Component

Mouse cystathionine gamma-lyase / Cth

Context-specific entity; species, compartment and exposure are stated on each claim.

10 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

Where it participates (unsigned role)

  1. The study linked cysteine-depletion-induced adipose browning and weight loss to sympathetic noradrenaline signaling through beta-3 adrenergic receptors.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse systemic depletion with sympathetic and adrenergic perturbations.
    limitations
    Does not establish that cysteine directly binds the adrenergic receptor or that dietary changes reproduce the genetic model.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    The whole-body response involved nerve-to-fat signaling.
    primary_references
    Cysteine depletion triggers adipose tissue thermogenesis and weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40461845/ · DOI 10.1038/s42255-025-01297-8
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 372–378

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse systemic depletion with sympathetic and adrenergic perturbations. · source_derived_draft · unverified_draft

    ## l-cysteine-adrenergic-depletion-response The whole-body response involved nerve-to-fat signaling. The study linked cysteine-depletion-induced adipose browning and weight loss to sympathetic noradrenaline signaling through beta-3 adrenergic receptors. Model: Mouse systemic depletion with sympathetic and adrenergic perturbations. Limitations: Does not establish that cysteine directly binds the adrenergic receptor or that dietary changes reproduce the genetic model. Evidence access: Primary full text Cysteine depletion triggers adipose tissue thermogenesis and weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40461845/ · DOI 10.1038/s42255-025-01297-8
    Complete structured claim and evidence
  2. After seven days of cysteine depletion, Cse-null mice repleted with cysteine but kept B5-deficient had persistently lower CoA and less weight recovery than mice receiving both nutrients, despite restored liver glutathione.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse cysteine repletion with or without dietary B5; subsequent tissue GSH/CoA and weight measurements.
    limitations
    A direct cross-nutrient repletion experiment in mice; not an established human treatment protocol. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Restoring one nutrient repaired one branch but left another branch short of its other substrate.
    primary_references
    Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 324–330

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse cysteine repletion with or without dietary B5; subsequent tissue GSH/CoA and weight measurements. · source_derived_draft · unverified_draft

    ## l-cysteine-b5-blocks-coa-recovery Restoring one nutrient repaired one branch but left another branch short of its other substrate. After seven days of cysteine depletion, Cse-null mice repleted with cysteine but kept B5-deficient had persistently lower CoA and less weight recovery than mice receiving both nutrients, despite restored liver glutathione. Model: Mouse cysteine repletion with or without dietary B5; subsequent tissue GSH/CoA and weight measurements. Limitations: A direct cross-nutrient repletion experiment in mice; not an established human treatment protocol. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8 Evidence access: Primary full text Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y
    Complete structured claim and evidence
  3. Adding B5 to drinking water after seven days on the cysteine-sufficient, B5-deficient recovery diet promptly rescued the weight-recovery difference.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse sequential nutrient-depletion/repletion experiment.
    limitations
    The endpoint was recovery from induced wasting, not weight gain or energy improvement in healthy people. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    A second missing nutrient limited recovery after the first was restored.
    primary_references
    Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 332–338

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse sequential nutrient-depletion/repletion experiment. · source_derived_draft · unverified_draft

    ## l-cysteine-b5-restores-weight-recovery A second missing nutrient limited recovery after the first was restored. Adding B5 to drinking water after seven days on the cysteine-sufficient, B5-deficient recovery diet promptly rescued the weight-recovery difference. Model: Mouse sequential nutrient-depletion/repletion experiment. Limitations: The endpoint was recovery from induced wasting, not weight gain or energy improvement in healthy people. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8 Evidence access: Primary full text Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y
    Complete structured claim and evidence
  4. Cth-null mice on a low cyst(e)ine diet developed reduced liver/muscle glutathione, acute skeletal myopathy and fatal paralysis in the reported model.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse Cth deletion with controlled low cyst(e)ine feeding.
    limitations
    Genetic plus dietary intervention; this does not establish a dose threshold for healthy people.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Diet became essential when the animal could not make enough internally.
    primary_references
    Cystathionine gamma-Lyase-deficient mice require dietary cysteine to protect against acute lethal myopathy and oxidative injury. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20566639/ · DOI 10.1074/jbc.M110.147439
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 300–306

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse Cth deletion with controlled low cyst(e)ine feeding. · source_derived_draft · unverified_draft

