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g-Aminobutyric acid (GABA) is the major known inhibitory neurotransmitter. The rate-limiting step in the synthesis of GABA is the decarboxylation of glutamate by glutamate decarboxylase (GAD; L-glutamate 1-carboxy-lyase, EC 4.1.115). In the CNS GAB is entirely restricted to GABAergic neurons. GAD is also present in the b-cells of the pancreas and autoantibodies to various GAD polypeptides are detected in insulin-dependent diabetes mellitus. Cloning of GAD genes have identified two subtypes: GAD65 (65 kDa; human 585 AA chromosome 10) and GAD67 (67 kDa; human 594 AA, chromosome 2) share approx. 65% amino acid homology. The N-terminus is the most divergent while the C-terminus is highly conserved. Although both GAD isoforms catalyzes the conversion of GABA but interact differently with the co-factor pyridoxal 5'-phosphate suggesting their activities are differentially regulated. GAD67 is cytosolic, while GAD65 is membrane associated. GAD65 is a major autoantigen in diabetes mellitus and stiff-man syndrome, a rare disease of the brain. ADI has produced antibodies to GAD65 and GAD67 using peptide sequences specific to each subtype.
 

r=rat; m=mouse; h=human; mk=monkey; AS=mouse ascites;

Control peptides, because of their small size, are not recommended for Western. They should be used in ELISA, dot blot or in antibody blocking studies. "Neat Antiserum" (unpurified crude antiserum) is suitable for ELISA and Western, whereas we recommend using "Affinity pure"(purified over the antigen columns) antibodies for Immunohistochemical applications.
 

© 2005 GENTAUR bvba
 

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