Component
Human MTARC1 p.Ala165Thr
Human MTARC1 p.Ala165Thr. 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.
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
Endogenous A165T MTARC1 showed substantial mislocalization outside the outer mitochondrial membrane in HepG2 cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/molybdenum-research/38723751.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5c4b7e298ad8a9760c515d21299d8c831692c6c07361857e3f6ff6509e9438db", "start_char": 0, "end_char": 1564, "text_sha256": "5c4b7e298ad8a9760c515d21299d8c831692c6c07361857e3f6ff6509e9438db"}
- experimental_model
- Endogenous CRISPR knock-in variants in HepG2 cells
- exposure
- A165T versus WT and catalytically inactive C273A
- limitations
- Cellular protein effects; the protective mechanism in human liver disease was not proven.
- nutrient_topic
- Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
- organism
- Homo sapiens
- plain_language
- The altered protein was not positioned like the usual enzyme.
- primary_references
- [mo-p38723751] Biochemical and functional characterization of the p.A165T missense variant of mitochondrial amidoxime-reducing component 1. (2024). https://pubmed.ncbi.nlm.nih.gov/38723751/ DOI: 10.1016/j.jbc.2024.107353
- tissue_or_cell_type
- Hepatoma cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1483–1494
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Endogenous CRISPR knock-in variants in HepG2 cells · source_derived_draft · unverified_draft
### mo-marc-a165t-location Endogenous A165T MTARC1 showed substantial mislocalization outside the outer mitochondrial membrane in HepG2 cells. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: The altered protein was not positioned like the usual enzyme. organism: Homo sapiens tissue_or_cell_type: Hepatoma cells experimental_model: Endogenous CRISPR knock-in variants in HepG2 cells limitations: Cellular protein effects; the protective mechanism in human liver disease was not proven. exposure: A165T versus WT and catalytically inactive C273A evidence_span: {"source_cache": "artifacts/molybdenum-research/38723751.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5c4b7e298ad8a9760c515d21299d8c831692c6c07361857e3f6ff6509e9438db", "start_char": 0, "end_char": 1564, "text_sha256": "5c4b7e298ad8a9760c515d21299d8c831692c6c07361857e3f6ff6509e9438db"} [mo-p38723751] Biochemical and functional characterization of the p.A165T missense variant of mitochondrial amidoxime-reducing component 1. (2024). https://pubmed.ncbi.nlm.nih.gov/38723751/ DOI: 10.1016/j.jbc.2024.107353
Complete structured claim and evidenceA165T MTARC1 showed increased ubiquitination and faster proteasomal degradation.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/molybdenum-research/38723751.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5c4b7e298ad8a9760c515d21299d8c831692c6c07361857e3f6ff6509e9438db", "start_char": 0, "end_char": 1564, "text_sha256": "5c4b7e298ad8a9760c515d21299d8c831692c6c07361857e3f6ff6509e9438db"}
- experimental_model
- Endogenous CRISPR knock-in variants in HepG2 cells
- exposure
- A165T versus WT and catalytically inactive C273A
- limitations
- Cellular protein effects; the protective mechanism in human liver disease was not proven.
- nutrient_topic
- Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
- organism
- Homo sapiens
- plain_language
- The cell removed the variant protein faster.
- primary_references
- [mo-p38723751] Biochemical and functional characterization of the p.A165T missense variant of mitochondrial amidoxime-reducing component 1. (2024). https://pubmed.ncbi.nlm.nih.gov/38723751/ DOI: 10.1016/j.jbc.2024.107353
- tissue_or_cell_type
- Hepatoma cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1496–1507
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Endogenous CRISPR knock-in variants in HepG2 cells · source_derived_draft · unverified_draft
### mo-marc-a165t-turnover A165T MTARC1 showed increased ubiquitination and faster proteasomal degradation. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell removed the variant protein faster. organism: Homo sapiens tissue_or_cell_type: Hepatoma cells experimental_model: Endogenous CRISPR knock-in variants in HepG2 cells limitations: Cellular protein effects; the protective mechanism in human liver disease was not proven. exposure: A165T versus WT and catalytically inactive C273A evidence_span: {"source_cache": "artifacts/molybdenum-research/38723751.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5c4b7e298ad8a9760c515d21299d8c831692c6c07361857e3f6ff6509e9438db", "start_char": 0, "end_char": 1564, "text_sha256": "5c4b7e298ad8a9760c515d21299d8c831692c6c07361857e3f6ff6509e9438db"} [mo-p38723751] Biochemical and functional characterization of the p.A165T missense variant of mitochondrial amidoxime-reducing component 1. (2024). https://pubmed.ncbi.nlm.nih.gov/38723751/ DOI: 10.1016/j.jbc.2024.107353
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.