Component

Human glutathione-specific gamma-glutamylcyclotransferase CHAC1

Human glutathione-specific gamma-glutamylcyclotransferase CHAC1. Species, exposure and limitations are retained in each linked claim.

3 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 it acts on

  1. CHAC1 overexpression depleted GSH in HEK293 cells; a catalytic mutation alleviated that depletion.

    Human glutathione-specific gamma-glutamylcyclotransferase CHAC1 → Cellular reduced-glutathione pool source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/25931127.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a561d11e802b38659805fe90dcab499bf0f434dbe91fa5510cf1eb4efb3460b1", "start_char": 0, "end_char": 1504, "text_sha256": "a561d11e802b38659805fe90dcab499bf0f434dbe91fa5510cf1eb4efb3460b1"}
    experimental_model
    Human promoter reporters, binding assays and overexpression
    exposure
    ER stress, ATF4 and CHAC1 expression
    limitations
    Cell experiments; CHAC1 induction is not a dietary GSH-deficiency diagnosis.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Human
    plain_language
    Low glutathione can reflect increased breakdown, not just poor supply.
    primary_references
    [glutathione-p25931127] Human CHAC1 Protein Degrades Glutathione, and mRNA Induction Is Regulated by the Transcription Factors ATF4 and ATF3 and a Bipartite ATF/CRE Regulatory Element. (2015). https://pubmed.ncbi.nlm.nih.gov/25931127/ DOI: 10.1074/jbc.m114.635144
    tissue_or_cell_type
    HEK293 and U2OS cells

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 580–591

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human promoter reporters, binding assays and overexpression · source_derived_draft · unverified_draft

    ### glutathione-chac1-gsh CHAC1 overexpression depleted GSH in HEK293 cells; a catalytic mutation alleviated that depletion. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low glutathione can reflect increased breakdown, not just poor supply. organism: Human tissue_or_cell_type: HEK293 and U2OS cells experimental_model: Human promoter reporters, binding assays and overexpression limitations: Cell experiments; CHAC1 induction is not a dietary GSH-deficiency diagnosis. exposure: ER stress, ATF4 and CHAC1 expression evidence_span: {"source_cache": "artifacts/glutathione-research/25931127.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a561d11e802b38659805fe90dcab499bf0f434dbe91fa5510cf1eb4efb3460b1", "start_char": 0, "end_char": 1504, "text_sha256": "a561d11e802b38659805fe90dcab499bf0f434dbe91fa5510cf1eb4efb3460b1"} [glutathione-p25931127] Human CHAC1 Protein Degrades Glutathione, and mRNA Induction Is Regulated by the Transcription Factors ATF4 and ATF3 and a Bipartite ATF/CRE Regulatory Element. (2015). https://pubmed.ncbi.nlm.nih.gov/25931127/ DOI: 10.1074/jbc.m114.635144
    Complete structured claim and evidence

  2. CHAC1 likewise lacked activity against GSSG in this comparison.

    Human glutathione-specific gamma-glutamylcyclotransferase CHAC1 → GSSG source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/27913623.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ddf397c2cb8fd60423c89cab28a0b54d124f0e34e0564a32d6bca36841530694", "start_char": 0, "end_char": 1617, "text_sha256": "ddf397c2cb8fd60423c89cab28a0b54d124f0e34e0564a32d6bca36841530694"}
    experimental_model
    Purified mammalian enzymes and expression comparison
    exposure
    CHAC1/CHAC2 substrate and kinetics comparison
    limitations
    Human kinetics and yeast structure are distinct; this does not establish a universal turnover rate in vivo.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Human and mouse enzymes; yeast structural homolog
    plain_language
    Substrate identity matters even within one degradation family.
    primary_references
    [glutathione-p27913623] ChaC2, an Enzyme for Slow Turnover of Cytosolic Glutathione. (2017). https://pubmed.ncbi.nlm.nih.gov/27913623/ DOI: 10.1074/jbc.m116.727479
    tissue_or_cell_type
    Cytosolic glutathione turnover

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 619–630

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified mammalian enzymes and expression comparison · source_derived_draft · unverified_draft

    ### glutathione-chac1-gssg-null CHAC1 likewise lacked activity against GSSG in this comparison. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Substrate identity matters even within one degradation family. organism: Human and mouse enzymes; yeast structural homolog tissue_or_cell_type: Cytosolic glutathione turnover experimental_model: Purified mammalian enzymes and expression comparison limitations: Human kinetics and yeast structure are distinct; this does not establish a universal turnover rate in vivo. exposure: CHAC1/CHAC2 substrate and kinetics comparison evidence_span: {"source_cache": "artifacts/glutathione-research/27913623.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ddf397c2cb8fd60423c89cab28a0b54d124f0e34e0564a32d6bca36841530694", "start_char": 0, "end_char": 1617, "text_sha256": "ddf397c2cb8fd60423c89cab28a0b54d124f0e34e0564a32d6bca36841530694"} [glutathione-p27913623] ChaC2, an Enzyme for Slow Turnover of Cytosolic Glutathione. (2017). https://pubmed.ncbi.nlm.nih.gov/27913623/ DOI: 10.1074/jbc.m116.727479
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. ATF4-responsive promoter elements supported human CHAC1 transcription in reporter experiments.

    Human activating transcription factor 4 / ATF4 → Human CHAC1 promoter activity and expression source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/25931127.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a561d11e802b38659805fe90dcab499bf0f434dbe91fa5510cf1eb4efb3460b1", "start_char": 0, "end_char": 1504, "text_sha256": "a561d11e802b38659805fe90dcab499bf0f434dbe91fa5510cf1eb4efb3460b1"}
    experimental_model
    Human promoter reporters, binding assays and overexpression
    exposure
    ER stress, ATF4 and CHAC1 expression
    limitations
    Cell experiments; CHAC1 induction is not a dietary GSH-deficiency diagnosis.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Human
    plain_language
    A stress-response factor can turn on glutathione breakdown.
    primary_references
    [glutathione-p25931127] Human CHAC1 Protein Degrades Glutathione, and mRNA Induction Is Regulated by the Transcription Factors ATF4 and ATF3 and a Bipartite ATF/CRE Regulatory Element. (2015). https://pubmed.ncbi.nlm.nih.gov/25931127/ DOI: 10.1074/jbc.m114.635144
    tissue_or_cell_type
    HEK293 and U2OS cells

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 567–578

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human promoter reporters, binding assays and overexpression · source_derived_draft · unverified_draft

    ### glutathione-atf4-chac1 ATF4-responsive promoter elements supported human CHAC1 transcription in reporter experiments. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: A stress-response factor can turn on glutathione breakdown. organism: Human tissue_or_cell_type: HEK293 and U2OS cells experimental_model: Human promoter reporters, binding assays and overexpression limitations: Cell experiments; CHAC1 induction is not a dietary GSH-deficiency diagnosis. exposure: ER stress, ATF4 and CHAC1 expression evidence_span: {"source_cache": "artifacts/glutathione-research/25931127.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a561d11e802b38659805fe90dcab499bf0f434dbe91fa5510cf1eb4efb3460b1", "start_char": 0, "end_char": 1504, "text_sha256": "a561d11e802b38659805fe90dcab499bf0f434dbe91fa5510cf1eb4efb3460b1"} [glutathione-p25931127] Human CHAC1 Protein Degrades Glutathione, and mRNA Induction Is Regulated by the Transcription Factors ATF4 and ATF3 and a Bipartite ATF/CRE Regulatory Element. (2015). https://pubmed.ncbi.nlm.nih.gov/25931127/ DOI: 10.1074/jbc.m114.635144
    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