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     Gel: 8%SDS-PAGE, Lysate: 40 μg, Lane 1-2: Mouse brain tissue, human fetal brain tissue, Primary antibody: P11777(GABRG2 Antibody) at dilution 1/300, Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution, Exposure time: 1 minute    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human thyroid cancer tissue using P11777(GABRG2 Antibody) at dilution 1/20. (Original magnification: ×200)    

  
  

The GABRG2 antibody targets the gamma-2 subunit (γ2) of the gamma-aminobutyric acid type A (GABA?) receptor, a critical ligand-gated chloride channel mediating inhibitory neurotransmission in the central nervous system. GABA? receptors are pentameric complexes, and the γ2 subunit, encoded by the GABRG2 gene, is essential for synaptic clustering, receptor trafficking, and benzodiazepine sensitivity. Autoantibodies against GABRG2 are rare but increasingly recognized in autoimmune encephalitis, often associated with seizures, cognitive decline, and psychiatric symptoms. These antibodies may disrupt GABAergic signaling by internalizing receptors or interfering with their function, leading to hyperexcitability and neuropsychiatric manifestations.

GABRG2-related autoimmunity is frequently detected alongside antibodies to other GABA? receptor subunits (e.g., α1. β3), complicating clinical characterization. Cases often respond to immunotherapies like corticosteroids, intravenous immunoglobulins, or rituximab, though residual deficits may persist. Beyond autoimmunity, GABRG2 germline mutations are linked to genetic epilepsy syndromes, such as Dravet syndrome and genetic epilepsy with febrile seizures plus (GEFS+), highlighting the subunit's broader role in neuronal excitability. Research continues to explore how GABRG2 antibodies contribute to disease mechanisms and whether their presence correlates with specific clinical phenotypes or treatment outcomes.