Phosphatidylinositol 4,5-bisphosphate

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/inositol-research/33875602.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "139eeba386e63329898f8e36ebe93ad741eed904819bbebe7fc2b1808130a19d", "start_char": 0, "end_char": 1108, "text_sha256": "139eeba386e63329898f8e36ebe93ad741eed904819bbebe7fc2b1808130a19d"}

experimental_model

Genetic small-vessel disease mouse model and lipid rescue

exposure

PIP2 depletion and soluble PIP2 administration

limitations

Mouse disease model; not evidence that oral inositol treats human cerebrovascular disease.

nutrient_topic

Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

organism

Mus musculus

plain_language

Replacing the deficient lipid signal restored a blood-flow response in these mice.

primary_references

[ino-p33875602] PIP2 corrects cerebral blood flow deficits in small vessel disease by rescuing capillary Kir2.1 activity. (2021). https://pubmed.ncbi.nlm.nih.gov/33875602/ DOI: 10.1073/pnas.2025998118

tissue_or_cell_type

Brain capillary endothelium and cerebral circulation

trigger_kind

machinery_impairment Imported condition classification; unverified.

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1029–1040

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic small-vessel disease mouse model and lipid rescue · source_derived_draft · unverified_draft

### ino-kir-flow-rescue Soluble PIP2 administration restored Kir2.1-dependent neurovascular responses in the studied mouse model. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Replacing the deficient lipid signal restored a blood-flow response in these mice. organism: Mus musculus tissue_or_cell_type: Brain capillary endothelium and cerebral circulation experimental_model: Genetic small-vessel disease mouse model and lipid rescue limitations: Mouse disease model; not evidence that oral inositol treats human cerebrovascular disease. exposure: PIP2 depletion and soluble PIP2 administration evidence_span: {"source_cache": "artifacts/inositol-research/33875602.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "139eeba386e63329898f8e36ebe93ad741eed904819bbebe7fc2b1808130a19d", "start_char": 0, "end_char": 1108, "text_sha256": "139eeba386e63329898f8e36ebe93ad741eed904819bbebe7fc2b1808130a19d"} [ino-p33875602] PIP2 corrects cerebral blood flow deficits in small vessel disease by rescuing capillary Kir2.1 activity. (2021). https://pubmed.ncbi.nlm.nih.gov/33875602/ DOI: 10.1073/pnas.2025998118

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/inositol-research/33875602.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "139eeba386e63329898f8e36ebe93ad741eed904819bbebe7fc2b1808130a19d", "start_char": 0, "end_char": 1108, "text_sha256": "139eeba386e63329898f8e36ebe93ad741eed904819bbebe7fc2b1808130a19d"}

experimental_model

Genetic small-vessel disease mouse model and lipid rescue

exposure

PIP2 depletion and soluble PIP2 administration

limitations

Mouse disease model; not evidence that oral inositol treats human cerebrovascular disease.

nutrient_topic

Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

organism

Mus musculus

plain_language

The potassium channel can fail because its supporting lipid is missing, even though the channel protein remains.

primary_references

[ino-p33875602] PIP2 corrects cerebral blood flow deficits in small vessel disease by rescuing capillary Kir2.1 activity. (2021). https://pubmed.ncbi.nlm.nih.gov/33875602/ DOI: 10.1073/pnas.2025998118

tissue_or_cell_type

Brain capillary endothelium and cerebral circulation

trigger_kind

machinery_impairment Imported condition classification; unverified.

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1016–1027

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic small-vessel disease mouse model and lipid rescue · source_derived_draft · unverified_draft

### ino-kir-pip2 PIP2 depletion in the studied mouse small-vessel disease model impaired endothelial Kir2.1 activity. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The potassium channel can fail because its supporting lipid is missing, even though the channel protein remains. organism: Mus musculus tissue_or_cell_type: Brain capillary endothelium and cerebral circulation experimental_model: Genetic small-vessel disease mouse model and lipid rescue limitations: Mouse disease model; not evidence that oral inositol treats human cerebrovascular disease. exposure: PIP2 depletion and soluble PIP2 administration evidence_span: {"source_cache": "artifacts/inositol-research/33875602.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "139eeba386e63329898f8e36ebe93ad741eed904819bbebe7fc2b1808130a19d", "start_char": 0, "end_char": 1108, "text_sha256": "139eeba386e63329898f8e36ebe93ad741eed904819bbebe7fc2b1808130a19d"} [ino-p33875602] PIP2 corrects cerebral blood flow deficits in small vessel disease by rescuing capillary Kir2.1 activity. (2021). https://pubmed.ncbi.nlm.nih.gov/33875602/ DOI: 10.1073/pnas.2025998118

