Component

The autoimmune polyendocrine syndrome type 2-associated autoantibody b96.11

The autoimmune polyendocrine syndrome type 2-associated autoantibody b96.11. Species, exposure and limitations are retained in each linked claim.

1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

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

Where it participates (unsigned role)

  1. Only GAD65 acts as a major autoantigen, frequently implicated in type 1 diabetes and other autoimmune diseases, hydrogen-deuterium exchange reveals local dynamics accompanying autoinactivation with the catalytic loop promoting collective motions at the C-terminal domain and pyridoxal-5-phosphate domain interface, in the complex with the autoantibody the heavy chain complementarity-determining regions dominate the interaction with a long CDRH3 bridging the GAD65 dimer, and thus intrinsic dynamics rather than sequence differences within epitopes appear to be responsible for the contrasting autoantigenicities of GAD65 and GAD67.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/gaba-research/40055307.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "832b0c18514e12230379ef877a5bd017fc67e23d762d3b9f00f5d59dc2f7efe2", "start_char": 0, "end_char": 1448, "text_sha256": "832b0c18514e12230379ef877a5bd017fc67e23d762d3b9f00f5d59dc2f7efe2"}
    experimental_model
    Hydrogen-deuterium exchange mass spectrometry, X-ray crystallography and cryo-electron microscopy of the enzyme with a human autoantibody
    exposure
    Apo and holo forms of GAD65 and the complex with the autoantibody b96.11
    limitations
    Structural and dynamic work on isolated protein. The conclusion about autoantigenicity is an interpretation of dynamics rather than an immunological measurement.
    nutrient_topic
    GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
    organism
    Human protein
    plain_language
    What makes one of the two enzymes the target of an autoimmune attack is how much it moves, not how its surface reads.
    primary_references
    [gb-p40055307] Structure and dynamics of GAD65 in complex with an autoimmune polyendocrine syndrome type 2-associated autoantibody. (2025). https://pubmed.ncbi.nlm.nih.gov/40055307/ DOI: 10.1038/s41467-025-57492-4
    tissue_or_cell_type
    Recombinant enzyme

    GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 144–155

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hydrogen-deuterium exchange mass spectrometry, X-ray crystallography and cryo-electron microscopy of the enzyme with a human autoantibody · source_derived_draft · unverified_draft

    ### gb-dynamics-not-sequence-make-the-autoantigen Only GAD65 acts as a major autoantigen, frequently implicated in type 1 diabetes and other autoimmune diseases, hydrogen-deuterium exchange reveals local dynamics accompanying autoinactivation with the catalytic loop promoting collective motions at the C-terminal domain and pyridoxal-5-phosphate domain interface, in the complex with the autoantibody the heavy chain complementarity-determining regions dominate the interaction with a long CDRH3 bridging the GAD65 dimer, and thus intrinsic dynamics rather than sequence differences within epitopes appear to be responsible for the contrasting autoantigenicities of GAD65 and GAD67. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: What makes one of the two enzymes the target of an autoimmune attack is how much it moves, not how its surface reads. organism: Human protein tissue_or_cell_type: Recombinant enzyme experimental_model: Hydrogen-deuterium exchange mass spectrometry, X-ray crystallography and cryo-electron microscopy of the enzyme with a human autoantibody limitations: Structural and dynamic work on isolated protein. The conclusion about autoantigenicity is an interpretation of dynamics rather than an immunological measurement. exposure: Apo and holo forms of GAD65 and the complex with the autoantibody b96.11 evidence_span: {"source_cache": "artifacts/gaba-research/40055307.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "832b0c18514e12230379ef877a5bd017fc67e23d762d3b9f00f5d59dc2f7efe2", "start_char": 0, "end_char": 1448, "text_sha256": "832b0c18514e12230379ef877a5bd017fc67e23d762d3b9f00f5d59dc2f7efe2"} [gb-p40055307] Structure and dynamics of GAD65 in complex with an autoimmune polyendocrine syndrome type 2-associated autoantibody. (2025). https://pubmed.ncbi.nlm.nih.gov/40055307/ DOI: 10.1038/s41467-025-57492-4
    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