Component

PDPK1 (3-phosphoinositide-dependent protein kinase 1)

PDPK1 (3-phosphoinositide-dependent protein kinase 1). Species, exposure and limitations are retained in each linked claim.

1 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.

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.

Recorded relationships

Where it participates (unsigned role)

  1. 5-InsP7 inhibited PDK1-dependent Akt phosphorylation and activation in the reported biochemical pathway.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/inositol-research/21145457.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0de0a9c3ea11cd8ce59bccff69a41139b11e11182fd9fd66016ec72ba329a5ce", "start_char": 0, "end_char": 889, "text_sha256": "0de0a9c3ea11cd8ce59bccff69a41139b11e11182fd9fd66016ec72ba329a5ce"}
    experimental_model
    Biochemical Akt regulation and targeted mouse Ip6k1 deletion
    exposure
    5-InsP7 and Ip6k1 knockout
    limitations
    Whole-gene deletion is not equivalent to adding or withdrawing free myo-inositol; the reported therapeutic proposal is not established treatment.
    nutrient_topic
    Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
    organism
    Mammalian enzymology and Mus musculus
    plain_language
    An inositol-derived signal can restrain insulin-pathway signaling rather than always increasing it.
    primary_references
    [ino-p21145457] Inositol pyrophosphates inhibit Akt signaling, thereby regulating insulin sensitivity and weight gain. (2010). https://pubmed.ncbi.nlm.nih.gov/21145457/ DOI: 10.1016/j.cell.2010.11.032
    tissue_or_cell_type
    Muscle, adipose tissue and liver

    Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 782–793

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical Akt regulation and targeted mouse Ip6k1 deletion · source_derived_draft · unverified_draft

    ### ino-ip7-akt 5-InsP7 inhibited PDK1-dependent Akt phosphorylation and activation in the reported biochemical pathway. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inositol-derived signal can restrain insulin-pathway signaling rather than always increasing it. organism: Mammalian enzymology and Mus musculus tissue_or_cell_type: Muscle, adipose tissue and liver experimental_model: Biochemical Akt regulation and targeted mouse Ip6k1 deletion limitations: Whole-gene deletion is not equivalent to adding or withdrawing free myo-inositol; the reported therapeutic proposal is not established treatment. exposure: 5-InsP7 and Ip6k1 knockout evidence_span: {"source_cache": "artifacts/inositol-research/21145457.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0de0a9c3ea11cd8ce59bccff69a41139b11e11182fd9fd66016ec72ba329a5ce", "start_char": 0, "end_char": 889, "text_sha256": "0de0a9c3ea11cd8ce59bccff69a41139b11e11182fd9fd66016ec72ba329a5ce"} [ino-p21145457] Inositol pyrophosphates inhibit Akt signaling, thereby regulating insulin sensitivity and weight gain. (2010). https://pubmed.ncbi.nlm.nih.gov/21145457/ DOI: 10.1016/j.cell.2010.11.032
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards