high-resolution cryo-electron microscopy structures of the human alpha1beta2gamma2 GABAA receptor the predominant isoform in the adult brain in complex with GABA and the benzodiazepine site antagonist flumazenil the first-line clinical treatment for benzodiazepine overdose
Study finds that optimal processing of aversive prediction errors is reduced in individuals genetically predisposed (polymorphisms in GABRB2 and ErbB4) towards decreased GABA neurotransmission.
The GABRB2 downregulation significantly inhibited the colony formation migration and invasion of the three PTC cell lines and GABRB2 plays important tumorigenic functions and acts as a novel oncogene in papillary thyroid carcinoma.
we report the discovery of a de novo heterozygous missense mutation in the GABRB2 gene that encodes the b2 subunit of the GABAA receptor. Our in vitro studies indicate that this mutation causes Early myoclonic encephalopathy via disruption of GABAergic inhibition in the brain
Deletion of the N-terminal extension and putative alpha-helix in heteromeric alpha1beta2gamma2 GABAA receptors in the beta2 subunit affected GABA sensitivity and desensitization.
Our findings underscore the need for further investigation into the mechanisms by which mutations in GABRB2 contribute to neurological and developmental dysfunction.
Mutation of GABA receptor beta2 subunit tyrosine residues in the binding pocket shifts the GABA concentration-response curve; GABA binding rates are reduced by mutation to binding pocket tyrosines.
This study demonistrated that GABRB2 expression was under epigenetic regulation that varied with development genotype and disease status and these regulatory mechanisms were observably disrupted in SCZ and BPD.
Data indicate the selectivity of some selected compounds were assessed in recombinant alpha(1)beta(2)gamma(2)L alpha(2)beta(1)gamma(2)L and alpha(5)beta(2)gamma(2)L GABA(A) receptors.
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