Component
Human mitochondrial methionyl-tRNA synthetase / MARS2
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
MARS2 is the mitochondrial methionyl-tRNA synthetase, connecting methionine to organelle translation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Established enzyme role described in the human MARS2 disease study.
- limitations
- This role statement is distinct from the patient-cell respiratory measurements.
- nutrient_topic
- L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
- plain_language
- Mitochondria need their own charging enzyme.
- primary_references
- Novel, compound heterozygous, single-nucleotide variants in MARS2 associated with developmental delay, poor growth, and sensorineural hearing loss. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25754315/ · DOI 10.1002/humu.22781
L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 92–98
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Established enzyme role described in the human MARS2 disease study. · source_derived_draft · unverified_draft
## methionine-mars2-charging Mitochondria need their own charging enzyme. MARS2 is the mitochondrial methionyl-tRNA synthetase, connecting methionine to organelle translation. Model: Established enzyme role described in the human MARS2 disease study. Limitations: This role statement is distinct from the patient-cell respiratory measurements. Evidence access: Primary abstract Novel, compound heterozygous, single-nucleotide variants in MARS2 associated with developmental delay, poor growth, and sensorineural hearing loss. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25754315/ · DOI 10.1002/humu.22781
Complete structured claim and evidenceBiallelic MARS2 variants lowered protein abundance; patient cells had complex I/IV defects, and wild-type MARS2 expression increased NDUFB8 and COXII proteins.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Two affected siblings; human fibroblasts/lymphoblasts and gene-expression rescue.
- limitations
- Genetic rescue is not proof that methionine supplementation rescues this disorder.
- nutrient_topic
- L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
- plain_language
- A faulty charging enzyme can impair respiratory machinery despite available methionine.
- primary_references
- Novel, compound heterozygous, single-nucleotide variants in MARS2 associated with developmental delay, poor growth, and sensorineural hearing loss. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25754315/ · DOI 10.1002/humu.22781
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 100–106
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Two affected siblings; human fibroblasts/lymphoblasts and gene-expression rescue. · source_derived_draft · unverified_draft
## methionine-mars2-loss A faulty charging enzyme can impair respiratory machinery despite available methionine. Biallelic MARS2 variants lowered protein abundance; patient cells had complex I/IV defects, and wild-type MARS2 expression increased NDUFB8 and COXII proteins. Model: Two affected siblings; human fibroblasts/lymphoblasts and gene-expression rescue. Limitations: Genetic rescue is not proof that methionine supplementation rescues this disorder. Evidence access: Primary abstract Novel, compound heterozygous, single-nucleotide variants in MARS2 associated with developmental delay, poor growth, and sensorineural hearing loss. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25754315/ · DOI 10.1002/humu.22781
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.