    ## l-cysteine-cth-diet-myopathy Diet became essential when the animal could not make enough internally. Cth-null mice on a low cyst(e)ine diet developed reduced liver/muscle glutathione, acute skeletal myopathy and fatal paralysis in the reported model. Model: Mouse Cth deletion with controlled low cyst(e)ine feeding. Limitations: Genetic plus dietary intervention; this does not establish a dose threshold for healthy people. Evidence access: Primary abstract Cystathionine gamma-Lyase-deficient mice require dietary cysteine to protect against acute lethal myopathy and oxidative injury. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20566639/ · DOI 10.1074/jbc.M110.147439
    Complete structured claim and evidence
  5. Cysteine-depleted Cse-null mice excreted more intermediary metabolites, including pyruvate, citrate, 2-oxoglutarate and orotate, with altered hepatic glycolytic and TCA-cycle metabolism.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse tissue/urine metabolomics during combined genetic and dietary depletion.
    limitations
    Metabolite abundance alone is not complete pathway flux or a human diagnostic signature. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    The shortage affected how efficiently the animal retained and used fuel.
    primary_references
    Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 316–322

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse tissue/urine metabolomics during combined genetic and dietary depletion. · source_derived_draft · unverified_draft

    ## l-cysteine-depletion-carbon-loss The shortage affected how efficiently the animal retained and used fuel. Cysteine-depleted Cse-null mice excreted more intermediary metabolites, including pyruvate, citrate, 2-oxoglutarate and orotate, with altered hepatic glycolytic and TCA-cycle metabolism. Model: Mouse tissue/urine metabolomics during combined genetic and dietary depletion. Limitations: Metabolite abundance alone is not complete pathway flux or a human diagnostic signature. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8 Evidence access: Primary full text Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y
    Complete structured claim and evidence
  6. Combined Cse loss and cysteine-free feeding reduced liver and muscle CoA, alongside glutathione depletion and major metabolic changes.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse genetic/dietary depletion; tissue CoA measurements at days 2 and 7.
    limitations
    CoA depletion accompanies several changes; do not assign all weight loss to one metabolite. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    A cysteine shortage reduced an energy-metabolism cofactor as well as an antioxidant.
    primary_references
    Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 308–314

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic/dietary depletion; tissue CoA measurements at days 2 and 7. · source_derived_draft · unverified_draft

    ## l-cysteine-depletion-coa A cysteine shortage reduced an energy-metabolism cofactor as well as an antioxidant. Combined Cse loss and cysteine-free feeding reduced liver and muscle CoA, alongside glutathione depletion and major metabolic changes. Model: Mouse genetic/dietary depletion; tissue CoA measurements at days 2 and 7. Limitations: CoA depletion accompanies several changes; do not assign all weight loss to one metabolite. Correction record: Author correction published 12 December 2025 (2026 issue), PMID 41388205, DOI 10.1038/s41586-025-09780-8: two incorrect day-3 muscle histology panels in Extended Data Fig. 2f,g duplicated day-7 panels and were replaced. The authors state that figure and paper conclusions were unaffected. This is a figure correction, not independent validation. https://www.nature.com/articles/s41586-025-09780-8 Evidence access: Primary full text Unravelling cysteine-deficiency-associated rapid weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40399674/ · DOI 10.1038/s41586-025-08996-y
    Complete structured claim and evidence
  7. Additional Fgf21 deletion in Cth-null mice did not prevent the rapid weight-loss phenotype during cysteine-free feeding.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Cth-null versus Cth/Fgf21 double-null mice on cysteine-free diet for five days.
    limitations
    Different genotype and diet from the combined methionine/cysteine restriction study; no universal FGF21 dependence is assigned.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    An increased hormone level did not make that hormone necessary for this outcome.
    primary_references
    Cysteine depletion triggers adipose tissue thermogenesis and weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40461845/ · DOI 10.1038/s42255-025-01297-8
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 364–370

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cth-null versus Cth/Fgf21 double-null mice on cysteine-free diet for five days. · source_derived_draft · unverified_draft