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/inositol-research/16707555.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b411ec23aa4b3ee2a861a8a9a99811acb039a03c18015a5954a1f90971d175ef", "start_char": 0, "end_char": 1640, "text_sha256": "b411ec23aa4b3ee2a861a8a9a99811acb039a03c18015a5954a1f90971d175ef"}

experimental_model

Cardiac patch clamp and lipid/ATP manipulation

exposure

ATP withdrawal, analogs and exogenous PIP2

limitations

The current was described as TRPM7-like; this experiment alone does not establish its molecular identity.

nutrient_topic

Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

organism

Pig, rat and guinea pig cardiac cells

plain_language

Restoring the membrane signal bypassed one consequence of ATP depletion in this assay.

primary_references

[ino-p16707555] ATP and PIP2 dependence of the magnesium-inhibited, TRPM7-like cation channel in cardiac myocytes. (2006). https://pubmed.ncbi.nlm.nih.gov/16707555/ DOI: 10.1152/ajpcell.00074.2006

tissue_or_cell_type

Cardiac magnesium-inhibited current

trigger_kind

machinery_impairment Imported condition classification; unverified.

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1003–1014

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cardiac patch clamp and lipid/ATP manipulation · source_derived_draft · unverified_draft

### ino-mic-pip2-rescue Exogenous PIP2 restored cardiac MIC current after rundown in ATP-depleted conditions. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring the membrane signal bypassed one consequence of ATP depletion in this assay. organism: Pig, rat and guinea pig cardiac cells tissue_or_cell_type: Cardiac magnesium-inhibited current experimental_model: Cardiac patch clamp and lipid/ATP manipulation limitations: The current was described as TRPM7-like; this experiment alone does not establish its molecular identity. exposure: ATP withdrawal, analogs and exogenous PIP2 evidence_span: {"source_cache": "artifacts/inositol-research/16707555.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b411ec23aa4b3ee2a861a8a9a99811acb039a03c18015a5954a1f90971d175ef", "start_char": 0, "end_char": 1640, "text_sha256": "b411ec23aa4b3ee2a861a8a9a99811acb039a03c18015a5954a1f90971d175ef"} [ino-p16707555] ATP and PIP2 dependence of the magnesium-inhibited, TRPM7-like cation channel in cardiac myocytes. (2006). https://pubmed.ncbi.nlm.nih.gov/16707555/ DOI: 10.1152/ajpcell.00074.2006

evidence_span

{"source_cache": "artifacts/inositol-research/11941371.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5b6343b08188b699a19591013fdcd2d9d604f8ae15adc5771b4bc677369d10b0", "start_char": 0, "end_char": 729, "text_sha256": "5b6343b08188b699a19591013fdcd2d9d604f8ae15adc5771b4bc677369d10b0"}

experimental_model

Electrophysiology and phosphoinositide manipulation

exposure

PLC activation and PIP2 depletion

limitations

PIP2 regulation is conditional; the 2007 study shows intracellular Mg and patch configuration can reverse the PLC response.

nutrient_topic

Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

organism

Mammalian heterologous cells and cardiac preparations

plain_language

A membrane inositol lipid helps regulate a channel that carries mineral ions; the response depends on the recording conditions.

primary_references

[ino-p11941371] The TRPM7 channel is inactivated by PIP(2) hydrolysis. (2002). https://pubmed.ncbi.nlm.nih.gov/11941371/ DOI: 10.1038/ncb781

tissue_or_cell_type

TRPM7-associated membrane currents

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 951–962

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electrophysiology and phosphoinositide manipulation · source_derived_draft · unverified_draft

