed phosphatase activity.

primary_references

Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 44–50

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Genetic screen, cell signaling and experimental tumor-growth models. · source_derived_draft · unverified_draft

## egcg-phosphatase Changing MYPT1 changed phosphatase activity. MYPT1 dephosphorylation accompanied activation of myosin phosphatase. Model: Genetic screen, cell signaling and experimental tumor-growth models. Limitations: Pathway dependency in these models does not establish human cancer treatment or a dietary threshold. Evidence access: primary abstract. Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200

experimental_model

Biochemical kinase assays plus MDA-MB-231 and A549 cell experiments.

limitations

PI3K isoform is not assigned from abstract; docking is a model, not a solved ligand structure.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG competed with the enzyme’s energy substrate.

primary_references

Epigallocatechin gallate (EGCG), a major component of green tea, is a dual phosphoinositide-3-kinase/mTOR inhibitor. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21300025/ · DOI 10.1016/j.bbrc.2011.02.010

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 212–218

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Biochemical kinase assays plus MDA-MB-231 and A549 cell experiments. · source_derived_draft · unverified_draft

## egcg-pi3k EGCG competed with the enzyme’s energy substrate. EGCG showed ATP-competitive inhibition with Ki 380 nanomolar in the reported enzyme assay. Model: Biochemical kinase assays plus MDA-MB-231 and A549 cell experiments. Limitations: PI3K isoform is not assigned from abstract; docking is a model, not a solved ligand structure. Evidence access: primary abstract. Epigallocatechin gallate (EGCG), a major component of green tea, is a dual phosphoinositide-3-kinase/mTOR inhibitor. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21300025/ · DOI 10.1016/j.bbrc.2011.02.010

experimental_model

Panel of 28 protein kinases.

limitations

Two inhibited kinases in this panel do not establish selectivity across the entire kinome.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

A kinase-panel experiment identified another target.

primary_references

The specificities of protein kinase inhibitors: an update. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12534346/ · DOI 10.1042/bj20021535

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 244–250

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Panel of 28 protein kinases. · source_derived_draft · unverified_draft

## egcg-prak A kinase-panel experiment identified another target. The kinase panel reported EGCG inhibition with IC50 1.0 micromolar. Model: Panel of 28 protein kinases. Limitations: Two inhibited kinases in this panel do not establish selectivity across the entire kinome. Evidence access: primary abstract. The specificities of protein kinase inhibitors: an update. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12534346/ · DOI 10.1042/bj20021535

experimental_model

Cancer-cell expression assays.

limitations

Dietary exposure and human disease outcomes were not established.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The study also checked gene expression, beyond a methylation signal.

primary_references

Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. · 2003 · https://pubmed.ncbi.nlm.nih.gov/14633667/

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 268–274

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-cell expression assays. · source_derived_draft · unverified_draft

## egcg-reactivation The study also checked gene expression, beyond a methylation signal. The promoter changes accompanied gene mRNA re-expression; RARbeta and hMLH1 protein re-expression was detected. Model: Cancer-cell expression assays. Limitations: Dietary exposure and human disease outcomes were not established. Evidence access: primary abstract. Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. · 2003 · https://pubmed.ncbi.nlm.nih.gov/14633667/

experimental_model

Receptor binding and cancer-cell expression experiments.

limitations

67LR is recorded as the receptor state, not equated with all functions of the 37-kDa RPSA precursor.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

A cell-surface receptor can make cells responsive to EGCG.

primary_references

A receptor for green tea polyphenol EGCG. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15024383/ · DOI 10.1038/nsmb743

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 20–26

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Receptor binding and cancer-cell expression experiments. · source_derived_draft · unverified_draft

## egcg-receptor A cell-surface receptor can make cells responsive to EGCG. Surface plasmon resonance supported nanomolar-affinity EGCG binding to 67LR; receptor expression conferred cellular responsiveness. Model: Receptor binding and cancer-cell expression experiments. Limitations: 67LR is recorded as the receptor state, not equated with all functions of the 37-kDa RPSA precursor. Evidence access: primary abstract. A receptor for green tea polyphenol EGCG. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15024383/ · DOI 10.1038/nsmb743

experimental_model

Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study.

