Component

Cysteine persulfide / CysSSH

Cysteine persulfide / CysSSH. Species, exposure and limitations are retained in each linked claim.

5 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 acts on it

  1. CARS2 disruption lowered cysteine-persulfide production in human cells, and wild-type or the C78/257D mutant restored it despite differing effects on translation.

    Human mitochondrial cysteinyl-tRNA synthetase / CARS2 → Cysteine persulfide / CysSSH source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human HEK293T knockout/rescue and LC–MS/MS persulfide assays.
    limitations
    Assay and mutation-dependent evidence; the proposed importance of this route is not proof of identical dominance in all human tissues.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    One enzyme had separable roles in protein synthesis and sulfur chemistry.
    primary_references
    Cysteinyl-tRNA synthetase governs cysteine polysulfidation and mitochondrial bioenergetics. · 2017 · https://pubmed.ncbi.nlm.nih.gov/29079736/ · DOI 10.1038/s41467-017-01311-y
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 164–170

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human HEK293T knockout/rescue and LC–MS/MS persulfide assays. · source_derived_draft · unverified_draft

    ## l-cysteine-cars2-persulfide One enzyme had separable roles in protein synthesis and sulfur chemistry. CARS2 disruption lowered cysteine-persulfide production in human cells, and wild-type or the C78/257D mutant restored it despite differing effects on translation. Model: Human HEK293T knockout/rescue and LC–MS/MS persulfide assays. Limitations: Assay and mutation-dependent evidence; the proposed importance of this route is not proof of identical dominance in all human tissues. Evidence access: Primary full text Cysteinyl-tRNA synthetase governs cysteine polysulfidation and mitochondrial bioenergetics. · 2017 · https://pubmed.ncbi.nlm.nih.gov/29079736/ · DOI 10.1038/s41467-017-01311-y
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Cars2-derived cysteine persulfide/H2S signaling promoted EBF2 persulfidation and interaction with PPARgamma or BRG1, supporting thermogenic gene recruitment.

    Mouse mitochondrial cysteinyl-tRNA synthetase / Cars2 → Mouse early B-cell factor 2 / Ebf2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse-centered brown-adipocyte and in vivo experimental program.
    limitations
    Abstract does not fully resolve each chemical intermediate; do not equate free H2S, CysSSH and protein-bound persulfides.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Sulfur chemistry fed back to the transcription machinery.
    primary_references
    Cars2-Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41849685/ · DOI 10.1002/advs.202522690

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 396–402

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse-centered brown-adipocyte and in vivo experimental program. · source_derived_draft · unverified_draft

    ## l-cysteine-cars2-ebf2-persulfidation Sulfur chemistry fed back to the transcription machinery. Cars2-derived cysteine persulfide/H2S signaling promoted EBF2 persulfidation and interaction with PPARgamma or BRG1, supporting thermogenic gene recruitment. Model: Mouse-centered brown-adipocyte and in vivo experimental program. Limitations: Abstract does not fully resolve each chemical intermediate; do not equate free H2S, CysSSH and protein-bound persulfides. Evidence access: Primary abstract Cars2-Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41849685/ · DOI 10.1002/advs.202522690
    Complete structured claim and evidence

  2. Loss of Cars2 in thermogenic fat impaired brown-fat formation and reduced thermogenesis and energy expenditure in mice.

    Mouse mitochondrial cysteinyl-tRNA synthetase / Cars2 → Brown-fat development and function in mouse Cars2 experiments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse thermogenic-fat Cars2 loss.
    limitations
    This is not the same intervention as Cth loss plus a cysteine-free diet.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    A tissue-specific enzyme defect produced a different response from whole-body nutrient withdrawal.
    primary_references
    Cars2-Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41849685/ · DOI 10.1002/advs.202522690
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 404–410

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse thermogenic-fat Cars2 loss. · source_derived_draft · unverified_draft

    ## l-cysteine-cars2-fat-loss A tissue-specific enzyme defect produced a different response from whole-body nutrient withdrawal. Loss of Cars2 in thermogenic fat impaired brown-fat formation and reduced thermogenesis and energy expenditure in mice. Model: Mouse thermogenic-fat Cars2 loss. Limitations: This is not the same intervention as Cth loss plus a cysteine-free diet. Evidence access: Primary abstract Cars2-Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41849685/ · DOI 10.1002/advs.202522690
    Complete structured claim and evidence

  3. CARS2-deficient human cells had fragmented or shrunken mitochondria; re-expression of wild-type or persulfide-competent C78/257D CARS2 improved morphology, unlike the tested persulfide-impaired lysine mutants.