    ## l-cysteine-fgf21-cysteine-only-limit An increased hormone level did not make that hormone necessary for this outcome. Additional Fgf21 deletion in Cth-null mice did not prevent the rapid weight-loss phenotype during cysteine-free feeding. Model: Cth-null versus Cth/Fgf21 double-null mice on cysteine-free diet for five days. Limitations: Different genotype and diet from the combined methionine/cysteine restriction study; no universal FGF21 dependence is assigned. Evidence access: Primary full text Cysteine depletion triggers adipose tissue thermogenesis and weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40461845/ · DOI 10.1038/s42255-025-01297-8
    Complete structured claim and evidence
  8. Whole-body Cth-null mice fed a cysteine-free diet developed rapid fat loss and adipose browning; restoring cysteine reversed the phenotype, whereas prolonged depletion could be lethal.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse genetic/dietary depletion and repletion; lean and obese models.
    limitations
    Severe induced deficiency is not evidence for a safe human weight-loss strategy.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Loss of the nutrient caused systemic stress, not simply a desirable fat-burning switch.
    primary_references
    Cysteine depletion triggers adipose tissue thermogenesis and weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40461845/ · DOI 10.1038/s42255-025-01297-8
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 356–362

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic/dietary depletion and repletion; lean and obese models. · source_derived_draft · unverified_draft

    ## l-cysteine-systemic-depletion-reversal Loss of the nutrient caused systemic stress, not simply a desirable fat-burning switch. Whole-body Cth-null mice fed a cysteine-free diet developed rapid fat loss and adipose browning; restoring cysteine reversed the phenotype, whereas prolonged depletion could be lethal. Model: Mouse genetic/dietary depletion and repletion; lean and obese models. Limitations: Severe induced deficiency is not evidence for a safe human weight-loss strategy. Evidence access: Primary full text Cysteine depletion triggers adipose tissue thermogenesis and weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40461845/ · DOI 10.1038/s42255-025-01297-8
    Complete structured claim and evidence
  9. Txndc17 knockout mice showed protection in the acute pancreatitis model, accompanied by Nrf2-pathway activation and increased transsulfuration.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse genetic deletion and experimental acute pancreatitis.
    limitations
    Not a recommendation to inhibit TRP14; the finding does not contradict its cystine-reduction role.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    An enzyme defect can trigger protective compensation in a specific stress model.
    primary_references
    TRP14 is the rate-limiting enzyme for intracellular cystine reduction and regulates proteome cysteinylation. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38811853/ · DOI 10.1038/s44318-024-00117-1
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply 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 · Mouse genetic deletion and experimental acute pancreatitis. · source_derived_draft · unverified_draft

    ## l-cysteine-trp14-mouse-adaptation An enzyme defect can trigger protective compensation in a specific stress model. Txndc17 knockout mice showed protection in the acute pancreatitis model, accompanied by Nrf2-pathway activation and increased transsulfuration. Model: Mouse genetic deletion and experimental acute pancreatitis. Limitations: Not a recommendation to inhibit TRP14; the finding does not contradict its cystine-reduction role. Evidence access: Primary full text TRP14 is the rate-limiting enzyme for intracellular cystine reduction and regulates proteome cysteinylation. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38811853/ · DOI 10.1038/s44318-024-00117-1
    Complete structured claim and evidence
  10. Cth/Ucp1 double-null mice still lost weight during cysteine deprivation; body-mass-adjusted energy expenditure was lower than in Cth-null mice in the reported comparison.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse double-knockout comparisons, six-day diet and metabolic-cage analysis.
    limitations
    UCP1-independent weight loss must not be generalized to UCP1-independent heat production or identical energy expenditure.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Persistence of weight loss does not mean every thermogenic measurement was unchanged.
    primary_references
    Cysteine depletion triggers adipose tissue thermogenesis and weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40461845/ · DOI 10.1038/s42255-025-01297-8
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 380–386

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse double-knockout comparisons, six-day diet and metabolic-cage analysis. · source_derived_draft · unverified_draft

    ## l-cysteine-ucp1-endpoint-limit Persistence of weight loss does not mean every thermogenic measurement was unchanged. Cth/Ucp1 double-null mice still lost weight during cysteine deprivation; body-mass-adjusted energy expenditure was lower than in Cth-null mice in the reported comparison. Model: Mouse double-knockout comparisons, six-day diet and metabolic-cage analysis. Limitations: UCP1-independent weight loss must not be generalized to UCP1-independent heat production or identical energy expenditure. Evidence access: Primary full text Cysteine depletion triggers adipose tissue thermogenesis and weight loss. · 2025 · https://pubmed.ncbi.nlm.nih.gov/40461845/ · DOI 10.1038/s42255-025-01297-8
    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