Component

D-Serine

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

9 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. Human serine racemase catalyzes the PLP-dependent formation of D-serine from L-serine; replacing Ser84 with alanine shifted its behavior toward serine dehydratase activity.

    Human serine racemase / SRR → D-Serine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Recombinant human serine racemase and serine dehydratase mutants with functional comparisons.
    limitations
    Engineered reaction switching does not mean the native enzymes have identical functions.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    One enzyme creates the D-form used in a distinct signaling pathway.
    primary_references
    Modulating the function of human serine racemase and human serine dehydratase by protein engineering. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23112234/ · DOI 10.1093/protein/gzs078

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 406–412

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human serine racemase and serine dehydratase mutants with functional comparisons. · source_derived_draft · unverified_draft

    ## l-serine-srr-racemization One enzyme creates the D-form used in a distinct signaling pathway. Human serine racemase catalyzes the PLP-dependent formation of D-serine from L-serine; replacing Ser84 with alanine shifted its behavior toward serine dehydratase activity. Model: Recombinant human serine racemase and serine dehydratase mutants with functional comparisons. Limitations: Engineered reaction switching does not mean the native enzymes have identical functions. Evidence access: Primary abstract Modulating the function of human serine racemase and human serine dehydratase by protein engineering. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23112234/ · DOI 10.1093/protein/gzs078
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Astrocytic Phgdh inhibition reduced newly synthesized L- and D-serine; neuronal serine-racemase deletion reduced D-serine synthesis to a similar extent.

    Mouse phosphoglycerate dehydrogenase / Phgdh → New D-serine synthesis in mouse neurons source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse genetic and hippocampal experiments with synthesis measurements.
    limitations
    This does not establish exclusive cell-type localization under every developmental or disease condition.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    Support cells can supply precursor while neurons perform the final conversion.
    primary_references
    The NMDA receptor activation by d-serine and glycine is controlled by an astrocytic Phgdh-dependent serine shuttle. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31548413/ · DOI 10.1073/pnas.1909458116
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 342–348

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic and hippocampal experiments with synthesis measurements. · source_derived_draft · unverified_draft

    ## l-serine-astrocyte-shuttle Support cells can supply precursor while neurons perform the final conversion. Astrocytic Phgdh inhibition reduced newly synthesized L- and D-serine; neuronal serine-racemase deletion reduced D-serine synthesis to a similar extent. Model: Mouse genetic and hippocampal experiments with synthesis measurements. Limitations: This does not establish exclusive cell-type localization under every developmental or disease condition. Evidence access: Primary abstract The NMDA receptor activation by d-serine and glycine is controlled by an astrocytic Phgdh-dependent serine shuttle. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31548413/ · DOI 10.1073/pnas.1909458116
    Complete structured claim and evidence

  2. Intracellular glycine tonically inhibited serine racemase in the study, while glycine exposure could transiently promote D-serine release through Asc-1.

    Glycine → Mouse serine racemase / Srr source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Biochemical assays, primary cultures and mouse microdialysis; Asc-1 knockout abolished the release response.
    limitations
    Inhibition of synthesis and stimulation of release are distinct endpoints, not contradictory directions for one reaction.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    The same neighboring amino acid can affect both production and release in different ways.
    primary_references
    The NMDA receptor activation by d-serine and glycine is controlled by an astrocytic Phgdh-dependent serine shuttle. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31548413/ · DOI 10.1073/pnas.1909458116

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 358–364

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Biochemical assays, primary cultures and mouse microdialysis; Asc-1 knockout abolished the release response. · source_derived_draft · unverified_draft

    ## l-serine-glycine-racemase The same neighboring amino acid can affect both production and release in different ways. Intracellular glycine tonically inhibited serine racemase in the study, while glycine exposure could transiently promote D-serine release through Asc-1. Model: Biochemical assays, primary cultures and mouse microdialysis; Asc-1 knockout abolished the release response. Limitations: Inhibition of synthesis and stimulation of release are distinct endpoints, not contradictory directions for one reaction. Evidence access: Primary abstract The NMDA receptor activation by d-serine and glycine is controlled by an astrocytic Phgdh-dependent serine shuttle. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31548413/ · DOI 10.1073/pnas.1909458116
    Complete structured claim and evidence

  3. Enzymatic removal of extracellular L-serine impaired hippocampal long-term potentiation, supporting a role for an intercellular serine supply route.