### ino-pip2-trpm7 TRPM7 currents depended on PI(4,5)P2 in the reported experiments, and PLC-mediated PIP2 hydrolysis inhibited the current. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A membrane inositol lipid helps regulate a channel that carries mineral ions; the response depends on the recording conditions. organism: Mammalian heterologous cells and cardiac preparations tissue_or_cell_type: TRPM7-associated membrane currents experimental_model: Electrophysiology and phosphoinositide manipulation limitations: PIP2 regulation is conditional; the 2007 study shows intracellular Mg and patch configuration can reverse the PLC response. exposure: PLC activation and PIP2 depletion evidence_span: {"source_cache": "artifacts/inositol-research/11941371.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5b6343b08188b699a19591013fdcd2d9d604f8ae15adc5771b4bc677369d10b0", "start_char": 0, "end_char": 729, "text_sha256": "5b6343b08188b699a19591013fdcd2d9d604f8ae15adc5771b4bc677369d10b0"} [ino-p11941371] The TRPM7 channel is inactivated by PIP(2) hydrolysis. (2002). https://pubmed.ncbi.nlm.nih.gov/11941371/ DOI: 10.1038/ncb781

cross_nutrient

false

experimental_model

X-ray complex PDB 3W68

exposure

Crystallized protein with alpha-tocopherol and PI(4,5)P2.

limitations

Structure is mouse protein; no dietary phosphorus requirement or human affinity value is inferred.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Mus musculus protein

plain_language

A membrane phosphoinositide interacts with the vitamin E transfer protein.

primary_references

[kono2013] Impaired α-TTP-PIPs interaction underlies familial vitamin E deficiency. (2013). https://pubmed.ncbi.nlm.nih.gov/23599266/ DOI: 10.1126/science.1233508

tissue_or_cell_type

Purified protein-lipid complex

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 324–335

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · X-ray complex PDB 3W68 · source_derived_draft · unverified_draft

### ve-transport-mouse-ttp-pip2-binding The deposited mouse alpha-TTP complex contains alpha-tocopherol and PI(4,5)P2, with phosphoinositide binding at the protein surface linked to opening of its ligand pocket. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: A membrane phosphoinositide interacts with the vitamin E transfer protein. organism: Mus musculus protein tissue_or_cell_type: Purified protein-lipid complex experimental_model: X-ray complex PDB 3W68 limitations: Structure is mouse protein; no dietary phosphorus requirement or human affinity value is inferred. exposure: Crystallized protein with alpha-tocopherol and PI(4,5)P2. cross_nutrient: false [kono2013] Impaired α-TTP-PIPs interaction underlies familial vitamin E deficiency. (2013). https://pubmed.ncbi.nlm.nih.gov/23599266/ DOI: 10.1126/science.1233508

evidence_span

{"source_cache": "artifacts/inositol-research/28882892.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "39494635d8bd1a8a8df3ac71f8aa6c5f6440bd3c6fa7cb4756e52d572a8f16db", "start_char": 0, "end_char": 1781, "text_sha256": "39494635d8bd1a8a8df3ac71f8aa6c5f6440bd3c6fa7cb4756e52d572a8f16db"}

experimental_model

Crystal structures and targeted human IPMK mutants

exposure

IP3 and PI(4,5)P2 substrate binding and phosphorylation

limitations

Human substrate specificity differs from yeast and plant orthologs; do not merge their regioselectivity.

nutrient_topic

Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

organism

Human protein

plain_language

One enzyme acts on both soluble inositol phosphates and a membrane lipid.

primary_references

[ino-p28882892] Structural features of human inositol phosphate multikinase rationalize its inositol phosphate kinase and phosphoinositide 3-kinase activities. (2017). https://pubmed.ncbi.nlm.nih.gov/28882892/ DOI: 10.1074/jbc.m117.801845

tissue_or_cell_type

Purified IPMK

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 691–702

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Crystal structures and targeted human IPMK mutants · source_derived_draft · unverified_draft

### ino-ipmk-pip3 Human IPMK also has PI(4,5)P2 3-kinase activity, producing PI(3,4,5)P3. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: One enzyme acts on both soluble inositol phosphates and a membrane lipid. organism: Human protein tissue_or_cell_type: Purified IPMK experimental_model: Crystal structures and targeted human IPMK mutants limitations: Human substrate specificity differs from yeast and plant orthologs; do not merge their regioselectivity. exposure: IP3 and PI(4,5)P2 substrate binding and phosphorylation evidence_span: {"source_cache": "artifacts/inositol-research/28882892.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "39494635d8bd1a8a8df3ac71f8aa6c5f6440bd3c6fa7cb4756e52d572a8f16db", "start_char": 0, "end_char": 1781, "text_sha256": "39494635d8bd1a8a8df3ac71f8aa6c5f6440bd3c6fa7cb4756e52d572a8f16db"} [ino-p28882892] Structural features of human inositol phosphate multikinase rationalize its inositol phosphate kinase and phosphoinositide 3-kinase activities. (2017). https://pubmed.ncbi.nlm.nih.gov/28882892/ DOI: 10.1074/jbc.m117.801845

