Component
Histamine
Histamine
15 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
Histamine-bound human H1 receptor was resolved with an engineered Gq-family protein complex, with binding and functional mutagenesis supporting ligand recognition and coupling.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays.
- limitations
- Structural stabilization, chimeric/mini G proteins and recombinant cells differ from native tissues; receptor engagement is not proof that oral histidine produces this response.
- nutrient_topic
- L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
- plain_language
- The same histidine-derived messenger can activate a distinct receptor route.
- primary_references
- Structural basis of ligand recognition and activation of the histamine receptor family. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39333117/ · DOI 10.1038/s41467-024-52585-y
L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 226–232
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays. · source_derived_draft · unverified_draft
## histidine-h1-activation The same histidine-derived messenger can activate a distinct receptor route. Histamine-bound human H1 receptor was resolved with an engineered Gq-family protein complex, with binding and functional mutagenesis supporting ligand recognition and coupling. Model: Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays. Limitations: Structural stabilization, chimeric/mini G proteins and recombinant cells differ from native tissues; receptor engagement is not proof that oral histidine produces this response. Evidence access: Primary full text Structural basis of ligand recognition and activation of the histamine receptor family. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39333117/ · DOI 10.1038/s41467-024-52585-y
Complete structured claim and evidenceHistamine-bound human H2 receptor was resolved with an engineered Gs-family protein complex, with binding and functional mutagenesis supporting ligand recognition and coupling.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays.
- limitations
- Structural stabilization, chimeric/mini G proteins and recombinant cells differ from native tissues; receptor engagement is not proof that oral histidine produces this response.
- nutrient_topic
- L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
- plain_language
- The same histidine-derived messenger can activate a distinct receptor route.
- primary_references
- Structural basis of ligand recognition and activation of the histamine receptor family. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39333117/ · DOI 10.1038/s41467-024-52585-y
L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 234–240
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays. · source_derived_draft · unverified_draft
## histidine-h2-activation The same histidine-derived messenger can activate a distinct receptor route. Histamine-bound human H2 receptor was resolved with an engineered Gs-family protein complex, with binding and functional mutagenesis supporting ligand recognition and coupling. Model: Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays. Limitations: Structural stabilization, chimeric/mini G proteins and recombinant cells differ from native tissues; receptor engagement is not proof that oral histidine produces this response. Evidence access: Primary full text Structural basis of ligand recognition and activation of the histamine receptor family. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39333117/ · DOI 10.1038/s41467-024-52585-y
Complete structured claim and evidenceHistamine-bound human H3 receptor was resolved with an engineered Gi-family protein complex, with binding and functional mutagenesis supporting ligand recognition and coupling.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays.
- limitations
- Structural stabilization, chimeric/mini G proteins and recombinant cells differ from native tissues; receptor engagement is not proof that oral histidine produces this response.
- nutrient_topic
- L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
- plain_language
- The same histidine-derived messenger can activate a distinct receptor route.
- primary_references
- Structural basis of ligand recognition and activation of the histamine receptor family. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39333117/ · DOI 10.1038/s41467-024-52585-y
L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 242–248
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays. · source_derived_draft · unverified_draft
## histidine-h3-activation The same histidine-derived messenger can activate a distinct receptor route. Histamine-bound human H3 receptor was resolved with an engineered Gi-family protein complex, with binding and functional mutagenesis supporting ligand recognition and coupling. Model: Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays. Limitations: Structural stabilization, chimeric/mini G proteins and recombinant cells differ from native tissues; receptor engagement is not proof that oral histidine produces this response. Evidence access: Primary full text Structural basis of ligand recognition and activation of the histamine receptor family. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39333117/ · DOI 10.1038/s41467-024-52585-y
Complete structured claim and evidenceHistamine-bound human H4 receptor was resolved with an engineered Gi-family protein complex, with binding and functional mutagenesis supporting ligand recognition and coupling.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays.
- limitations
- Structural stabilization, chimeric/mini G proteins and recombinant cells differ from native tissues; receptor engagement is not proof that oral histidine produces this response.
- nutrient_topic
- L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
- plain_language
- The same histidine-derived messenger can activate a distinct receptor route.
