Component

SCLY

PLP-dependent enzyme that releases selenium from free selenocysteine; not itself a selenoprotein.

7 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. Human SCLY has two cofactor-containing active sites at its homodimer interface, with both subunits contributing to each site.

    SCLY → PLP source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    B6-dependent machinery participates in selenium metabolism.
    existing_related_claim_ids
    ["54d5691e-ef60-5f20-a204-abc3fcef9c21", "b6605dbc-466c-5591-965b-0a11b1b3c6fc"]
    experimental_model
    Recombinant human SCLY; structures and substrate assays
    limitations
    Structural/biochemical evidence; dietary B6 withdrawal was not tested.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    The selenium enzyme has a shared B6-binding architecture.
    primary_references
    [b6-scly-2012] Biochemical Discrimination between Selenium and Sulfur 1: A Single Residue Provides Selenium Specificity to Human Selenocysteine Lyase (2012). https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0030581 DOI: 10.1371/journal.pone.0030581
    tissue_or_cell_type
    Purified recombinant protein; no intact tissue

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 924–935

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human SCLY; structures and substrate assays · source_derived_draft · unverified_draft

    ### b6-met-scly-structure Human SCLY has two cofactor-containing active sites at its homodimer interface, with both subunits contributing to each site. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The selenium enzyme has a shared B6-binding architecture. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human SCLY; structures and substrate assays limitations: Structural/biochemical evidence; dietary B6 withdrawal was not tested. cross_nutrient: B6-dependent machinery participates in selenium metabolism. existing_related_claim_ids: ["54d5691e-ef60-5f20-a204-abc3fcef9c21", "b6605dbc-466c-5591-965b-0a11b1b3c6fc"] [b6-scly-2012] Biochemical Discrimination between Selenium and Sulfur 1: A Single Residue Provides Selenium Specificity to Human Selenocysteine Lyase (2012). https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0030581 DOI: 10.1371/journal.pone.0030581
    Complete structured claim and evidence

  2. Jurkat cells retained efficient SELENOP utilization without SCLY.

    SCLY → Selenoprotein biosynthesis source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    Jurkat
    experimental_model
    SCLY disruption
    limitations
    Alternative recovery chemistry is unresolved.
    organism
    human

    Selenium: literature corrections and mechanism additions · lines 582–592

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · SCLY disruption · secondary_verified · secondary_verified

    ## jurkat-selenop-use-persists-without-scly This cell line used a SCLY-independent recovery route. Jurkat cells retained efficient SELENOP utilization without SCLY. Organism: human Cell type: Jurkat Experimental model: SCLY disruption Limitations: Alternative recovery chemistry is unresolved. Primary reference: [An efficient selenium transport pathway of selenoprotein P utilizing a high-affinity ApoER2 receptor variant and being independent of selenocysteine lyase](https://pubmed.ncbi.nlm.nih.gov/37406814/)
    Complete structured claim and evidence

  3. RD cells used a lysosomal SELENOP recovery route dependent on SCLY.

    SCLY → Selenoprotein biosynthesis source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    RD rhabdomyosarcoma
    experimental_model
    Perturbation assays
    limitations
    Dependency does not locate SCLY catalysis inside lysosomes.
    organism
    human

    Selenium: literature corrections and mechanism additions · lines 570–580

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Perturbation assays · secondary_verified · secondary_verified

    ## rd-lysosomal-selenop-recovery-requires-scly These rhabdomyosarcoma cells required SCLY for SELENOP selenium recovery. RD cells used a lysosomal SELENOP recovery route dependent on SCLY. Organism: human Cell type: RD rhabdomyosarcoma Experimental model: Perturbation assays Limitations: Dependency does not locate SCLY catalysis inside lysosomes. Primary reference: [An efficient selenium transport pathway of selenoprotein P utilizing a high-affinity ApoER2 receptor variant and being independent of selenocysteine lyase](https://pubmed.ncbi.nlm.nih.gov/37406814/)
    Complete structured claim and evidence

  4. SCLY decomposes free L-selenocysteine, yielding L-alanine and released selenium.

    SCLY → Sec source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    liver-derived enzyme
    experimental_model
    Purified and recombinant enzyme
    limitations
    The original assay described elemental selenium; intracellular speciation remains separate.
    organism
    mouse

    Selenium: literature corrections and mechanism additions · lines 510–520

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Purified and recombinant enzyme · secondary_verified · secondary_verified

