Component

Human mitochondrial m-AAA protease AFG3L2

Human mitochondrial m-AAA protease AFG3L2. Species, exposure and limitations are retained in each linked 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

What it acts on

  1. AFG3L2 mediated SLC25A39 degradation through matrix loop 1.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/38157846.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8910cd64daf32714af4c954a4781163c2c5be3270e58eba14f7ff481e8a2cc71", "start_char": 0, "end_char": 1145, "text_sha256": "8910cd64daf32714af4c954a4781163c2c5be3270e58eba14f7ff481e8a2cc71"}
    experimental_model
    Protein-interaction proteomics, knockout and neuronal regulation
    exposure
    AFG3L2 deletion and iron-sulfur sensing experiments
    limitations
    Protein-turnover regulation; no quantitative intake requirement is inferred.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Human carrier in mammalian systems
    plain_language
    The cell regulates carrier abundance by breaking down the protein.
    primary_references
    [glutathione-p38157846] Dual regulation of SLC25A39 by AFG3L2 and iron controls mitochondrial glutathione homeostasis. (2024). https://pubmed.ncbi.nlm.nih.gov/38157846/ DOI: 10.1016/j.molcel.2023.12.008
    tissue_or_cell_type
    Mitochondrial matrix-facing loop

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 541–552

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein-interaction proteomics, knockout and neuronal regulation · source_derived_draft · unverified_draft

    ### glutathione-afg3l2-a39 AFG3L2 mediated SLC25A39 degradation through matrix loop 1. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell regulates carrier abundance by breaking down the protein. organism: Human carrier in mammalian systems tissue_or_cell_type: Mitochondrial matrix-facing loop experimental_model: Protein-interaction proteomics, knockout and neuronal regulation limitations: Protein-turnover regulation; no quantitative intake requirement is inferred. exposure: AFG3L2 deletion and iron-sulfur sensing experiments evidence_span: {"source_cache": "artifacts/glutathione-research/38157846.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8910cd64daf32714af4c954a4781163c2c5be3270e58eba14f7ff481e8a2cc71", "start_char": 0, "end_char": 1145, "text_sha256": "8910cd64daf32714af4c954a4781163c2c5be3270e58eba14f7ff481e8a2cc71"} [glutathione-p38157846] Dual regulation of SLC25A39 by AFG3L2 and iron controls mitochondrial glutathione homeostasis. (2024). https://pubmed.ncbi.nlm.nih.gov/38157846/ DOI: 10.1016/j.molcel.2023.12.008
    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