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Human TTP-expressing cells with membrane-targeted inositol phosphatase; Figure 5

exposure

IPP-CAAX expression; pulse loading with 10 µM serum-complexed NBD-alpha-tocopherol.

limitations

Phosphoinositide machinery perturbation and fluorescent analog; not dietary phosphorus or vitamin E deprivation as the causal contrast.

nutrient_topic

Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E

organism

Rattus norvegicus cells; Homo sapiens TTP

plain_language

A membrane lipid signal was needed for efficient reporter export.

primary_references

[chung2016] Vitamin E and Phosphoinositides Regulate the Intracellular Localization of the Hepatic α-Tocopherol Transfer Protein. (2016). https://pubmed.ncbi.nlm.nih.gov/27307040/ DOI: 10.1074/jbc.m116.734210

tissue_or_cell_type

Hepatoma cells

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 363–374

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human TTP-expressing cells with membrane-targeted inositol phosphatase; Figure 5 · source_derived_draft · unverified_draft

### ve-transport-pip2-depletion-ttp-export Engineered depletion of plasma-membrane PI(4,5)P2 impaired TTP-dependent NBD-alpha-tocopherol secretion in McARH7777 cells. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: A membrane lipid signal was needed for efficient reporter export. organism: Rattus norvegicus cells; Homo sapiens TTP tissue_or_cell_type: Hepatoma cells experimental_model: Human TTP-expressing cells with membrane-targeted inositol phosphatase; Figure 5 limitations: Phosphoinositide machinery perturbation and fluorescent analog; not dietary phosphorus or vitamin E deprivation as the causal contrast. exposure: IPP-CAAX expression; pulse loading with 10 µM serum-complexed NBD-alpha-tocopherol. cross_nutrient: false [chung2016] Vitamin E and Phosphoinositides Regulate the Intracellular Localization of the Hepatic α-Tocopherol Transfer Protein. (2016). https://pubmed.ncbi.nlm.nih.gov/27307040/ DOI: 10.1074/jbc.m116.734210

evidence_span

{"source_cache": "artifacts/inositol-research/19548880.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ae150d47bf139d7352c8a5a128e0d6b071340f8c47d78700d5f398a549d3cd8", "start_char": 0, "end_char": 1766, "text_sha256": "5ae150d47bf139d7352c8a5a128e0d6b071340f8c47d78700d5f398a549d3cd8"}

experimental_model

Human splice-isoform expression, localization and kinase assay

exposure

PIP5K1C_i4 and i5 characterization

limitations

Isoforms have different localizations; a bulk lipid concentration cannot describe every local pool.

nutrient_topic

Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

organism

Human proteins in cellular expression assays

plain_language

This isoform can make PI(4,5)P2 from PI4P.

primary_references

[ino-p19548880] Two novel phosphatidylinositol-4-phosphate 5-kinase type Igamma splice variants expressed in human cells display distinctive cellular targeting. (2009). https://pubmed.ncbi.nlm.nih.gov/19548880/ DOI: 10.1042/bj20090638

tissue_or_cell_type

Nuclear and vesicular compartments

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 574–585

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human splice-isoform expression, localization and kinase assay · source_derived_draft · unverified_draft