limitations

Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

A conjugated metabolite reached exposure comparable to free EGCG.

primary_references

4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 292–298

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. · source_derived_draft · unverified_draft

## egcg-sulfate-exposure A conjugated metabolite reached exposure comparable to free EGCG. Human plasma EGCG-4″-sulfate Cmax was 177.9 nM versus 233.5 nM free EGCG; AUC was 715.2 versus 664.1 nM·h. Model: Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. Limitations: Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG. Evidence access: primary abstract. 4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150

experimental_model

Allosteric binding/kinetic model; weak active-site binding also observed.

limitations

Substrate status and inhibition are separate questions; not proof of altered melatonin or hormone levels in people.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG can trap this enzyme in a slower-cycling state.

primary_references

Isozyme Specific Allosteric Regulation of Human Sulfotransferase 1A1. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27356022/ · DOI 10.1021/acs.biochem.6b00401

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 308–314

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Allosteric binding/kinetic model; weak active-site binding also observed. · source_derived_draft · unverified_draft

## egcg-sult-cap EGCG can trap this enzyme in a slower-cycling state. EGCG stabilized the closed SULT1A1 active-site cap, slowed nucleotide release and inhibited turnover; nucleotide-bound enzyme showed 17-fold tighter EGCG binding. Model: Allosteric binding/kinetic model; weak active-site binding also observed. Limitations: Substrate status and inhibition are separate questions; not proof of altered melatonin or hormone levels in people. Evidence access: primary abstract. Isozyme Specific Allosteric Regulation of Human Sulfotransferase 1A1. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27356022/ · DOI 10.1021/acs.biochem.6b00401

experimental_model

Fibril binding/assay-interference experiments.

limitations

Use independent structural and toxicity measurements to distinguish remodeling from dye displacement.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

A lower dye signal alone can be mistaken for less amyloid.

primary_references

Toward the molecular mechanism(s) by which EGCG treatment remodels mature amyloid fibrils. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23611538/ · DOI 10.1021/ja3115696

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 388–394

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Fibril binding/assay-interference experiments. · source_derived_draft · unverified_draft

## egcg-tht A lower dye signal alone can be mistaken for less amyloid. Both oxidized and unoxidized EGCG bound fibrils and prevented Thioflavin T binding. Model: Fibril binding/assay-interference experiments. Limitations: Use independent structural and toxicity measurements to distinguish remodeling from dye displacement. Evidence access: primary abstract. Toward the molecular mechanism(s) by which EGCG treatment remodels mature amyloid fibrils. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23611538/ · DOI 10.1021/ja3115696

experimental_model

Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract.

limitations

Family nodes preserve the unresolved species. This is not evidence of treating systemic human inflammation.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The cells expressed less of the tested inflammatory receptor.

primary_references

TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20511545/ · DOI 10.4049/jimmunol.0903742

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 108–114

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract. · source_derived_draft · unverified_draft

## egcg-tlr4 The cells expressed less of the tested inflammatory receptor. EGCG reduced TLR4 expression through 67LR. Model: Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract. Limitations: Family nodes preserve the unresolved species. This is not evidence of treating systemic human inflammation. Evidence access: primary abstract. TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20511545/ · DOI 10.4049/jimmunol.0903742

experimental_model

Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract.

limitations

Family nodes preserve the unresolved species. This is not evidence of treating systemic human inflammation.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

EGCG increased a brake on inflammatory signaling.

primary_references

TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20511545/ · DOI 10.4049/jimmunol.0903742

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 100–106

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract. · source_derived_draft · unverified_draft

## egcg-tollip EGCG increased a brake on inflammatory signaling. EGCG rapidly increased Tollip expression; 67LR silencing or antibody blockade prevented this. Model: Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract. Limitations: Family nodes preserve the unresolved species. This is not evidence of treating systemic human inflammation. Evidence access: primary abstract. TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20511545/ · DOI 10.4049/jimmunol.0903742

experimental_model

Equilibrium binding and pre-steady-state human SULT enzyme experiments.

