IP3

compartment_description

Nonmitochondrial intracellular store to cytosol

experimental_model

Permeabilized rat pancreatic acinar cells

limitations

Permeabilized-cell application; receptor isoform and dietary status were not established.

nutrient_topic

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

organism

Rattus norvegicus

plain_language

IP3 releases stored calcium inside acinar cells.

primary_references

[ca-streb1983] Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate (1983). https://pubmed.ncbi.nlm.nih.gov/6605482/ DOI: 10.1038/306067a0

research_relationship_category

mechanism

tissue_or_cell_type

Pancreatic acinar cells

transport_or_reaction_direction

Intracellular store to cytosol

Calcium: mechanism-first literature curation (2026-09-17) · lines 464–476

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Permeabilized rat pancreatic acinar cells · source_derived_draft · unverified_draft

### ca-ip3-mobilizes-store Applied IP3 releases calcium from a nonmitochondrial intracellular store in permeabilized pancreatic acinar cells. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: IP3 releases stored calcium inside acinar cells. organism: Rattus norvegicus tissue_or_cell_type: Pancreatic acinar cells experimental_model: Permeabilized rat pancreatic acinar cells limitations: Permeabilized-cell application; receptor isoform and dietary status were not established. research_relationship_category: mechanism transport_or_reaction_direction: Intracellular store to cytosol compartment_description: Nonmitochondrial intracellular store to cytosol [ca-streb1983] Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate (1983). https://pubmed.ncbi.nlm.nih.gov/6605482/ DOI: 10.1038/306067a0

cell_type

· T cell

evidence_scope

Source-derived draft; primary-source verification required

organism

· Human

Selenium in immune cells · lines 30–38

Selenium immune-cell mechanism draft · supports · Source draft; model details require primary-source verification · source_derived_draft · unverified_draft

5. TCR → LCK → ZAP70 → LAT → PLCγ1 → PIP₂ → IP₃ + DAG 6. IP₃ → IP3R → ER Ca²⁺ release → store depletion 7. STIM1 oligomerizes → ORAI1 → CRAC channel → sustained Ca²⁺ entry 8. Ca²⁺/calmodulin → CALCINEURIN (PP2B) → dephosphorylates NFAT 9. NFAT → nucleus → partners with AP-1 → IL2, IFNG, CD25 transcription

evidence_access

Primary full text

experimental_model

Monkey COS-7; 10 mM LiCl, 1 mM myo-inositol rescue.

limitations

Cell-culture rescue is not a clinical supplement recommendation.

nutrient_topic

Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium

plain_language

Availability of the precursor changes a signaling messenger.

primary_references

Lithium induces autophagy by inhibiting inositol monophosphatase. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16186256/ · DOI 10.1083/jcb.200504035

Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 80–86

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Monkey COS-7; 10 mM LiCl, 1 mM myo-inositol rescue. · source_derived_draft · unverified_draft

## lithium-ip3-decrease Availability of the precursor changes a signaling messenger. Lithium lowered IP3 in the COS-7 experiments; added myo-inositol raised it relative to lithium alone. Model: Monkey COS-7; 10 mM LiCl, 1 mM myo-inositol rescue. Limitations: Cell-culture rescue is not a clinical supplement recommendation. Evidence access: Primary full text Lithium induces autophagy by inhibiting inositol monophosphatase. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16186256/ · DOI 10.1083/jcb.200504035

evidence_span

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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

Soluble IP3 can be redirected into a more highly phosphorylated molecule.

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 678–689

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-ip4 Human IPMK has IP3 3-kinase activity, producing inositol 1,3,4,5-tetrakisphosphate. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Soluble IP3 can be redirected into a more highly phosphorylated molecule. 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

evidence_span

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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

cell_type

· T cell

evidence_scope

Source-derived draft; primary-source verification required

organism

· Human

Selenium in immune cells · lines 30–38

Selenium immune-cell mechanism draft · supports · Source draft; model details require primary-source verification · source_derived_draft · unverified_draft

5. TCR → LCK → ZAP70 → LAT → PLCγ1 → PIP₂ → IP₃ + DAG 6. IP₃ → IP3R → ER Ca²⁺ release → store depletion 7. STIM1 oligomerizes → ORAI1 → CRAC channel → sustained Ca²⁺ entry 8. Ca²⁺/calmodulin → CALCINEURIN (PP2B) → dephosphorylates NFAT 9. NFAT → nucleus → partners with AP-1 → IL2, IFNG, CD25 transcription

evidence_access

Primary abstract

experimental_model

Rabbit osteoclast pathway perturbations.