### ino-pip5k-i4 Human PIP5K1C_i4 displayed PI4P 5-kinase activity in vitro. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: This isoform can make PI(4,5)P2 from PI4P. organism: Human proteins in cellular expression assays tissue_or_cell_type: Nuclear and vesicular compartments experimental_model: Human splice-isoform expression, localization and kinase assay limitations: Isoforms have different localizations; a bulk lipid concentration cannot describe every local pool. exposure: PIP5K1C_i4 and i5 characterization evidence_span: {"source_cache": "artifacts/inositol-research/19548880.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ae150d47bf139d7352c8a5a128e0d6b071340f8c47d78700d5f398a549d3cd8", "start_char": 0, "end_char": 1766, "text_sha256": "5ae150d47bf139d7352c8a5a128e0d6b071340f8c47d78700d5f398a549d3cd8"} [ino-p19548880] Two novel phosphatidylinositol-4-phosphate 5-kinase type Igamma splice variants expressed in human cells display distinctive cellular targeting. (2009). https://pubmed.ncbi.nlm.nih.gov/19548880/ DOI: 10.1042/bj20090638

evidence_span

{"source_cache": "artifacts/inositol-research/19548880.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ae150d47bf139d7352c8a5a128e0d6b071340f8c47d78700d5f398a549d3cd8", "start_char": 0, "end_char": 1766, "text_sha256": "5ae150d47bf139d7352c8a5a128e0d6b071340f8c47d78700d5f398a549d3cd8"}

experimental_model

Human splice-isoform expression, localization and kinase assay

exposure

PIP5K1C_i4 and i5 characterization

limitations

Isoforms have different localizations; a bulk lipid concentration cannot describe every local pool.

nutrient_topic

Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

organism

Human proteins in cellular expression assays

plain_language

A separately identified isoform can carry out the same chemical step.

primary_references

[ino-p19548880] Two novel phosphatidylinositol-4-phosphate 5-kinase type Igamma splice variants expressed in human cells display distinctive cellular targeting. (2009). https://pubmed.ncbi.nlm.nih.gov/19548880/ DOI: 10.1042/bj20090638

tissue_or_cell_type

Nuclear and vesicular compartments

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 587–598

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human splice-isoform expression, localization and kinase assay · source_derived_draft · unverified_draft

### ino-pip5k-i5 Human PIP5K1C_i5 also displayed PI4P 5-kinase activity in vitro. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A separately identified isoform can carry out the same chemical step. organism: Human proteins in cellular expression assays tissue_or_cell_type: Nuclear and vesicular compartments experimental_model: Human splice-isoform expression, localization and kinase assay limitations: Isoforms have different localizations; a bulk lipid concentration cannot describe every local pool. exposure: PIP5K1C_i4 and i5 characterization evidence_span: {"source_cache": "artifacts/inositol-research/19548880.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ae150d47bf139d7352c8a5a128e0d6b071340f8c47d78700d5f398a549d3cd8", "start_char": 0, "end_char": 1766, "text_sha256": "5ae150d47bf139d7352c8a5a128e0d6b071340f8c47d78700d5f398a549d3cd8"} [ino-p19548880] Two novel phosphatidylinositol-4-phosphate 5-kinase type Igamma splice variants expressed in human cells display distinctive cellular targeting. (2009). https://pubmed.ncbi.nlm.nih.gov/19548880/ DOI: 10.1042/bj20090638

evidence_span

{"source_cache": "artifacts/inositol-research/37991948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7", "start_char": 0, "end_char": 1735, "text_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7"}

experimental_model

Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis

exposure

G-alpha-q and G-beta-gamma stimulation

limitations

Reconstituted biochemical regulation; not an oral inositol intervention. Product generation and lipid depletion occur in the same reaction.

nutrient_topic

Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

organism

Recombinant mammalian signaling proteins

plain_language

The second product stays in the membrane rather than becoming soluble IP3.

primary_references

[ino-p37991948] The mechanism of Gαq regulation of PLCβ3-catalyzed PIP2 hydrolysis. (2023). https://pubmed.ncbi.nlm.nih.gov/37991948/ DOI: 10.1073/pnas.2315011120

tissue_or_cell_type

Defined membrane bilayers

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 639–650

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis · source_derived_draft · unverified_draft

### ino-plc-dag Diacylglycerol was the lipid product of PLCB3-catalyzed PI(4,5)P2 hydrolysis. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The second product stays in the membrane rather than becoming soluble IP3. organism: Recombinant mammalian signaling proteins tissue_or_cell_type: Defined membrane bilayers experimental_model: Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis limitations: Reconstituted biochemical regulation; not an oral inositol intervention. Product generation and lipid depletion occur in the same reaction. exposure: G-alpha-q and G-beta-gamma stimulation evidence_span: {"source_cache": "artifacts/inositol-research/37991948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7", "start_char": 0, "end_char": 1735, "text_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7"} [ino-p37991948] The mechanism of Gαq regulation of PLCβ3-catalyzed PIP2 hydrolysis. (2023). https://pubmed.ncbi.nlm.nih.gov/37991948/ DOI: 10.1073/pnas.2315011120

evidence_span

{"source_cache": "artifacts/inositol-research/37991948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7", "start_char": 0, "end_char": 1735, "text_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7"}

experimental_model

Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis

exposure

G-alpha-q and G-beta-gamma stimulation

limitations

Reconstituted biochemical regulation; not an oral inositol intervention. Product generation and lipid depletion occur in the same reaction.

nutrient_topic

Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

organism

Recombinant mammalian signaling proteins

plain_language

Splitting one membrane lipid creates two different signaling products.

primary_references

[ino-p37991948] The mechanism of Gαq regulation of PLCβ3-catalyzed PIP2 hydrolysis. (2023). https://pubmed.ncbi.nlm.nih.gov/37991948/ DOI: 10.1073/pnas.2315011120

tissue_or_cell_type

Defined membrane bilayers

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 626–637

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis · source_derived_draft · unverified_draft

### ino-plc-ip3 PLCB3 hydrolyzed PI(4,5)P2 to produce soluble IP3 and membrane-associated diacylglycerol. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Splitting one membrane lipid creates two different signaling products. organism: Recombinant mammalian signaling proteins tissue_or_cell_type: Defined membrane bilayers experimental_model: Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis limitations: Reconstituted biochemical regulation; not an oral inositol intervention. Product generation and lipid depletion occur in the same reaction. exposure: G-alpha-q and G-beta-gamma stimulation evidence_span: {"source_cache": "artifacts/inositol-research/37991948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7", "start_char": 0, "end_char": 1735, "text_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7"} [ino-p37991948] The mechanism of Gαq regulation of PLCβ3-catalyzed PIP2 hydrolysis. (2023). https://pubmed.ncbi.nlm.nih.gov/37991948/ DOI: 10.1073/pnas.2315011120

evidence_span

{"source_cache": "artifacts/inositol-research/9593664.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "118dd3dacb2fa7be09cb0258dd0f6de1193cf2553142c94a5750d82c5f00a248", "start_char": 0, "end_char": 1012, "text_sha256": "118dd3dacb2fa7be09cb0258dd0f6de1193cf2553142c94a5750d82c5f00a248"}

experimental_model

Phosphatase assays and human cell expression

exposure

Wild-type versus catalytic-mutant PTEN

limitations

Cellular overexpression and enzymology do not imply that inositol supplements activate PTEN.

nutrient_topic

Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)

organism

Human protein and HEK293 cells

plain_language

A phosphatase reverses a signaling-lipid phosphorylation step.

primary_references

[ino-p9593664] The tumor suppressor, PTEN/MMAC1, dephosphorylates the lipid second messenger, phosphatidylinositol 3,4,5-trisphosphate. (1998). https://pubmed.ncbi.nlm.nih.gov/9593664/ DOI: 10.1074/jbc.273.22.13375

tissue_or_cell_type

Purified enzyme and cultured cells

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 717–728

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phosphatase assays and human cell expression · source_derived_draft · unverified_draft

### ino-pten-pip3 Human PTEN removed the 3-phosphate from PI(3,4,5)P3, forming PI(4,5)P2. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A phosphatase reverses a signaling-lipid phosphorylation step. organism: Human protein and HEK293 cells tissue_or_cell_type: Purified enzyme and cultured cells experimental_model: Phosphatase assays and human cell expression limitations: Cellular overexpression and enzymology do not imply that inositol supplements activate PTEN. exposure: Wild-type versus catalytic-mutant PTEN evidence_span: {"source_cache": "artifacts/inositol-research/9593664.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "118dd3dacb2fa7be09cb0258dd0f6de1193cf2553142c94a5750d82c5f00a248", "start_char": 0, "end_char": 1012, "text_sha256": "118dd3dacb2fa7be09cb0258dd0f6de1193cf2553142c94a5750d82c5f00a248"} [ino-p9593664] The tumor suppressor, PTEN/MMAC1, dephosphorylates the lipid second messenger, phosphatidylinositol 3,4,5-trisphosphate. (1998). https://pubmed.ncbi.nlm.nih.gov/9593664/ DOI: 10.1074/jbc.273.22.13375