limitations

This differs from the later SULT1A1 assignment; assay and product-identification differences require comparison.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

An earlier enzyme study gives a different substrate assignment.

primary_references

Isozyme Specific Allosteric Regulation of Human Sulfotransferase 1A1. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27356022/ · DOI 10.1021/acs.biochem.6b00401

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 300–306

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Equilibrium binding and pre-steady-state human SULT enzyme experiments. · source_derived_draft · unverified_draft

## egcg-sult-not-substrate An earlier enzyme study gives a different substrate assignment. The 2016 SULT1A1 allostery study explicitly reported that EGCG was not a SULT1A1 substrate but was sulfonated by SULT2A1. Model: Equilibrium binding and pre-steady-state human SULT enzyme experiments. Limitations: This differs from the later SULT1A1 assignment; assay and product-identification differences require comparison. Evidence access: primary abstract. Isozyme Specific Allosteric Regulation of Human Sulfotransferase 1A1. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27356022/ · DOI 10.1021/acs.biochem.6b00401

experimental_model

Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study.

limitations

Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

One study identifies this enzyme as a route for processing EGCG.

primary_references

4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 276–282

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. · source_derived_draft · unverified_draft

## egcg-sult1a1-substrate One study identifies this enzyme as a route for processing EGCG. The 2022 study assigned hepatic EGCG sulfation to SULT1A1. Model: Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. Limitations: Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG. Evidence access: primary abstract. 4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150

experimental_model

Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study.

limitations

Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

A different enzyme contributed in the intestinal preparation.

primary_references

4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 284–290

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. · source_derived_draft · unverified_draft

## egcg-sult1a3 A different enzyme contributed in the intestinal preparation. The same study assigned intestinal EGCG sulfation to SULT1A3. Model: Human liver/intestinal cytosol, enzyme assignment and a human ingestion pharmacokinetic study. Limitations: Formation rate and metabolite exposure do not prove identical biological effects of free and conjugated EGCG. Evidence access: primary abstract. 4″-Sulfation Is the Major Metabolic Pathway of Epigallocatechin-3-gallate in Humans: Characterization of Metabolites, Enzymatic Analysis, and Pharmacokinetic Profiling. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35786898/ · DOI 10.1021/acs.jafc.2c02150

experimental_model

Cancer-cell experiments and mouse xenografts in the 2013 study.

limitations

Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Lipid breakdown was part of the experimental death signal.

primary_references

67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 76–82

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-cell experiments and mouse xenografts in the 2013 study. · source_derived_draft · unverified_draft

## egcg-asm Lipid breakdown was part of the experimental death signal. Acid sphingomyelinase participated downstream of PKC delta in 67LR-dependent cell death. Model: Cancer-cell experiments and mouse xenografts in the 2013 study. Limitations: Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety. Evidence access: primary abstract. 67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

experimental_model

CHO-cell experiments.

limitations

Rescue implicates peroxide in this setting; it does not establish oral catalase or antioxidant combinations as treatment.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Removing peroxide reduced the observed cell injury.

primary_references

Different cytotoxic and clastogenic effects of epigallocatechin gallate in various cell-culture media due to variable rates of its oxidation in the culture medium. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17851114/ · DOI 10.1016/j.mrgentox.2007.07.009

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 340–346

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · CHO-cell experiments. · source_derived_draft · unverified_draft

## egcg-catalase Removing peroxide reduced the observed cell injury. Added catalase substantially reduced EGCG cytotoxicity in the culture comparison. Model: CHO-cell experiments. Limitations: Rescue implicates peroxide in this setting; it does not establish oral catalase or antioxidant combinations as treatment. Evidence access: primary abstract. Different cytotoxic and clastogenic effects of epigallocatechin gallate in various cell-culture media due to variable rates of its oxidation in the culture medium. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17851114/ · DOI 10.1016/j.mrgentox.2007.07.009

experimental_model

Cancer-cell experiments and mouse xenografts in the 2013 study.

limitations

Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The receptor signal passed through cGMP.

