Component

Human Epac1 / RAPGEF3

Context-specific entity; species, compartment and exposure are stated on each claim.

2 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

What it acts on

  1. Epac1 siRNA, unlike PKA catalytic-subunit siRNA, blocked resveratrol-induced AMPK/ACC phosphorylation in human HeLa cells.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    HeLa experiments selected to avoid myogenesis confounding; 50 micromolar resveratrol.
    limitations
    RNAi does not make all tissue responses Epac1-dependent.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    A cAMP effector is a tested dependency.
    primary_references
    Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 238–244

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · HeLa experiments selected to avoid myogenesis confounding; 50 micromolar resveratrol. · source_derived_draft · unverified_draft

    ## resveratrol-epac-loss A cAMP effector is a tested dependency. Epac1 siRNA, unlike PKA catalytic-subunit siRNA, blocked resveratrol-induced AMPK/ACC phosphorylation in human HeLa cells. Model: HeLa experiments selected to avoid myogenesis confounding; 50 micromolar resveratrol. Limitations: RNAi does not make all tissue responses Epac1-dependent. Evidence access: Primary full text Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    Complete structured claim and evidence
  2. Epac1 siRNA prevented the resveratrol-induced NAD increase and PGC-1alpha deacetylation in human HeLa experiments.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Same cellular mechanism study.
    limitations
    NAD measurement and substrate deacetylation do not establish direct SIRT1 binding.
    nutrient_topic
    Resveratrol collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Resveratrol
    plain_language
    Calcium/cAMP signaling connects to NAD-dependent regulation.
    primary_references
    Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Resveratrol: metabolites, target selectivity and cross-nutrient mechanisms (2026-09-19) · lines 246–252

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same cellular mechanism study. · source_derived_draft · unverified_draft

    ## resveratrol-epac-nad-loss Calcium/cAMP signaling connects to NAD-dependent regulation. Epac1 siRNA prevented the resveratrol-induced NAD increase and PGC-1alpha deacetylation in human HeLa experiments. Model: Same cellular mechanism study. Limitations: NAD measurement and substrate deacetylation do not establish direct SIRT1 binding. Evidence access: Primary full text Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22304913/ · DOI 10.1016/j.cell.2012.01.017
    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