    ## scly-decomposes-selenocysteine SCLY recovers selenium from free selenocysteine. SCLY decomposes free L-selenocysteine, yielding L-alanine and released selenium. Organism: mouse Cell type: liver-derived enzyme Experimental model: Purified and recombinant enzyme Limitations: The original assay described elemental selenium; intracellular speciation remains separate. Primary reference: [cDNA cloning, purification, and characterization of mouse liver selenocysteine lyase. Candidate for selenium delivery protein in selenoprotein synthesis](https://pubmed.ncbi.nlm.nih.gov/10692412/)
    Complete structured claim and evidence

  5. SCLY knockdown reduced incorporation of SELENOP-derived selenium into newly synthesized selenoproteins in HeLa cells.

    SCLY → Selenoprotein biosynthesis source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    HeLa
    experimental_model
    75Se-labeled SELENOP and RNA interference
    limitations
    Cell-specific dependency; not a universal uptake sequence.
    organism
    human

    Selenium: literature corrections and mechanism additions · lines 534–544

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · 75Se-labeled SELENOP and RNA interference · secondary_verified · secondary_verified

    ## scly-supports-selenop-selenium-reuse These cells needed SCLY for efficient selenium reuse. SCLY knockdown reduced incorporation of SELENOP-derived selenium into newly synthesized selenoproteins in HeLa cells. Organism: human Cell type: HeLa Experimental model: 75Se-labeled SELENOP and RNA interference Limitations: Cell-specific dependency; not a universal uptake sequence. Primary reference: [Mammalian Selenocysteine Lyase Is Involved in Selenoprotein Biosynthesis](https://www.jstage.jst.go.jp/article/jnsv/57/4/57_4_298/_article/-char/en)
    Complete structured claim and evidence

What acts on it

  1. SCLY is a pyridoxal-phosphate-dependent enzyme.

    PLP → SCLY source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    liver-derived enzyme
    experimental_model
    Enzyme characterization
    limitations
    Not evidence that extra vitamin B6 improves selenium recycling.
    organism
    mouse

    Selenium: literature corrections and mechanism additions · lines 522–532

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Enzyme characterization · secondary_verified · secondary_verified

    ## plp-supports-scly-catalysis SCLY uses a vitamin B6-derived cofactor. SCLY is a pyridoxal-phosphate-dependent enzyme. Organism: mouse Cell type: liver-derived enzyme Experimental model: Enzyme characterization Limitations: Not evidence that extra vitamin B6 improves selenium recycling. Primary reference: [cDNA cloning, purification, and characterization of mouse liver selenocysteine lyase. Candidate for selenium delivery protein in selenoprotein synthesis](https://pubmed.ncbi.nlm.nih.gov/10692412/)
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Replacing Asp146 with lysine gave human SCLY detectable cysteine-desulfurase activity absent from wild-type activity assays.

    Human SCLY Asp146Lys variant → L-Cysteine source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Protein architecture distinguishes sulfur from selenium at a B6-dependent enzyme.
    experimental_model
    Recombinant human SCLY; structures and substrate assays
    limitations
    Engineered gain of function; physiological rates and clinical effects were not tested.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    A specific enzyme residue helps distinguish selenium from sulfur substrates.
    primary_references
    [b6-scly-2012] Biochemical Discrimination between Selenium and Sulfur 1: A Single Residue Provides Selenium Specificity to Human Selenocysteine Lyase (2012). https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0030581 DOI: 10.1371/journal.pone.0030581
    tissue_or_cell_type
    Purified recombinant protein; no intact tissue
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 937–947

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human SCLY; structures and substrate assays · source_derived_draft · unverified_draft

    ### b6-met-scly-specificity Replacing Asp146 with lysine gave human SCLY detectable cysteine-desulfurase activity absent from wild-type activity assays. Condition category: machinery_impairment nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A specific enzyme residue helps distinguish selenium from sulfur substrates. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human SCLY; structures and substrate assays limitations: Engineered gain of function; physiological rates and clinical effects were not tested. cross_nutrient: Protein architecture distinguishes sulfur from selenium at a B6-dependent enzyme. [b6-scly-2012] Biochemical Discrimination between Selenium and Sulfur 1: A Single Residue Provides Selenium Specificity to Human Selenocysteine Lyase (2012). https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0030581 DOI: 10.1371/journal.pone.0030581
    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