primary_references

67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 60–66

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-cell experiments and mouse xenografts in the 2013 study. · source_derived_draft · unverified_draft

## egcg-cgmp The receptor signal passed through cGMP. EGCG activation of 67LR increased cGMP, a rate-limiting signal for cell death in the model. Model: Cancer-cell experiments and mouse xenografts in the 2013 study. Limitations: Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety. Evidence access: primary abstract. 67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

experimental_model

Genetic screen, cell signaling and experimental tumor-growth models.

limitations

Pathway dependency in these models does not establish human cancer treatment or a dietary threshold.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The surface signal depends on an intracellular relay.

primary_references

Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 28–34

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Genetic screen, cell signaling and experimental tumor-growth models. · source_derived_draft · unverified_draft

## egcg-eef1a The surface signal depends on an intracellular relay. A genetic screen identified eEF1A as a component of 67LR-dependent EGCG signaling. Model: Genetic screen, cell signaling and experimental tumor-growth models. Limitations: Pathway dependency in these models does not establish human cancer treatment or a dietary threshold. Evidence access: primary abstract. Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200

experimental_model

Purified chicken FAS kinetics.

limitations

This does not show that niacin supplementation cancels EGCG or improves a clinical outcome.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The enzyme’s reducing cofactor altered EGCG inhibition.

primary_references

Green tea epigallocatechin gallate: a natural inhibitor of fatty-acid synthase. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11700039/ · DOI 10.1006/bbrc.2001.5923

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 204–210

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified chicken FAS kinetics. · source_derived_draft · unverified_draft

## egcg-fasn-nadph The enzyme’s reducing cofactor altered EGCG inhibition. NADPH protected against inhibition, and ketoacyl-reductase experiments supported competition near the NADPH-binding function. Model: Purified chicken FAS kinetics. Limitations: This does not show that niacin supplementation cancels EGCG or improves a clinical outcome. Evidence access: primary abstract. Green tea epigallocatechin gallate: a natural inhibitor of fatty-acid synthase. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11700039/ · DOI 10.1006/bbrc.2001.5923

experimental_model

Polyphenon E providing 400, 800 or 1200 mg EGCG; 10 subjects per dose group.

limitations

Mixture and high experimental doses; greater exposure is not a recommendation to take extracts fasting. Nausea was most frequent at 1200 mg fasting.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Food changed how much free EGCG reached the blood.

primary_references

Effects of dosing condition on the oral bioavailability of green tea catechins after single-dose administration of Polyphenon E in healthy individuals. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15958649/ · DOI 10.1158/1078-0432.ccr-04-2549

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 460–466

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Polyphenon E providing 400, 800 or 1200 mg EGCG; 10 subjects per dose group. · source_derived_draft · unverified_draft

## egcg-fasting Food changed how much free EGCG reached the blood. In a 30-person crossover study, fasting produced more than 3.5-fold higher free-EGCG peak concentrations than fed administration. Model: Polyphenon E providing 400, 800 or 1200 mg EGCG; 10 subjects per dose group. Limitations: Mixture and high experimental doses; greater exposure is not a recommendation to take extracts fasting. Nausea was most frequent at 1200 mg fasting. Evidence access: primary abstract. Effects of dosing condition on the oral bioavailability of green tea catechins after single-dose administration of Polyphenon E in healthy individuals. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15958649/ · DOI 10.1158/1078-0432.ccr-04-2549

availability_state

nutrient_deficiency Imported condition classification; unverified.

experimental_model

Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally.

limitations

Do not relabel the purified enzymes as human DHFR or infer that normal tea intake causes folate deficiency.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Low folate made the cultured cells more sensitive.

primary_references

The antifolate activity of tea catechins. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15781612/ · DOI 10.1158/0008-5472.can-04-3469

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 140–146

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally. · source_derived_draft · unverified_draft

## egcg-folate-low Low folate made the cultured cells more sensitive. Folate depletion increased lymphoma-cell sensitivity to EGCG; the reported growth IC50 was 20 micromolar. Model: Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally. Limitations: Do not relabel the purified enzymes as human DHFR or infer that normal tea intake causes folate deficiency. Evidence access: primary abstract. The antifolate activity of tea catechins. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15781612/ · DOI 10.1158/0008-5472.can-04-3469

experimental_model

Women aged 18–40; all groups received extract; selected MTHFR and DHFR genotypes considered.