- primary_references
- Structural basis of ligand recognition and activation of the histamine receptor family. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39333117/ · DOI 10.1038/s41467-024-52585-y
L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 250–256
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays. · source_derived_draft · unverified_draft
## histidine-h4-activation The same histidine-derived messenger can activate a distinct receptor route. Histamine-bound human H4 receptor was resolved with an engineered Gi-family protein complex, with binding and functional mutagenesis supporting ligand recognition and coupling. Model: Engineered human receptor complexes produced in insect cells, cryo-EM and HEK293 binding/G-protein assays. Limitations: Structural stabilization, chimeric/mini G proteins and recombinant cells differ from native tissues; receptor engagement is not proof that oral histidine produces this response. Evidence access: Primary full text Structural basis of ligand recognition and activation of the histamine receptor family. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39333117/ · DOI 10.1038/s41467-024-52585-y
Complete structured claim and evidence
What acts on it
Human diamine oxidase has a substrate pocket adapted to diamines including histamine, distinct from that of AOC3.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/copper-research/19764817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9a01d0dba5caec8a33a77fdbe7190d7a05bdd6e691a570a890eb6b19d4c692b6", "start_char": 0, "end_char": 1343, "text_sha256": "9a01d0dba5caec8a33a77fdbe7190d7a05bdd6e691a570a890eb6b19d4c692b6"}
- experimental_model
- Crystallography of recombinant human diamine oxidase and inhibitor complexes
- exposure
- Native structure and inhibitor binding
- limitations
- Copper/TPQ dependence is molecular evidence, not a trial of copper for histamine intolerance; DAO activity can have multiple determinants.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Human AOC1 expressed in insect cells
- plain_language
- Related copper enzymes process different amines.
- primary_references
- [copper-p19764817] Structure and inhibition of human diamine oxidase. (2009). https://pubmed.ncbi.nlm.nih.gov/19764817/ DOI: 10.1021/bi9014192
- tissue_or_cell_type
- Purified protein
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1027–1038
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Crystallography of recombinant human diamine oxidase and inhibitor complexes · source_derived_draft · unverified_draft
### copper-aoc1-histamine-specificity Human diamine oxidase has a substrate pocket adapted to diamines including histamine, distinct from that of AOC3. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Related copper enzymes process different amines. organism: Human AOC1 expressed in insect cells tissue_or_cell_type: Purified protein experimental_model: Crystallography of recombinant human diamine oxidase and inhibitor complexes limitations: Copper/TPQ dependence is molecular evidence, not a trial of copper for histamine intolerance; DAO activity can have multiple determinants. exposure: Native structure and inhibitor binding evidence_span: {"source_cache": "artifacts/copper-research/19764817.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9a01d0dba5caec8a33a77fdbe7190d7a05bdd6e691a570a890eb6b19d4c692b6", "start_char": 0, "end_char": 1343, "text_sha256": "9a01d0dba5caec8a33a77fdbe7190d7a05bdd6e691a570a890eb6b19d4c692b6"} [copper-p19764817] Structure and inhibition of human diamine oxidase. (2009). https://pubmed.ncbi.nlm.nih.gov/19764817/ DOI: 10.1021/bi9014192
Complete structured claim and evidenceRecombinant human HDC catalyzes PLP-dependent histidine decarboxylation to histamine.
Experimental context and source evidence
- experimental_model
- Recombinant engineered human HDC; crystallography and enzyme assays
- exposure
- Recombinant HDC enzyme-activity assays.
- limitations
- Engineered soluble HDC construct; histamine release and allergy outcomes were not tested.
- nutrient_topic
- Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
- organism
- Homo sapiens
- plain_language
- Activated B6 supports histamine synthesis.
- primary_references
- [komori-2012-hdc] Structural Study Reveals That Ser-354 Determines Substrate Specificity on Human Histidine Decarboxylase (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3436558/ DOI: 10.1074/jbc.M112.381897
- tissue_or_cell_type
- Purified recombinant protein; no intact tissue
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1047–1057
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant engineered human HDC; crystallography and enzyme assays · source_derived_draft · unverified_draft
### b6-neuro-hdc-histamine Recombinant human HDC catalyzes PLP-dependent histidine decarboxylation to histamine. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activated B6 supports histamine synthesis. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant engineered human HDC; crystallography and enzyme assays limitations: Engineered soluble HDC construct; histamine release and allergy outcomes were not tested. exposure: Recombinant HDC enzyme-activity assays. [komori-2012-hdc] Structural Study Reveals That Ser-354 Determines Substrate Specificity on Human Histidine Decarboxylase (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3436558/ DOI: 10.1074/jbc.M112.381897
Complete structured claim and evidenceLuteolin reduced stimulated histamine release from human LAD2 mast cells; tetramethoxyluteolin was more potent.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human mast-cell cultures; 1–100 micromolar pretreatment.
- limitations
- Do not assign the analog’s animal or calcium results to luteolin.
- nutrient_topic
- Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
- plain_language
- Related flavones have different potencies.