    L-Serine → Mouse hippocampal serine-shuttle-dependent plasticity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse hippocampal synaptic experiments.
    limitations
    L-serine supplies D-serine; this is not evidence that L-serine directly substitutes at the NMDAR coagonist site.
    nutrient_topic
    L-Serine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Serine
    plain_language
    Removing extracellular precursor can disrupt a downstream signaling response.
    primary_references
    The NMDA receptor activation by d-serine and glycine is controlled by an astrocytic Phgdh-dependent serine shuttle. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31548413/ · DOI 10.1073/pnas.1909458116
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Serine: synthesis, one-carbon metabolism, lipids and cross-nutrient mechanisms (2026-09-19) · lines 350–356

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse hippocampal synaptic experiments. · source_derived_draft · unverified_draft

    ## l-serine-shuttle-ltp Removing extracellular precursor can disrupt a downstream signaling response. Enzymatic removal of extracellular L-serine impaired hippocampal long-term potentiation, supporting a role for an intercellular serine supply route. Model: Mouse hippocampal synaptic experiments. Limitations: L-serine supplies D-serine; this is not evidence that L-serine directly substitutes at the NMDAR coagonist site. Evidence access: Primary abstract The NMDA receptor activation by d-serine and glycine is controlled by an astrocytic Phgdh-dependent serine shuttle. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31548413/ · DOI 10.1073/pnas.1909458116
    Complete structured claim and evidence

  4. Compared with age-adjusted controls, NKH patients had higher CSF threonine, lower serine and higher glycine.

    L-Threonine → CSF threonine in genetically confirmed nonketotic hyperglycinemia source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    61 genetically confirmed patients versus reference data from 274 controls; stereoselective serine analysis in a smaller subset.
    limitations
    Association does not identify a unique transport mechanism or justify treating an isolated CSF ratio.
    nutrient_topic
    L-Threonine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Threonine
    plain_language
    A high amino-acid measurement can accompany a defect in a neighboring pathway.
    primary_references
    Cerebrospinal fluid amino acids glycine, serine, and threonine in nonketotic hyperglycinemia. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35357708/ · DOI 10.1002/jimd.12500
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    L-Threonine: translation, intestinal barrier, metabolism and cross-nutrient mechanisms (2026-09-19) · lines 418–424

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 61 genetically confirmed patients versus reference data from 274 controls; stereoselective serine analysis in a smaller subset. · source_derived_draft · unverified_draft

    ## l-threonine-nkh-amino-acid-pattern A high amino-acid measurement can accompany a defect in a neighboring pathway. Compared with age-adjusted controls, NKH patients had higher CSF threonine, lower serine and higher glycine. Model: 61 genetically confirmed patients versus reference data from 274 controls; stereoselective serine analysis in a smaller subset. Limitations: Association does not identify a unique transport mechanism or justify treating an isolated CSF ratio. Evidence access: Primary abstract Cerebrospinal fluid amino acids glycine, serine, and threonine in nonketotic hyperglycinemia. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35357708/ · DOI 10.1002/jimd.12500
    Complete structured claim and evidence

  5. Mg2+ and ATP increased recombinant serine-racemase serine racemization and pyruvate production by approximately five- to ten-fold in the study assay.

