Component

Human cytosolic methionyl-tRNA synthetase / MARS1

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

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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. Human MARS1 catalyzes methionylation of cognate tRNA; the study compared this activity with stress-induced charging of non-cognate tRNAs.

    Human cytosolic methionyl-tRNA synthetase / MARS1 → Human cytosolic methionyl-tRNA source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human MRS/MARS1 biochemical and HeLa-cell experiments.
    limitations
    Baseline charging and stress-related mistranslation are separate observations.
    nutrient_topic
    L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
    plain_language
    A dedicated enzyme attaches methionine to the translation machinery.
    primary_references
    Promiscuous methionyl-tRNA synthetase mediates adaptive mistranslation to protect cells against oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25097229/ · DOI 10.1242/jcs.152470

    L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 60–66

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human MRS/MARS1 biochemical and HeLa-cell experiments. · source_derived_draft · unverified_draft

    ## methionine-mars-charging A dedicated enzyme attaches methionine to the translation machinery. Human MARS1 catalyzes methionylation of cognate tRNA; the study compared this activity with stress-induced charging of non-cognate tRNAs. Model: Human MRS/MARS1 biochemical and HeLa-cell experiments. Limitations: Baseline charging and stress-related mistranslation are separate observations. Evidence access: Primary full text Promiscuous methionyl-tRNA synthetase mediates adaptive mistranslation to protect cells against oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25097229/ · DOI 10.1242/jcs.152470
    Complete structured claim and evidence

  2. Phosphorylation-mimicking MARS1 favored non-cognate tRNAs and increased methionine incorporation at normally non-methionine positions.

    Human cytosolic methionyl-tRNA synthetase / MARS1 → Methionylation of non-cognate human tRNAs source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human MARS1 mutants and cultured-cell/protein assays.
    limitations
    Not evidence that all altered proteins retain normal function or that methionine loading is protective.
    nutrient_topic
    L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
    plain_language
    Cells can trade some translation accuracy for a stress response.
    primary_references
    Promiscuous methionyl-tRNA synthetase mediates adaptive mistranslation to protect cells against oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25097229/ · DOI 10.1242/jcs.152470

    L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 76–82

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human MARS1 mutants and cultured-cell/protein assays. · source_derived_draft · unverified_draft

    ## methionine-mars-mischarging Cells can trade some translation accuracy for a stress response. Phosphorylation-mimicking MARS1 favored non-cognate tRNAs and increased methionine incorporation at normally non-methionine positions. Model: Human MARS1 mutants and cultured-cell/protein assays. Limitations: Not evidence that all altered proteins retain normal function or that methionine loading is protective. Evidence access: Primary full text Promiscuous methionyl-tRNA synthetase mediates adaptive mistranslation to protect cells against oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25097229/ · DOI 10.1242/jcs.152470
    Complete structured claim and evidence

  3. Expression of the MARS1 S209D/S825D phosphorylation mimic reduced ROS and cell death in the tested stress conditions.

    Human cytosolic methionyl-tRNA synthetase / MARS1 → ROS and cell death in the MARS1 phosphorylation-mutant experiment source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human cell experiments with engineered MARS1.
    limitations
    Not a clinical antioxidant intervention.
    nutrient_topic
    L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
    plain_language
    Changing the enzyme affected stress survival in cultured cells.
    primary_references
    Promiscuous methionyl-tRNA synthetase mediates adaptive mistranslation to protect cells against oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25097229/ · DOI 10.1242/jcs.152470

    L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 84–90

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cell experiments with engineered MARS1. · source_derived_draft · unverified_draft

    ## methionine-mars-redox-outcome Changing the enzyme affected stress survival in cultured cells. Expression of the MARS1 S209D/S825D phosphorylation mimic reduced ROS and cell death in the tested stress conditions. Model: Human cell experiments with engineered MARS1. Limitations: Not a clinical antioxidant intervention. Evidence access: Primary full text Promiscuous methionyl-tRNA synthetase mediates adaptive mistranslation to protect cells against oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25097229/ · DOI 10.1242/jcs.152470
    Complete structured claim and evidence

What acts on it

  1. Oxidative-stress experiments identified ERK-dependent MARS1 phosphorylation at Ser209 and Ser825.

    Human ERK1/ERK2 kinases → Human cytosolic methionyl-tRNA synthetase / MARS1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human HeLa/HEK293T cells, kinase assays and site-directed mutants.
    limitations
    Arsenite/peroxide and engineered constructs do not represent routine dietary exposure.
    nutrient_topic
    L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
    plain_language
    Stress signaling changes how the charging enzyme behaves.
    primary_references
    Promiscuous methionyl-tRNA synthetase mediates adaptive mistranslation to protect cells against oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25097229/ · DOI 10.1242/jcs.152470

    L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 68–74

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human HeLa/HEK293T cells, kinase assays and site-directed mutants. · source_derived_draft · unverified_draft

    ## methionine-mars-phosphorylation Stress signaling changes how the charging enzyme behaves. Oxidative-stress experiments identified ERK-dependent MARS1 phosphorylation at Ser209 and Ser825. Model: Human HeLa/HEK293T cells, kinase assays and site-directed mutants. Limitations: Arsenite/peroxide and engineered constructs do not represent routine dietary exposure. Evidence access: Primary full text Promiscuous methionyl-tRNA synthetase mediates adaptive mistranslation to protect cells against oxidative stress. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25097229/ · DOI 10.1242/jcs.152470
    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