Component
Human SHMT2 gene
Gene-level perturbation target; individual exposure and alleles are recorded in scenario metadata.
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
SHMT2-null Jurkat cells failed to maintain normal mitochondrial formylmethionyl-tRNA pools.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- CRISPR and tRNA assays
- exposure
- Assay conditions described in the linked primary study.
- limitations
- Several downstream mitochondrial consequences may coexist.
- nutrient_topic
- Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
- organism
- Homo sapiens
- plain_language
- Mitochondrial serine breakdown helps prepare the tRNA that starts translation.
- primary_references
- [minton-2018] Serine Catabolism by SHMT2 Is Required for Proper Mitochondrial Translation Initiation and Maintenance of Formylmethionyl-tRNAs (2018). https://pubmed.ncbi.nlm.nih.gov/29452640/ DOI: 10.1016/j.molcel.2018.01.024
- tissue_or_cell_type
- Jurkat cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1109–1119
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CRISPR and tRNA assays · source_derived_draft · unverified_draft
### shmt2-loss-formyltrna SHMT2-null Jurkat cells failed to maintain normal mitochondrial formylmethionyl-tRNA pools. Condition category: machinery_impairment nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mitochondrial serine breakdown helps prepare the tRNA that starts translation. organism: Homo sapiens tissue_or_cell_type: Jurkat cells experimental_model: CRISPR and tRNA assays limitations: Several downstream mitochondrial consequences may coexist. exposure: Assay conditions described in the linked primary study. [minton-2018] Serine Catabolism by SHMT2 Is Required for Proper Mitochondrial Translation Initiation and Maintenance of Formylmethionyl-tRNAs (2018). https://pubmed.ncbi.nlm.nih.gov/29452640/ DOI: 10.1016/j.molcel.2018.01.024
Complete structured claim and evidenceSHMT2 deletion reduced synthesis of mitochondrially encoded proteins while cytosolic protein labeling was preserved.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Radiolabeled protein synthesis
- exposure
- Assay conditions described in the linked primary study.
- limitations
- Cell-line response; no clinical supplementation conclusion.
- nutrient_topic
- Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
- organism
- Homo sapiens
- plain_language
- The translation defect was concentrated in mitochondria.
- primary_references
- [minton-2018] Serine Catabolism by SHMT2 Is Required for Proper Mitochondrial Translation Initiation and Maintenance of Formylmethionyl-tRNAs (2018). https://pubmed.ncbi.nlm.nih.gov/29452640/ DOI: 10.1016/j.molcel.2018.01.024
- tissue_or_cell_type
- Jurkat cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1121–1131
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabeled protein synthesis · source_derived_draft · unverified_draft
### shmt2-loss-mito-translation SHMT2 deletion reduced synthesis of mitochondrially encoded proteins while cytosolic protein labeling was preserved. Condition category: machinery_impairment nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The translation defect was concentrated in mitochondria. organism: Homo sapiens tissue_or_cell_type: Jurkat cells experimental_model: Radiolabeled protein synthesis limitations: Cell-line response; no clinical supplementation conclusion. exposure: Assay conditions described in the linked primary study. [minton-2018] Serine Catabolism by SHMT2 Is Required for Proper Mitochondrial Translation Initiation and Maintenance of Formylmethionyl-tRNAs (2018). https://pubmed.ncbi.nlm.nih.gov/29452640/ DOI: 10.1016/j.molcel.2018.01.024
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.