Host: Rabbit

Target Protein: phospho-GABRG2 (Ser366)

IR: Immunogen Range:KP(p-S)KD

Clonality: Polyclonal

Isotype: IgG

Entrez Gene: 2566

Swiss Prot: P18507

Source: KLH conjugated synthesised phosphopeptide derived from human GABRG2 around the phosphorylation site of Ser366:KP(p-S)KD 

Purification: affinity purified by Protein A

Storage: 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.

Background: GAD-65 and GAD-67, glutamate decarboxylases, function to catalyze the production of GABA (gamma-aminobutyric acid). In the central nervous system, GABA functions as the main inhibitory transmitter by increasing a Cl- (chloride) conductance that inhibits neuronal firing. GABA has been shown to activate both ionotropic (GABAA) and metabotropic (GABAB) receptors, as well as a third class of receptors called GABAC. The ?subunit of GABAA receptors are important for benzodiazepine binding and modulation of GABA-mediated Cl- current. GABAA R? is a 467 amino acid mulit-pass membrane protein localized to the postsynaptic cell membrane. Present as a pentamer with other GABAA receptor chains (Alpha, Beta, Gamma, Delta and Epsilon), the GABAA ligand-gated Cl- channels selectively complex with D5DR to enable mutual inhibitory functional interactions between the two receptor systems. Defects in the gene encoding GABAA R Gamma 2 have been found to be the cause of childhood absence epilepsy type 2, familial febrile convulsions type 8, generalized epilepsy with febrile seizures plus type 3 and severe myoclonic epilepsy in infancy.