Component

Human SLC25A38

Inner mitochondrial membrane carrier implicated in PLP accumulation.

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 it acts on

  1. SLC25A38 loss reduced deuterated-serine incorporation into glycine and glycine-derived glutathione under low-B6 conditions.

    Human SLC25A38 → Serine-derived glycine synthesis in human K562 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 K562 knockout, isotope tracing and controlled B6 culture conditions.
    limitations
    Tracing reflects pathway flux; it does not establish direct PLP transport by SLC25A38.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    A mitochondrial cofactor problem reduced the cell's ability to make glycine.
    primary_references
    SLC25A38 is required for mitochondrial pyridoxal 5'-phosphate (PLP) accumulation. · 2025 · https://pubmed.ncbi.nlm.nih.gov/39856062/ · DOI 10.1038/s41467-025-56130-3
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 114–120

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human K562 knockout, isotope tracing and controlled B6 culture conditions. · source_derived_draft · unverified_draft

    ## glycine-s38-glycine-synthesis A mitochondrial cofactor problem reduced the cell's ability to make glycine. SLC25A38 loss reduced deuterated-serine incorporation into glycine and glycine-derived glutathione under low-B6 conditions. Model: Human K562 knockout, isotope tracing and controlled B6 culture conditions. Limitations: Tracing reflects pathway flux; it does not establish direct PLP transport by SLC25A38. Evidence access: Primary full text SLC25A38 is required for mitochondrial pyridoxal 5'-phosphate (PLP) accumulation. · 2025 · https://pubmed.ncbi.nlm.nih.gov/39856062/ · DOI 10.1038/s41467-025-56130-3
    Complete structured claim and evidence

  2. The biochemical characterization reported glycine transport by human SLC25A38; human SLC25A38 expression complemented heme-pathway defects in yeast lacking Hem25.

    Human SLC25A38 → Glycine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human/yeast carrier biochemistry and yeast genetic complementation.
    limitations
    Primary abstract access; later PLP-homeostasis findings broaden interpretation. This claim does not establish exclusive substrate specificity.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    A mitochondrial carrier connects access to glycine with heme production.
    primary_references
    Characterization of Human and Yeast Mitochondrial Glycine Carriers with Implications for Heme Biosynthesis and Anemia. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27476175/ · DOI 10.1074/jbc.M116.736876
    transport_effect
    raises Human expression complemented heme-pathway defects in yeast lacking Hem25, which is matrix glycine supply.
    transport_pool
    the mitochondrial matrix Human expression complemented heme-pathway defects in yeast lacking Hem25, which is matrix glycine supply.

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 82–88

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human/yeast carrier biochemistry and yeast genetic complementation. · source_derived_draft · unverified_draft

    ## glycine-s38-glycine-transport A mitochondrial carrier connects access to glycine with heme production. The biochemical characterization reported glycine transport by human SLC25A38; human SLC25A38 expression complemented heme-pathway defects in yeast lacking Hem25. Model: Human/yeast carrier biochemistry and yeast genetic complementation. Limitations: Primary abstract access; later PLP-homeostasis findings broaden interpretation. This claim does not establish exclusive substrate specificity. Evidence access: Primary abstract Characterization of Human and Yeast Mitochondrial Glycine Carriers with Implications for Heme Biosynthesis and Anemia. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27476175/ · DOI 10.1074/jbc.M116.736876
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. At 10 nM extracellular PN, SLC25A38-null K562 mitochondria had about 3.9-fold lower PLP despite no whole-cell depletion.

    Human SLC25A38 knockout genotype → PLP source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Supplementary Figure 3E-F
    experimental_model
    Human K562 knockout cells, Mito-IP, LC-MS and isotope tracing.
    exposure
    10 nM PN culture condition.
    limitations
    Not proof that SLC25A38 directly transports PLP.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    A normal whole-cell pool can hide mitochondrial depletion.
    primary_references
    [pena2025] SLC25A38 is required for mitochondrial pyridoxal 5'-phosphate (PLP) accumulation. (2025). https://pubmed.ncbi.nlm.nih.gov/39856062/ DOI: 10.1038/s41467-025-56130-3
    tissue_or_cell_type
    K562 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 452–463