- primary_references
- The novel flavone tetramethoxyluteolin is a potent inhibitor of human mast cells. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25498791/ · DOI 10.1016/j.jaci.2014.10.032
Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 388–394
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human mast-cell cultures; 1–100 micromolar pretreatment. · source_derived_draft · unverified_draft
## luteolin-mast-histamine Related flavones have different potencies. Luteolin reduced stimulated histamine release from human LAD2 mast cells; tetramethoxyluteolin was more potent. Model: Human mast-cell cultures; 1–100 micromolar pretreatment. Limitations: Do not assign the analog’s animal or calcium results to luteolin. Evidence access: Primary abstract The novel flavone tetramethoxyluteolin is a potent inhibitor of human mast cells. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25498791/ · DOI 10.1016/j.jaci.2014.10.032
Complete structured claim and evidenceSS-FA at 0.1-10 micrograms/mL reduced PMA/calcium-ionophore-induced histamine release from KU812 cells.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human basophilic leukemia KU812 cells; 15-minute pretreatment, PMA 20 nM plus A23187 1 micromolar.
- limitations
- Sludge-derived research material is not a dietary ingredient recommendation. This does not establish human allergy treatment or direct calcium chelation.
- nutrient_topic
- Fulvic acid collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Fulvic acid (heterogeneous humic fraction)
- plain_language
- One preparation reduced triggered mediator release.
- primary_references
- Microarray analysis of immediate-type allergy in KU812 cells in response to fulvic acid. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21331654/ · DOI 10.1007/s10616-010-9333-6
Fulvic acid: mixture identity, mineral chemistry, signaling and cross-nutrient mechanisms (2026-09-19) · lines 108–114
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human basophilic leukemia KU812 cells; 15-minute pretreatment, PMA 20 nM plus A23187 1 micromolar. · source_derived_draft · unverified_draft
## fulvic-acid-histamine One preparation reduced triggered mediator release. SS-FA at 0.1-10 micrograms/mL reduced PMA/calcium-ionophore-induced histamine release from KU812 cells. Model: Human basophilic leukemia KU812 cells; 15-minute pretreatment, PMA 20 nM plus A23187 1 micromolar. Limitations: Sludge-derived research material is not a dietary ingredient recommendation. This does not establish human allergy treatment or direct calcium chelation. Evidence access: Primary abstract Microarray analysis of immediate-type allergy in KU812 cells in response to fulvic acid. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21331654/ · DOI 10.1007/s10616-010-9333-6
Complete structured claim and evidenceMyricetin inhibited anti-IgE-stimulated histamine release from cultured human cord-blood mast cells.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested.
- limitations
- No oral allergy trial; reduced phosphorylation is not direct kinase inhibition.
- nutrient_topic
- Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
- plain_language
- The allergic response involves multiple independently recorded steps.
- primary_references
- Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15912140/ · DOI 10.1038/sj.bjp.0706246
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 420–426
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested. · source_derived_draft · unverified_draft
## myricetin-mast-histamine The allergic response involves multiple independently recorded steps. Myricetin inhibited anti-IgE-stimulated histamine release from cultured human cord-blood mast cells. Model: Human cord-blood-derived mast cells; 15-minute pretreatment, 0.01–100 micromolar tested. Limitations: No oral allergy trial; reduced phosphorylation is not direct kinase inhibition. Evidence access: Primary abstract Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15912140/ · DOI 10.1038/sj.bjp.0706246
Complete structured claim and evidence
Where it participates (unsigned role)
Tartrazine at 0.1-1 mM augmented A23187-triggered histamine release in the rat mast-cell assay.
Experimental context and source evidence
- dose
- Tartrazine 0.1-1 mM with calcium ionophore A23187
- duration
- Maximum augmentation with 0-5 min preincubation
- evidence_access
- Primary PubMed abstract; unrecovered method details explicitly retained.
- evidence_scope
- literature_reviewed; source-specific experimental curation
- experimental_model
- Purified rat peritoneal mast cells
- limitations
- The ionophore interaction cannot be generalized to every mast-cell stimulus; higher concentrations had a small inhibitory effect.
- nutrient_topic
- Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
- organism
- Purified rat peritoneal mast cells
- plain_language
- Tartrazine at 0.1-1 mM augmented A23187-triggered histamine release in the rat mast-cell assay.