limitations

No extract-free control, pregnancy outcome or long-term depletion test. Abstract dose terminology is inconsistent; no pure-EGCG dose is inferred.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

This short human study did not reproduce folate depletion.

primary_references

Evaluating the Effect of Epigallocatechin Gallate (EGCG) in Reducing Folate Levels in Reproductive Aged Women by MTHFR and DHFR Genotype in Combination With Letrozole or Clomiphene. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40077973/ · DOI 10.1111/cts.70189

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 156–162

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Women aged 18–40; all groups received extract; selected MTHFR and DHFR genotypes considered. · source_derived_draft · unverified_draft

## egcg-human-folate This short human study did not reproduce folate depletion. In 39 women studied for 30 days, folate stayed in the normal range across EGCG-containing-extract groups, including groups receiving clomiphene or letrozole. Model: Women aged 18–40; all groups received extract; selected MTHFR and DHFR genotypes considered. Limitations: No extract-free control, pregnancy outcome or long-term depletion test. Abstract dose terminology is inconsistent; no pure-EGCG dose is inferred. Evidence access: primary abstract. Evaluating the Effect of Epigallocatechin Gallate (EGCG) in Reducing Folate Levels in Reproductive Aged Women by MTHFR and DHFR Genotype in Combination With Letrozole or Clomiphene. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40077973/ · DOI 10.1111/cts.70189

availability_state

machinery_impairment Imported condition classification; unverified.

experimental_model

Genetic screen, cell signaling and experimental tumor-growth models.

limitations

Pathway dependency in these models does not establish human cancer treatment or a dietary threshold.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Removing pathway components prevented the observed response.

primary_references

Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200

trigger_kind

machinery_impairment Imported condition classification; unverified.

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 52–58

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Genetic screen, cell signaling and experimental tumor-growth models. · source_derived_draft · unverified_draft

## egcg-machinery Removing pathway components prevented the observed response. Silencing MYPT1, eEF1A or 67LR abrogated EGCG-mediated tumor-growth inhibition in the tested models. Model: Genetic screen, cell signaling and experimental tumor-growth models. Limitations: Pathway dependency in these models does not establish human cancer treatment or a dietary threshold. Evidence access: primary abstract. Green tea polyphenol epigallocatechin-3-gallate signaling pathway through 67-kDa laminin receptor. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18079119/ · DOI 10.1074/jbc.m707892200

experimental_model

Amyloid-beta 1–40 and IAPP/Sup35 fragment preparations.

limitations

Fragment and in-vitro oxidation contexts limit generalization.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The oxidation state helped determine aggregate remodeling.

primary_references

Toward the molecular mechanism(s) by which EGCG treatment remodels mature amyloid fibrils. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23611538/ · DOI 10.1021/ja3115696

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 380–386

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Amyloid-beta 1–40 and IAPP/Sup35 fragment preparations. · source_derived_draft · unverified_draft

## egcg-oxidation-remodel The oxidation state helped determine aggregate remodeling. Remodeling of the tested mature amyloid preparations depended on EGCG autooxidation. Model: Amyloid-beta 1–40 and IAPP/Sup35 fragment preparations. Limitations: Fragment and in-vitro oxidation contexts limit generalization. Evidence access: primary abstract. Toward the molecular mechanism(s) by which EGCG treatment remodels mature amyloid fibrils. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23611538/ · DOI 10.1021/ja3115696

experimental_model

Cancer-cell experiments and mouse xenografts in the 2013 study.

limitations

Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

An enzyme that removes cGMP can limit the response.

primary_references

67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 84–90

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-cell experiments and mouse xenografts in the 2013 study. · source_derived_draft · unverified_draft

## egcg-pde5 An enzyme that removes cGMP can limit the response. Overexpressed PDE5 attenuated the cGMP-dependent anticancer signal. Model: Cancer-cell experiments and mouse xenografts in the 2013 study. Limitations: Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety. Evidence access: primary abstract. 67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

experimental_model

Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally.

limitations

Rescue supports pathway involvement but does not prove DHFR is the only target.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Supplying salvage-pathway ingredients partly bypassed the growth effect.

primary_references

The antifolate activity of tea catechins. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15781612/ · DOI 10.1158/0008-5472.can-04-3469

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 148–154

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally. · source_derived_draft · unverified_draft

## egcg-salvage Supplying salvage-pathway ingredients partly bypassed the growth effect. Hypoxanthine plus thymidine attenuated EGCG growth inhibition, consistent with involvement of folate-dependent nucleotide supply. Model: Purified bovine/chicken DHFR and lymphoma-cell experiments; human DHFR interaction was modeled computationally. Limitations: Rescue supports pathway involvement but does not prove DHFR is the only target. Evidence access: primary abstract. The antifolate activity of tea catechins. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15781612/ · DOI 10.1158/0008-5472.can-04-3469

availability_state

machinery_impairment Imported condition classification; unverified.

experimental_model

Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract.

limitations

Family nodes preserve the unresolved species. This is not evidence of treating systemic human inflammation.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

The anti-inflammatory response depended on Tollip.

primary_references

TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20511545/ · DOI 10.4049/jimmunol.0903742

trigger_kind

machinery_impairment Imported condition classification; unverified.

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 116–122

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract. · source_derived_draft · unverified_draft

## egcg-tollip-gate The anti-inflammatory response depended on Tollip. Tollip silencing impaired EGCG inhibition of TLR4 signaling. Model: Macrophage LPS-response experiments, EGCG 1 micromolar; organism not assigned from abstract. Limitations: Family nodes preserve the unresolved species. This is not evidence of treating systemic human inflammation. Evidence access: primary abstract. TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20511545/ · DOI 10.4049/jimmunol.0903742

experimental_model

Cancer-cell experiments and mouse xenografts in the 2013 study.

limitations

Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Blocking the opposing enzyme strengthened the response in these models.

primary_references

67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 92–98

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cancer-cell experiments and mouse xenografts in the 2013 study. · source_derived_draft · unverified_draft

## egcg-vardenafil Blocking the opposing enzyme strengthened the response in these models. PDE5 inhibition with vardenafil potentiated EGCG-dependent apoptosis and prolonged survival in a mouse xenograft experiment. Model: Cancer-cell experiments and mouse xenografts in the 2013 study. Limitations: Preclinical combination experiments; normal-cell selectivity in tested preparations is not universal safety. Evidence access: primary abstract. 67-kDa laminin receptor increases cGMP to induce cancer-selective apoptosis. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23348740/ · DOI 10.1172/jci64768

experimental_model

In-vitro gastric/small-intestinal digestion with HPLC recovery.

limitations

Recovery is chemical survival, not measured human absorption or clinical synergy.

nutrient_topic

EGCG collection; comparator and shared-pathway records retain their actual intervention. · Epigallocatechin-3-gallate (EGCG)

plain_language

Vitamin C protected EGCG in a simulated digestive system.

primary_references

Common tea formulations modulate in vitro digestive recovery of green tea catechins. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17688297/ · DOI 10.1002/mnfr.200700086

EGCG: receptor signaling, metabolism, nutrient interactions and discovery questions (2026-09-18) · lines 452–458

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · In-vitro gastric/small-intestinal digestion with HPLC recovery. · source_derived_draft · unverified_draft

## egcg-vitc-stability Vitamin C protected EGCG in a simulated digestive system. Adding 30 mg ascorbic acid to 250 mL tea increased EGCG recovery after simulated digestion to 54%, versus at most 10% without protective formulation. Model: In-vitro gastric/small-intestinal digestion with HPLC recovery. Limitations: Recovery is chemical survival, not measured human absorption or clinical synergy. Evidence access: primary abstract. Common tea formulations modulate in vitro digestive recovery of green tea catechins. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17688297/ · DOI 10.1002/mnfr.200700086