    Human mitochondrial cysteinyl-tRNA synthetase / CARS2 → Mitochondrial morphology in human CARS2-deficient cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human HEK293T imaging and mutant rescue.
    limitations
    This does not show that free-cysteine supplementation repairs mitochondrial disease.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Sulfur chemistry contributed to mitochondrial behavior beyond protein production.
    primary_references
    Cysteinyl-tRNA synthetase governs cysteine polysulfidation and mitochondrial bioenergetics. · 2017 · https://pubmed.ncbi.nlm.nih.gov/29079736/ · DOI 10.1038/s41467-017-01311-y
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 172–178

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human HEK293T imaging and mutant rescue. · source_derived_draft · unverified_draft

    ## l-cysteine-cars2-mitochondrial-shape Sulfur chemistry contributed to mitochondrial behavior beyond protein production. CARS2-deficient human cells had fragmented or shrunken mitochondria; re-expression of wild-type or persulfide-competent C78/257D CARS2 improved morphology, unlike the tested persulfide-impaired lysine mutants. Model: Human HEK293T imaging and mutant rescue. Limitations: This does not show that free-cysteine supplementation repairs mitochondrial disease. Evidence access: Primary full text Cysteinyl-tRNA synthetase governs cysteine polysulfidation and mitochondrial bioenergetics. · 2017 · https://pubmed.ncbi.nlm.nih.gov/29079736/ · DOI 10.1038/s41467-017-01311-y
    Complete structured claim and evidence

  4. SUOX-deficient cells accumulated persulfidated glutathione and cysteine.

    Human sulfite oxidase / SUOX → Glutathione persulfide / GSSH source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/33271457.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "619710a31160db0927e01193e458277773ebe5e5423629e7dab58888ab6bc617", "start_char": 0, "end_char": 1479, "text_sha256": "619710a31160db0927e01193e458277773ebe5e5423629e7dab58888ab6bc617"}
    experimental_model
    CRISPR SUOX/GOT1/GOT2 perturbations and sulfur-metabolite assays
    exposure
    Cysteine-sulfinate and H2S pathway experiments
    limitations
    Cell-specific contributions; a higher concentration is not a direct measurement of pathway flux.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Homo sapiens
    plain_language
    Glutathione and cysteine sulfur chemistry also changed.
    primary_references
    [mo-p33271457] The role of glutamate oxaloacetate transaminases in sulfite biosynthesis and H<sub>2</sub>S metabolism. (2021). https://pubmed.ncbi.nlm.nih.gov/33271457/ DOI: 10.1016/j.redox.2020.101800
    tissue_or_cell_type
    HEK293T cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 716–727

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CRISPR SUOX/GOT1/GOT2 perturbations and sulfur-metabolite assays · source_derived_draft · unverified_draft

    ### mo-suox-persulfides SUOX-deficient cells accumulated persulfidated glutathione and cysteine. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutathione and cysteine sulfur chemistry also changed. organism: Homo sapiens tissue_or_cell_type: HEK293T cells experimental_model: CRISPR SUOX/GOT1/GOT2 perturbations and sulfur-metabolite assays limitations: Cell-specific contributions; a higher concentration is not a direct measurement of pathway flux. exposure: Cysteine-sulfinate and H2S pathway experiments evidence_span: {"source_cache": "artifacts/molybdenum-research/33271457.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "619710a31160db0927e01193e458277773ebe5e5423629e7dab58888ab6bc617", "start_char": 0, "end_char": 1479, "text_sha256": "619710a31160db0927e01193e458277773ebe5e5423629e7dab58888ab6bc617"} [mo-p33271457] The role of glutamate oxaloacetate transaminases in sulfite biosynthesis and H<sub>2</sub>S metabolism. (2021). https://pubmed.ncbi.nlm.nih.gov/33271457/ DOI: 10.1016/j.redox.2020.101800
    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