    Serine-racemase cofactor assay, construct species unresolved here → Magnesium/ATP stimulation of serine-racemase activity source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Recombinant enzyme and cell-extract experiments; construct species not resolved in accessed abstract.
    limitations
    This is a shared-machinery connection, not a demonstrated magnesium effect on D-aspartate flux.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Mineral and energy cofactors affect this enzyme, but the measured substrate was serine.
    primary_references
    Cofactors of serine racemase that physiologically stimulate the synthesis of the N-methyl-D-aspartate (NMDA) receptor coagonist D-serine. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12393813/ · DOI 10.1073/pnas.222421299

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 64–70

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant enzyme and cell-extract experiments; construct species not resolved in accessed abstract. · source_derived_draft · unverified_draft

    ## d-aspartate-srr-mg-atp Mineral and energy cofactors affect this enzyme, but the measured substrate was serine. Mg2+ and ATP increased recombinant serine-racemase serine racemization and pyruvate production by approximately five- to ten-fold in the study assay. Model: Recombinant enzyme and cell-extract experiments; construct species not resolved in accessed abstract. Limitations: This is a shared-machinery connection, not a demonstrated magnesium effect on D-aspartate flux. Evidence access: Primary abstract Cofactors of serine racemase that physiologically stimulate the synthesis of the N-methyl-D-aspartate (NMDA) receptor coagonist D-serine. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12393813/ · DOI 10.1073/pnas.222421299
    Complete structured claim and evidence

  6. Srr deletion lowered D-aspartate in mouse frontal cortex and hippocampus, while cerebellum and testes were unchanged.

    Mouse serine racemase / Srr → Mouse regional brain free D-aspartate pool source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Srr-knockout mice; regional amino-acid measurements.
    limitations
    Not dietary deficiency or proof that a supplement repairs the knockout.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Dependence on the same enzyme varies by tissue.
    primary_references
    Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 40–46

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Srr-knockout mice; regional amino-acid measurements. · source_derived_draft · unverified_draft

    ## d-aspartate-srr-mouse-loss Dependence on the same enzyme varies by tissue. Srr deletion lowered D-aspartate in mouse frontal cortex and hippocampus, while cerebellum and testes were unchanged. Model: Srr-knockout mice; regional amino-acid measurements. Limitations: Not dietary deficiency or proof that a supplement repairs the knockout. Evidence access: Primary abstract Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
    Complete structured claim and evidence

  7. Deleting endogenous SRR in rat PC12 cells lowered D-serine but left D-aspartate production unchanged.

    Rat serine racemase / Srr → D-aspartate pool in rat PC12 cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Rat PC12 SRR knockout.
    limitations
    The alternative synthesis route was not identified.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    The cells retained another way to maintain D-aspartate.
    primary_references
    Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 32–38

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat PC12 SRR knockout. · source_derived_draft · unverified_draft

    ## d-aspartate-srr-pc12-loss The cells retained another way to maintain D-aspartate. Deleting endogenous SRR in rat PC12 cells lowered D-serine but left D-aspartate production unchanged. Model: Rat PC12 SRR knockout. Limitations: The alternative synthesis route was not identified. Evidence access: Primary abstract Serine racemase is involved in d-aspartate biosynthesis. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27387750/ · DOI 10.1093/jb/mvw043
    Complete structured claim and evidence

  8. The 1.89-angstrom human serine-racemase holoenzyme structure included its bound pyridoxal-phosphate cofactor.

    PLP → Human serine racemase / SRR source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Purified human SRR crystal structure.
    limitations
    Structural cofactor binding does not establish dietary B6 control of human D-aspartate or an effective supplementation threshold.
    nutrient_topic
    D-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · D-Aspartate
    plain_language
    Vitamin B6-derived PLP is part of the shared racemase machinery.
    primary_references
    Conformational flexibility within the small domain of human serine racemase. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32039887/ · DOI 10.1107/S2053230X20001193

    D-Aspartate: synthesis, clearance, neural and endocrine mechanisms (2026-09-19) · lines 56–62

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified human SRR crystal structure. · source_derived_draft · unverified_draft

    ## d-aspartate-srr-plp Vitamin B6-derived PLP is part of the shared racemase machinery. The 1.89-angstrom human serine-racemase holoenzyme structure included its bound pyridoxal-phosphate cofactor. Model: Purified human SRR crystal structure. Limitations: Structural cofactor binding does not establish dietary B6 control of human D-aspartate or an effective supplementation threshold. Evidence access: Primary abstract Conformational flexibility within the small domain of human serine racemase. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32039887/ · DOI 10.1107/S2053230X20001193
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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