limitations

Absence of IP3 dependence here is not absence of calcium signaling in every strontium response.

nutrient_topic

Strontium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Strontium

plain_language

Similar ions need not use identical intracellular messengers.

primary_references

The calcium-sensing receptor is involved in strontium ranelate-induced osteoclast apoptosis. New insights into the associated signaling pathways. · 2009 · https://pubmed.ncbi.nlm.nih.gov/18927086/ · DOI 10.1074/jbc.M801668200

Strontium: calcium interactions, cellular mechanisms and mineralization (2026-09-19) · lines 230–236

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rabbit osteoclast pathway perturbations. · source_derived_draft · unverified_draft

## strontium-rabbit-ip3-difference Similar ions need not use identical intracellular messengers. Unlike calcium in the same experimental program, strontium-associated osteoclast apoptosis was independent of inositol 1,4,5-trisphosphate action. Model: Rabbit osteoclast pathway perturbations. Limitations: Absence of IP3 dependence here is not absence of calcium signaling in every strontium response. Evidence access: Primary abstract The calcium-sensing receptor is involved in strontium ranelate-induced osteoclast apoptosis. New insights into the associated signaling pathways. · 2009 · https://pubmed.ncbi.nlm.nih.gov/18927086/ · DOI 10.1074/jbc.M801668200

compartment_description

Cytosolic regulatory regions of ER channel

experimental_model

Recombinant human ITPR3; cryo-EM in ligand-bound gating states

limitations

Structural populations do not define a universal calcium threshold or prove all calcium-bound channels are active.

nutrient_topic

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

organism

Homo sapiens

plain_language

Calcium helps control ITPR3 opening; binding does not guarantee that the channel stays open.

primary_references

[ca-schmitz2022] Structural basis for activation and gating of IP3 receptors (2022). https://pubmed.ncbi.nlm.nih.gov/35301323/ DOI: 10.1038/s41467-022-29073-2

research_relationship_category

regulation

tissue_or_cell_type

Recombinant ITPR3

Calcium: mechanism-first literature curation (2026-09-17) · lines 492–503

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human ITPR3; cryo-EM in ligand-bound gating states · source_derived_draft · unverified_draft

### ca-itpr3-calcium-coactivation Calcium binding participates in ITPR3 gating after IP3/ATP priming, with both active and inactive calcium-bound conformations resolved. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium helps control ITPR3 opening; binding does not guarantee that the channel stays open. organism: Homo sapiens tissue_or_cell_type: Recombinant ITPR3 experimental_model: Recombinant human ITPR3; cryo-EM in ligand-bound gating states limitations: Structural populations do not define a universal calcium threshold or prove all calcium-bound channels are active. research_relationship_category: regulation compartment_description: Cytosolic regulatory regions of ER channel [ca-schmitz2022] Structural basis for activation and gating of IP3 receptors (2022). https://pubmed.ncbi.nlm.nih.gov/35301323/ DOI: 10.1038/s41467-022-29073-2

compartment_description

ER membrane

experimental_model

Recombinant human ITPR3; cryo-EM in ligand-bound gating states

limitations

Structure specifies ITPR3; it must not be relabeled as ITPR1 or a measurement of every receptor subtype.

nutrient_topic

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

organism

Homo sapiens

plain_language

ITPR3 provides a route for calcium to leave the ER.

primary_references

[ca-schmitz2022] Structural basis for activation and gating of IP3 receptors (2022). https://pubmed.ncbi.nlm.nih.gov/35301323/ DOI: 10.1038/s41467-022-29073-2

research_relationship_category

transport

tissue_or_cell_type

Recombinant ITPR3

transport_effect

raises A calcium-release channel: the recorded direction is ER lumen to cytosol.

transport_or_reaction_direction

ER lumen to cytosol

transport_pool

cytosolic calcium A calcium-release channel: the recorded direction is ER lumen to cytosol.

Calcium: mechanism-first literature curation (2026-09-17) · lines 478–490

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human ITPR3; cryo-EM in ligand-bound gating states · source_derived_draft · unverified_draft

### ca-itpr3-er-calcium-channel Human ITPR3 forms a calcium-release channel with an open pore in the IP3/ATP/Ca2+-bound structural state. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: ITPR3 provides a route for calcium to leave the ER. organism: Homo sapiens tissue_or_cell_type: Recombinant ITPR3 experimental_model: Recombinant human ITPR3; cryo-EM in ligand-bound gating states limitations: Structure specifies ITPR3; it must not be relabeled as ITPR1 or a measurement of every receptor subtype. research_relationship_category: transport transport_or_reaction_direction: ER lumen to cytosol compartment_description: ER membrane [ca-schmitz2022] Structural basis for activation and gating of IP3 receptors (2022). https://pubmed.ncbi.nlm.nih.gov/35301323/ DOI: 10.1038/s41467-022-29073-2

evidence_access

Primary abstract

experimental_model

Rat receptor cloning and functional expression study.

limitations

This does not demonstrate that oral inositol or calcium increases the response.

nutrient_topic

L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate

plain_language

A glutamate receptor can trigger an internal signaling cascade instead of forming the ion pore itself.

primary_references

Sequence and expression of a metabotropic glutamate receptor. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1847995/ · DOI 10.1038/349760a0

L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling 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 · Rat receptor cloning and functional expression study. · source_derived_draft · unverified_draft

## glutamate-mgr1-ip-calcium A glutamate receptor can trigger an internal signaling cascade instead of forming the ion pore itself. The cloned rat metabotropic glutamate receptor coupled receptor activation to inositol-phosphate/calcium signaling. Model: Rat receptor cloning and functional expression study. Limitations: This does not demonstrate that oral inositol or calcium increases the response. Evidence access: Primary abstract Sequence and expression of a metabotropic glutamate receptor. · 1991 · https://pubmed.ncbi.nlm.nih.gov/1847995/ · DOI 10.1038/349760a0

evidence_span

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experimental_model

Human cDNA cloning and recombinant kinase characterization

exposure

IP3 phosphorylation and product analysis

limitations

Enzyme activity and expression-system localization do not establish dietary effects or a single obligatory route for all cells.

nutrient_topic

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

organism

Human protein expressed in bacteria and mammalian cells

plain_language

The multikinase supplies a route from IP3 toward the five-phosphate precursor of InsP6.

primary_references

[ino-p12027805] The human homologue of yeast ArgRIII protein is an inositol phosphate multikinase with predominantly nuclear localization. (2002). https://pubmed.ncbi.nlm.nih.gov/12027805/ DOI: 10.1042/bj20020327

tissue_or_cell_type

Recombinant enzyme and tagged-protein localization

Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 704–715

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cDNA cloning and recombinant kinase characterization · source_derived_draft · unverified_draft

### ino-ipmk-ip5 Recombinant human IPMK phosphorylated IP3 at positions 3 and 6, reaching inositol 1,3,4,5,6-pentakisphosphate. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The multikinase supplies a route from IP3 toward the five-phosphate precursor of InsP6. organism: Human protein expressed in bacteria and mammalian cells tissue_or_cell_type: Recombinant enzyme and tagged-protein localization experimental_model: Human cDNA cloning and recombinant kinase characterization limitations: Enzyme activity and expression-system localization do not establish dietary effects or a single obligatory route for all cells. exposure: IP3 phosphorylation and product analysis evidence_span: {"source_cache": "artifacts/inositol-research/12027805.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d015b4f1e5198aceb869411c91fd2ab00da093fb573c1b195305fe8adfe66b26", "start_char": 0, "end_char": 1282, "text_sha256": "d015b4f1e5198aceb869411c91fd2ab00da093fb573c1b195305fe8adfe66b26"} [ino-p12027805] The human homologue of yeast ArgRIII protein is an inositol phosphate multikinase with predominantly nuclear localization. (2002). https://pubmed.ncbi.nlm.nih.gov/12027805/ DOI: 10.1042/bj20020327

evidence_span

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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/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 related phosphate-removal reaction was observed on a soluble molecule.

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 730–741

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-soluble PTEN also showed 3-phosphatase activity toward soluble inositol 1,3,4,5-tetrakisphosphate. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A related phosphate-removal reaction was observed on a soluble molecule. 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