- primary_references
- The effect of tartrazine on histamine release from rat peritoneal mast cells. (1984). https://pubmed.ncbi.nlm.nih.gov/6204951/ DOI: 10.1016/0192-0561(84)90021-3
- route
- In vitro preincubation and challenge
- tissue
- Calcium-ionophore-triggered histamine release
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 468–477
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Purified rat peritoneal mast cells · source_derived_draft · unverified_draft
## tartrazine-mast-cell-augmentation Tartrazine at 0.1-1 mM augmented A23187-triggered histamine release in the rat mast-cell assay. Model/species: Purified rat peritoneal mast cells Tissue: Calcium-ionophore-triggered histamine release Exposure: Tartrazine 0.1-1 mM with calcium ionophore A23187 Route: In vitro preincubation and challenge Duration: Maximum augmentation with 0-5 min preincubation Limits: The ionophore interaction cannot be generalized to every mast-cell stimulus; higher concentrations had a small inhibitory effect. Primary reference: The effect of tartrazine on histamine release from rat peritoneal mast cells. (1984). https://pubmed.ncbi.nlm.nih.gov/6204951/ DOI: 10.1016/0192-0561(84)90021-3 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidenceTartrazine inhibited compound-48/80- and antigen-triggered histamine release from rat peritoneal mast cells.
Experimental context and source evidence
- dose
- Tartrazine 10 micromolar-10 mM with compound 48/80 or egg-albumin challenge
- duration
- Acute release assay; antigen inhibition strongest with simultaneous addition
- evidence_access
- Primary PubMed abstract; unrecovered method details explicitly retained.
- evidence_scope
- literature_reviewed; source-specific experimental curation
- experimental_model
- Purified rat peritoneal mast cells
- limitations
- Secretagogue and timing alter the response. This is not a demonstration of spontaneous histamine release or a human allergic mechanism.
- nutrient_topic
- Tartrazine food-colorant chapter; nutrient, drug and peptide interactions retain their models and limits. · Tartrazine
- organism
- Purified rat peritoneal mast cells
- plain_language
- Tartrazine inhibited compound-48/80- and antigen-triggered histamine release from rat peritoneal mast cells.
- primary_references
- The effect of tartrazine on histamine release from rat peritoneal mast cells. (1984). https://pubmed.ncbi.nlm.nih.gov/6204951/ DOI: 10.1016/0192-0561(84)90021-3
- route
- In vitro co-exposure
- tissue
- Secretagogue-induced histamine release
Tartrazine: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 457–466
Original AI-assisted curation of eighteen primary studies. Study-specific citations, negative findings and limitations retained. Not publisher full text. · supports · Purified rat peritoneal mast cells · source_derived_draft · unverified_draft
## tartrazine-mast-cell-inhibition Tartrazine inhibited compound-48/80- and antigen-triggered histamine release from rat peritoneal mast cells. Model/species: Purified rat peritoneal mast cells Tissue: Secretagogue-induced histamine release Exposure: Tartrazine 10 micromolar-10 mM with compound 48/80 or egg-albumin challenge Route: In vitro co-exposure Duration: Acute release assay; antigen inhibition strongest with simultaneous addition Limits: Secretagogue and timing alter the response. This is not a demonstration of spontaneous histamine release or a human allergic mechanism. Primary reference: The effect of tartrazine on histamine release from rat peritoneal mast cells. (1984). https://pubmed.ncbi.nlm.nih.gov/6204951/ DOI: 10.1016/0192-0561(84)90021-3 Access: Primary PubMed abstract; unrecovered method details explicitly retained.
Complete structured claim and evidenceHuman H2 receptor W222A/V mutations abolished measured Gs activation while retaining Gq responses; the structural Gq complex used a G-alpha-s/q chimera.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Recombinant human receptor mutagenesis and G-protein dissociation assays.
- limitations
- Do not label H2 as exclusively Gs-coupled; chimera-supported structure and native Gq signaling are distinct evidence types.
- nutrient_topic
- L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
- plain_language
- A receptor can use more than one signaling partner, with separable structural requirements.
- primary_references
- Structural basis of ligand recognition and activation of the histamine receptor family. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39333117/ · DOI 10.1038/s41467-024-52585-y
L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 258–264
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human receptor mutagenesis and G-protein dissociation assays. · source_derived_draft · unverified_draft
## histidine-h2-coupling-selectivity A receptor can use more than one signaling partner, with separable structural requirements. Human H2 receptor W222A/V mutations abolished measured Gs activation while retaining Gq responses; the structural Gq complex used a G-alpha-s/q chimera. Model: Recombinant human receptor mutagenesis and G-protein dissociation assays. Limitations: Do not label H2 as exclusively Gs-coupled; chimera-supported structure and native Gq signaling are distinct evidence types. Evidence access: Primary full text Structural basis of ligand recognition and activation of the histamine receptor family. · 2024 · https://pubmed.ncbi.nlm.nih.gov/39333117/ · DOI 10.1038/s41467-024-52585-y
Complete structured claim and evidenceHuman HNMT methylates histamine using SAM; structural complexes locate histamine and the reaction product SAH at the enzyme.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Purified recombinant human enzyme; ternary structures and steady-state kinetics.
