Component

YTHDF1 in the tumor study, species unresolved here

Context-specific entity; species, compartment and exposure are stated on each 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. Methionine-derived SAM supported m6A modification and YTHDF1-associated translation of PD-L1 and VISTA transcripts in the tumor study.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Tumor-cell and mouse experiments; construct species unresolved in accessed abstract.
    limitations
    Does not mean all methionine methylation suppresses immunity.
    nutrient_topic
    L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
    plain_language
    The same donor can support an immune-evasion pathway in a different cell.
    primary_references
    Methionine deficiency facilitates antitumour immunity by altering m6A methylation of immune checkpoint transcripts. · 2023 · https://pubmed.ncbi.nlm.nih.gov/35803704/ · DOI 10.1136/gutjnl-2022-326928

    L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 444–450

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Tumor-cell and mouse experiments; construct species unresolved in accessed abstract. · source_derived_draft · unverified_draft

    ## methionine-checkpoint-rna The same donor can support an immune-evasion pathway in a different cell. Methionine-derived SAM supported m6A modification and YTHDF1-associated translation of PD-L1 and VISTA transcripts in the tumor study. Model: Tumor-cell and mouse experiments; construct species unresolved in accessed abstract. Limitations: Does not mean all methionine methylation suppresses immunity. Evidence access: Primary abstract Methionine deficiency facilitates antitumour immunity by altering m6A methylation of immune checkpoint transcripts. · 2023 · https://pubmed.ncbi.nlm.nih.gov/35803704/ · DOI 10.1136/gutjnl-2022-326928
    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