Component
Intracellular myo-inositol availability
Intracellular myo-inositol availability. Species, exposure and limitations are retained in each linked claim.
3 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 acts on it
HMIT-null mice did not show altered inositol transport or homeostasis in the reported analyses.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/inositol-research/19607714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8b8bd010f44dd8b055efc345c57791e88547114b0a2f27d782183674fc53f984", "start_char": 0, "end_char": 1332, "text_sha256": "8b8bd010f44dd8b055efc345c57791e88547114b0a2f27d782183674fc53f984"}
- experimental_model
- Immunolocalization, neuronal electrophysiology and knockout
- exposure
- Native localization and HMIT-null comparisons
- limitations
- Native localization qualifies earlier heterologous uptake findings; it is an explained context difference, not evidence that one experiment is false.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Rat and human brain; mouse knockout
- plain_language
- Removing this one candidate transporter did not produce the predicted general uptake failure.
- primary_references
- [ino-p19607714] Evaluation of expression and function of the H+/myo-inositol transporter HMIT. (2009). https://pubmed.ncbi.nlm.nih.gov/19607714/ DOI: 10.1186/1471-2121-10-54
- tissue_or_cell_type
- Brain neurons and cultured neurons
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 392–403
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Immunolocalization, neuronal electrophysiology and knockout · source_derived_draft · unverified_draft
### ino-hmit-null HMIT-null mice did not show altered inositol transport or homeostasis in the reported analyses. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing this one candidate transporter did not produce the predicted general uptake failure. organism: Rat and human brain; mouse knockout tissue_or_cell_type: Brain neurons and cultured neurons experimental_model: Immunolocalization, neuronal electrophysiology and knockout limitations: Native localization qualifies earlier heterologous uptake findings; it is an explained context difference, not evidence that one experiment is false. exposure: Native localization and HMIT-null comparisons evidence_span: {"source_cache": "artifacts/inositol-research/19607714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8b8bd010f44dd8b055efc345c57791e88547114b0a2f27d782183674fc53f984", "start_char": 0, "end_char": 1332, "text_sha256": "8b8bd010f44dd8b055efc345c57791e88547114b0a2f27d782183674fc53f984"} [ino-p19607714] Evaluation of expression and function of the H+/myo-inositol transporter HMIT. (2009). https://pubmed.ncbi.nlm.nih.gov/19607714/ DOI: 10.1186/1471-2121-10-54
Complete structured claim and evidenceAt 0.6 mM valproate, yeast expressing human ISYNA1 had approximately 25% less intracellular inositol; purified ISYNA1 was not inhibited at that concentration.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/inositol-research/15024000.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac", "start_char": 0, "end_char": 1427, "text_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac"}
- experimental_model
- Recombinant human enzyme and complementation of yeast ino1 deletion
- exposure
- Substrate, NAD+, cation and valproate experiments
- limitations
- Purified-enzyme and yeast results do not establish supplement effects or a human dietary deficiency threshold.
- 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 yeast
- plain_language
- The effect depended on the cellular setting rather than direct inhibition of the isolated enzyme.
- primary_references
- [ino-p15024000] Human 1-D-myo-inositol-3-phosphate synthase is functional in yeast. (2004). https://pubmed.ncbi.nlm.nih.gov/15024000/ DOI: 10.1074/jbc.m312078200
- tissue_or_cell_type
- Purified enzyme; yeast cultures
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 223–234
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human enzyme and complementation of yeast ino1 deletion · source_derived_draft · unverified_draft
### ino-valproate-yeast At 0.6 mM valproate, yeast expressing human ISYNA1 had approximately 25% less intracellular inositol; purified ISYNA1 was not inhibited at that concentration. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: The effect depended on the cellular setting rather than direct inhibition of the isolated enzyme. organism: Human protein expressed in bacteria and yeast tissue_or_cell_type: Purified enzyme; yeast cultures experimental_model: Recombinant human enzyme and complementation of yeast ino1 deletion limitations: Purified-enzyme and yeast results do not establish supplement effects or a human dietary deficiency threshold. exposure: Substrate, NAD+, cation and valproate experiments evidence_span: {"source_cache": "artifacts/inositol-research/15024000.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac", "start_char": 0, "end_char": 1427, "text_sha256": "5ab3a8eda77989c3e4a681b4a971fb7e969c285d3e5c8e41bc31713a7f88c9ac"} [ino-p15024000] Human 1-D-myo-inositol-3-phosphate synthase is functional in yeast. (2004). https://pubmed.ncbi.nlm.nih.gov/15024000/ DOI: 10.1074/jbc.m312078200
Complete structured claim and evidence
Where it participates (unsigned role)
Gain- and loss-of-function experiments supported redundant contributions of ISYNA1 synthesis and SLC5A3 transport to intracellular inositol and AML-cell fitness.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/inositol-research/34531253.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27", "start_char": 0, "end_char": 1431, "text_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27"}
- experimental_model
- Genetic screening, gain/loss of function and patient sample profiling
- exposure
- SLC5A3/ISYNA1 perturbation
- limitations
- Restricted to an epigenetically defined subset; no evidence that dietary inositol restriction treats leukemia.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Human AML cells and in vivo leukemia models
- plain_language
- Restoring synthesis can remove dependence on the same import route.
- primary_references
- [ino-p34531253] SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia. (2022). https://pubmed.ncbi.nlm.nih.gov/34531253/ DOI: 10.1158/2159-8290.cd-20-1849
- tissue_or_cell_type
- Acute myeloid leukemia
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 418–429
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic screening, gain/loss of function and patient sample profiling · source_derived_draft · unverified_draft
### ino-aml-redundancy Gain- and loss-of-function experiments supported redundant contributions of ISYNA1 synthesis and SLC5A3 transport to intracellular inositol and AML-cell fitness. Condition category: machinery_impairment nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring synthesis can remove dependence on the same import route. organism: Human AML cells and in vivo leukemia models tissue_or_cell_type: Acute myeloid leukemia experimental_model: Genetic screening, gain/loss of function and patient sample profiling limitations: Restricted to an epigenetically defined subset; no evidence that dietary inositol restriction treats leukemia. exposure: SLC5A3/ISYNA1 perturbation evidence_span: {"source_cache": "artifacts/inositol-research/34531253.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27", "start_char": 0, "end_char": 1431, "text_sha256": "e709021b8916a9b38a3a52f092732c2b587c55247c0bd9bd3f96438e74ad4b27"} [ino-p34531253] SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia. (2022). https://pubmed.ncbi.nlm.nih.gov/34531253/ DOI: 10.1158/2159-8290.cd-20-1849
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.