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human K562 knockout cells, Mito-IP, LC-MS and isotope tracing. · source_derived_draft · unverified_draft

    ### b6-transport-slc25a38-pools At 10 nM extracellular PN, SLC25A38-null K562 mitochondria had about 3.9-fold lower PLP despite no whole-cell depletion. Condition category: machinery_impairment nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A normal whole-cell pool can hide mitochondrial depletion. organism: Homo sapiens tissue_or_cell_type: K562 cells experimental_model: Human K562 knockout cells, Mito-IP, LC-MS and isotope tracing. limitations: Not proof that SLC25A38 directly transports PLP. exposure: 10 nM PN culture condition. evidence_location: Supplementary Figure 3E-F [pena2025] SLC25A38 is required for mitochondrial pyridoxal 5'-phosphate (PLP) accumulation. (2025). https://pubmed.ncbi.nlm.nih.gov/39856062/ DOI: 10.1038/s41467-025-56130-3
    Complete structured claim and evidence

  2. R134C add-back failed to restore mitochondrial PLP accumulation in SLC25A38-null cells, unlike wild-type add-back.

    Human SLC25A38 Arg134Cys → PLP source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Figures 3F and 4C-D
    experimental_model
    Human K562 knockout cells, Mito-IP, LC-MS and isotope tracing.
    exposure
    Variant versus wild-type expression.
    limitations
    No direct PLP transport conclusion.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    A disease-associated variant failed the cellular rescue test.
    primary_references
    [pena2025] SLC25A38 is required for mitochondrial pyridoxal 5'-phosphate (PLP) accumulation. (2025). https://pubmed.ncbi.nlm.nih.gov/39856062/ DOI: 10.1038/s41467-025-56130-3
    tissue_or_cell_type
    K562 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 478–489

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human K562 knockout cells, Mito-IP, LC-MS and isotope tracing. · source_derived_draft · unverified_draft

    ### b6-transport-slc25a38-r134c R134C add-back failed to restore mitochondrial PLP accumulation in SLC25A38-null cells, unlike wild-type add-back. Condition category: machinery_impairment nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A disease-associated variant failed the cellular rescue test. organism: Homo sapiens tissue_or_cell_type: K562 cells experimental_model: Human K562 knockout cells, Mito-IP, LC-MS and isotope tracing. limitations: No direct PLP transport conclusion. exposure: Variant versus wild-type expression. evidence_location: Figures 3F and 4C-D [pena2025] SLC25A38 is required for mitochondrial pyridoxal 5'-phosphate (PLP) accumulation. (2025). https://pubmed.ncbi.nlm.nih.gov/39856062/ DOI: 10.1038/s41467-025-56130-3
    Complete structured claim and evidence

  3. Formate at 1 mM rescued the low-B6 proliferation defect of SLC25A38-null K562 cells, while glycine, serine and folate did not under the tested conditions.

    Formate → Growth of SLC25A38-null human K562 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 leukemia cells, knockout and metabolite-rescue experiment.
    limitations
    Culture rescue is not a nutritional recommendation; this growth endpoint differs from zebrafish hemoglobin.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    Restoring a downstream one-carbon source worked where adding an amino acid did not.
    primary_references
    SLC25A38 is required for mitochondrial pyridoxal 5'-phosphate (PLP) accumulation. · 2025 · https://pubmed.ncbi.nlm.nih.gov/39856062/ · DOI 10.1038/s41467-025-56130-3
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 122–128

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human leukemia cells, knockout and metabolite-rescue experiment. · source_derived_draft · unverified_draft

    ## glycine-s38-formate-rescue Restoring a downstream one-carbon source worked where adding an amino acid did not. Formate at 1 mM rescued the low-B6 proliferation defect of SLC25A38-null K562 cells, while glycine, serine and folate did not under the tested conditions. Model: Human leukemia cells, knockout and metabolite-rescue experiment. Limitations: Culture rescue is not a nutritional recommendation; this growth endpoint differs from zebrafish hemoglobin. Evidence access: Primary full text SLC25A38 is required for mitochondrial pyridoxal 5'-phosphate (PLP) accumulation. · 2025 · https://pubmed.ncbi.nlm.nih.gov/39856062/ · DOI 10.1038/s41467-025-56130-3
    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