Component

Mouse protein tyrosine phosphatase 1B / Ptpn1

Mouse protein tyrosine phosphatase 1B / Ptpn1. Species, exposure and limitations are retained in each linked claim.

4 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. Hippocampal neuronal-specific PTP1B deletion prevented olanzapine-induced synaptic and cognitive deficits in mice.

    Mouse protein tyrosine phosphatase 1B / Ptpn1 → Mouse cognitive/synaptic response during antipsychotic exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Cell-type-specific mouse genetic intervention.
    limitations
    Does not mean ergothioneine reproduces every consequence of genetic deletion.
    nutrient_topic
    Ergothioneine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Ergothioneine
    plain_language
    Removing the proposed target tested its role in the injury pathway.
    primary_references
    Gut microbiota-derived ergothioneine alleviates antipsychotic-induced synaptic and cognitive impairments. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42013837/ · DOI 10.1016/j.chom.2026.03.020
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Ergothioneine: transport, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 448–454

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Cell-type-specific mouse genetic intervention. · source_derived_draft · unverified_draft

    ## ergothioneine-mouse-ptp1b-deletion Removing the proposed target tested its role in the injury pathway. Hippocampal neuronal-specific PTP1B deletion prevented olanzapine-induced synaptic and cognitive deficits in mice. Model: Cell-type-specific mouse genetic intervention. Limitations: Does not mean ergothioneine reproduces every consequence of genetic deletion. Evidence access: Primary abstract Gut microbiota-derived ergothioneine alleviates antipsychotic-induced synaptic and cognitive impairments. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42013837/ · DOI 10.1016/j.chom.2026.03.020
    Complete structured claim and evidence

What acts on it

  1. Ergothioneine supplementation inhibited hippocampal PTP1B-associated signaling and mitigated synaptic/cognitive impairment in olanzapine-treated mice.

    L-Ergothioneine → Mouse protein tyrosine phosphatase 1B / Ptpn1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse gut-brain study with supplementation.
    limitations
    Abstract supports inhibition but does not establish a direct binding site or human efficacy.
    nutrient_topic
    Ergothioneine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Ergothioneine
    plain_language
    A phosphatase links the compound to a brain signaling pathway.
    primary_references
    Gut microbiota-derived ergothioneine alleviates antipsychotic-induced synaptic and cognitive impairments. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42013837/ · DOI 10.1016/j.chom.2026.03.020

    Ergothioneine: transport, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 440–446

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse gut-brain study with supplementation. · source_derived_draft · unverified_draft

    ## ergothioneine-mouse-ptp1b-inhibition A phosphatase links the compound to a brain signaling pathway. Ergothioneine supplementation inhibited hippocampal PTP1B-associated signaling and mitigated synaptic/cognitive impairment in olanzapine-treated mice. Model: Mouse gut-brain study with supplementation. Limitations: Abstract supports inhibition but does not establish a direct binding site or human efficacy. Evidence access: Primary abstract Gut microbiota-derived ergothioneine alleviates antipsychotic-induced synaptic and cognitive impairments. · 2026 · https://pubmed.ncbi.nlm.nih.gov/42013837/ · DOI 10.1016/j.chom.2026.03.020
    Complete structured claim and evidence

  2. Lipoic acid reduced phosphatase activity and PTP1B thiol reactivity in 3T3-L1 cells.

    Lipoic acid → Mouse protein tyrosine phosphatase 1B / Ptpn1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ala-research/12948866.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9", "start_char": 0, "end_char": 1489, "text_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9"}
    experimental_model
    Protein-thiol, phosphorylation and glucose-uptake assays
    exposure
    Alpha-lipoic-acid stimulation with redox/thiol inhibitors
    limitations
    Cell-culture redox signaling; not proof that lipoic acid invariably lowers oxidation in all settings.
    nutrient_topic
    Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid
    organism
    Mouse
    plain_language
    The exposure weakened a phosphatase brake on phosphorylation signaling.
    primary_references
    [ala-p12948866] Alpha-lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes. (2003). https://pubmed.ncbi.nlm.nih.gov/12948866/ DOI: 10.1016/s0006-2952(03)00395-2
    tissue_or_cell_type
    3T3-L1 adipocytes

    Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 949–960

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein-thiol, phosphorylation and glucose-uptake assays · source_derived_draft · unverified_draft

    ### ala-adipocyte-ptp1b Lipoic acid reduced phosphatase activity and PTP1B thiol reactivity in 3T3-L1 cells. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The exposure weakened a phosphatase brake on phosphorylation signaling. organism: Mouse tissue_or_cell_type: 3T3-L1 adipocytes experimental_model: Protein-thiol, phosphorylation and glucose-uptake assays limitations: Cell-culture redox signaling; not proof that lipoic acid invariably lowers oxidation in all settings. exposure: Alpha-lipoic-acid stimulation with redox/thiol inhibitors evidence_span: {"source_cache": "artifacts/ala-research/12948866.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9", "start_char": 0, "end_char": 1489, "text_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9"} [ala-p12948866] Alpha-lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes. (2003). https://pubmed.ncbi.nlm.nih.gov/12948866/ DOI: 10.1016/s0006-2952(03)00395-2
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Lipoic acid increased glucose uptake in 3T3-L1 adipocytes; intracellular thiol modification or inhibition of the upstream oxidant response blocked stimulation.

    Lipoic acid → Mouse adipocyte glucose uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ala-research/12948866.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9", "start_char": 0, "end_char": 1489, "text_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9"}
    experimental_model
    Protein-thiol, phosphorylation and glucose-uptake assays
    exposure
    Alpha-lipoic-acid stimulation with redox/thiol inhibitors
    limitations
    Cell-culture redox signaling; not proof that lipoic acid invariably lowers oxidation in all settings.
    nutrient_topic
    Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. · Lipoic acid
    organism
    Mouse
    plain_language
    The glucose response depended on the cell’s redox-signaling machinery.
    primary_references
    [ala-p12948866] Alpha-lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes. (2003). https://pubmed.ncbi.nlm.nih.gov/12948866/ DOI: 10.1016/s0006-2952(03)00395-2
    tissue_or_cell_type
    3T3-L1 adipocytes

    Alpha-lipoic acid: cofactor assembly, redox signaling and nutrient interactions (2026-09-17) · lines 962–973

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Protein-thiol, phosphorylation and glucose-uptake assays · source_derived_draft · unverified_draft

    ### ala-adipocyte-glucose Lipoic acid increased glucose uptake in 3T3-L1 adipocytes; intracellular thiol modification or inhibition of the upstream oxidant response blocked stimulation. Condition category: normal nutrient_topic: Alpha-lipoic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose response depended on the cell’s redox-signaling machinery. organism: Mouse tissue_or_cell_type: 3T3-L1 adipocytes experimental_model: Protein-thiol, phosphorylation and glucose-uptake assays limitations: Cell-culture redox signaling; not proof that lipoic acid invariably lowers oxidation in all settings. exposure: Alpha-lipoic-acid stimulation with redox/thiol inhibitors evidence_span: {"source_cache": "artifacts/ala-research/12948866.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9", "start_char": 0, "end_char": 1489, "text_sha256": "0440cb8edaf0213af3824367ee799d1a1916ed2340c9da99588d83c7581804b9"} [ala-p12948866] Alpha-lipoic acid decreases thiol reactivity of the insulin receptor and protein tyrosine phosphatase 1B in 3T3-L1 adipocytes. (2003). https://pubmed.ncbi.nlm.nih.gov/12948866/ DOI: 10.1016/s0006-2952(03)00395-2
    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