Component

Intracellular creatine content

Intracellular creatine content. Species, exposure and limitations are retained in each linked 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. AGAT reporter expression fell with intracellular creatine, with a reported intracellular IC50 of approximately 1–2 mM.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/creatine-research/38104212.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936", "start_char": 0, "end_char": 1889, "text_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936"}
    experimental_model
    CRISPR AGAT reporter, transporter knockout and rescue
    exposure
    Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8
    limitations
    Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Human HAP1 cells
    plain_language
    Cells responded to the creatine inside them when regulating the first synthesis enzyme.
    primary_references
    [creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. (2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1
    tissue_or_cell_type
    Cultured cells

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 308–319

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CRISPR AGAT reporter, transporter knockout and rescue · source_derived_draft · unverified_draft

    ### creatine-intracellular-feedback AGAT reporter expression fell with intracellular creatine, with a reported intracellular IC50 of approximately 1–2 mM. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells responded to the creatine inside them when regulating the first synthesis enzyme. organism: Human HAP1 cells tissue_or_cell_type: Cultured cells experimental_model: CRISPR AGAT reporter, transporter knockout and rescue limitations: Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified. exposure: Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8 evidence_span: {"source_cache": "artifacts/creatine-research/38104212.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936", "start_char": 0, "end_char": 1889, "text_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936"} [creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. (2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1
    Complete structured claim and evidence

What acts on it

  1. The high-affinity component of creatine accumulation and AGAT regulation depended on SLC6A8, whereas a nonsaturable component remained without the transporter.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/creatine-research/38104212.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936", "start_char": 0, "end_char": 1889, "text_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936"}
    experimental_model
    CRISPR AGAT reporter, transporter knockout and rescue
    exposure
    Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8
    limitations
    Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Human HAP1 cells
    plain_language
    The usual transporter shaped feedback, but the engineered cells also showed a separate low-affinity route.
    primary_references
    [creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. (2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1
    tissue_or_cell_type
    Cultured cells

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 321–332

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CRISPR AGAT reporter, transporter knockout and rescue · source_derived_draft · unverified_draft

    ### creatine-feedback-transporter-component The high-affinity component of creatine accumulation and AGAT regulation depended on SLC6A8, whereas a nonsaturable component remained without the transporter. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The usual transporter shaped feedback, but the engineered cells also showed a separate low-affinity route. organism: Human HAP1 cells tissue_or_cell_type: Cultured cells experimental_model: CRISPR AGAT reporter, transporter knockout and rescue limitations: Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified. exposure: Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8 evidence_span: {"source_cache": "artifacts/creatine-research/38104212.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936", "start_char": 0, "end_char": 1889, "text_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936"} [creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. (2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1
    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