- limitations
- A shared SAM requirement does not prove clinically important methyl depletion from histamine turnover.
- nutrient_topic
- L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
- plain_language
- Histamine disposal connects to the cellular methyl-donor system.
- primary_references
- Two polymorphic forms of human histamine methyltransferase: structural, thermal, and kinetic comparisons. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11566133/ · DOI 10.1016/s0969-2126(01)00643-8
L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 210–216
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified recombinant human enzyme; ternary structures and steady-state kinetics. · source_derived_draft · unverified_draft
## histidine-hnmt-methylation Histamine disposal connects to the cellular methyl-donor system. Human HNMT methylates histamine using SAM; structural complexes locate histamine and the reaction product SAH at the enzyme. Model: Purified recombinant human enzyme; ternary structures and steady-state kinetics. Limitations: A shared SAM requirement does not prove clinically important methyl depletion from histamine turnover. Evidence access: Primary abstract Two polymorphic forms of human histamine methyltransferase: structural, thermal, and kinetic comparisons. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11566133/ · DOI 10.1016/s0969-2126(01)00643-8
Complete structured claim and evidenceRecombinant Ile105 HNMT had about 16 percent lower specific activity and higher apparent Km for SAM and histamine than Thr105 across 25-45 degrees C.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human recombinant enzyme comparison.
- limitations
- Results paragraph reports increased Km; the abstract conclusion says lowered Km. Numerical results are retained as a source wording discrepancy, not two independent experiments. No clinical symptom prediction.
- nutrient_topic
- L-Histidine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Histidine
- plain_language
- A common enzyme variant changed the measured reaction kinetics.
- primary_references
- Two polymorphic forms of human histamine methyltransferase: structural, thermal, and kinetic comparisons. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11566133/ · DOI 10.1016/s0969-2126(01)00643-8
L-Histidine: supply, catabolism, histamine, receptors and cross-nutrient mechanisms (2026-09-19) · lines 218–224
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human recombinant enzyme comparison. · source_derived_draft · unverified_draft
## histidine-hnmt-variant A common enzyme variant changed the measured reaction kinetics. Recombinant Ile105 HNMT had about 16 percent lower specific activity and higher apparent Km for SAM and histamine than Thr105 across 25-45 degrees C. Model: Human recombinant enzyme comparison. Limitations: Results paragraph reports increased Km; the abstract conclusion says lowered Km. Numerical results are retained as a source wording discrepancy, not two independent experiments. No clinical symptom prediction. Evidence access: Primary abstract Two polymorphic forms of human histamine methyltransferase: structural, thermal, and kinetic comparisons. · 2001 · https://pubmed.ncbi.nlm.nih.gov/11566133/ · DOI 10.1016/s0969-2126(01)00643-8
Complete structured claim and evidenceCarnosine treatment reduced infarct size in both wild-type and histidine-decarboxylase-null mice after permanent MCAO.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse cerebral ischemia with Hdc knockout.
- limitations
- Preclinical intervention; not stroke treatment guidance.
- nutrient_topic
- Carnosine collection; isomer, preparation, species, exposure and manipulation remain explicit. · L-Carnosine / beta-alanyl-L-histidine
- plain_language
- Protection in this model did not require histamine synthesis.
- primary_references
- Carnosine protects against permanent cerebral ischemia in histidine decarboxylase knockout mice by reducing glutamate excitotoxicity. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20043985/ · DOI 10.1016/j.freeradbiomed.2009.12.021
Carnosine: synthesis, transport, carbonyl chemistry and nutrient interactions (2026-09-19) · lines 460–466
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse cerebral ischemia with Hdc knockout. · source_derived_draft · unverified_draft
## carnosine-ischemia-hdc Protection in this model did not require histamine synthesis. Carnosine treatment reduced infarct size in both wild-type and histidine-decarboxylase-null mice after permanent MCAO. Model: Mouse cerebral ischemia with Hdc knockout. Limitations: Preclinical intervention; not stroke treatment guidance. Evidence access: Primary abstract Carnosine protects against permanent cerebral ischemia in histidine decarboxylase knockout mice by reducing glutamate excitotoxicity. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20043985/ · DOI 10.1016/j.freeradbiomed.2009.12.021
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