GAD2/GAD65 Antibody

Glutamic Acid Decarboxylase (GAD) catalyzes the conversion of L-glutamate to g-aminobutyric acid (GABA), the principal inhibitory neurotransmitter in the brain, and a putative paracrine signal molecule in pancreatic islets.1, 3 GAD has a restricted tissue distribution. It is highly expressed in the cytoplasm of GABAergic neurons in the central nervous system (CNS) and pancreatic $-cells. It is also present in other non-neuronal tissues such as testis, oviduct and ovary.1-5 GAD is also transiently expressed in non-GABAergic cells of the embryonic and adult nervous system, suggesting its involvement in development and plasticity.6 GAD exists as two isoforms, GAD 65 and GAD 67 (molecular masses of 65 and 67 kD, respectively) that are encoded by two different genes.2,7,8 GAD65 is an ampiphilic, membraneanchored protein, (585 amino acid residues) and is encoded on human chromosome 10. GAD 67 is a cytoplasmic protein (594 amino acid residues) and is encoded on chromosome 2. There is 64% amino acid identity between the two isoforms, with the highest diversity located at the N-terminus, which in GAD 65 is required for targeting the enzyme to GABA-containing secretory vesicles. The two isoforms appear to have distinct intraneuronal distribution in the brain.9 GAD 65 has been identified as an autoantigen in insulindependent diabetes mellitus (IDDM) and stiff-man syndrome (SMS), 10,11 IDDM is an autoimmune disease that results from T cell mediated destruction of pancreatic insulin-secreting $-cells. Islet-reactive T cells and antibodies primarily to GAD 65 (also named $-cell autoantigen) can be detected in peripheral blood of 80% of recent-onset IDD patients and in pre-diabetic high-risk subjects before onset of clinical symptoms. This suggests that GAD may be an important marker in the early stages of the disease.11 Also, autoantibodies to GAD 65 and GAD 67 are detected in animal models of IDDM, including the non-obese diabetes (NOD) mouse. In the NOD mouse, T cell reactivity is initially restricted to the C-terminal regions of GAD 65, but later spreads to other parts of GAD 65.12,13 Stiff-man syndrome (SMS), a rare disorder of the CNS, is characterized by progressive rigidity of the body musculature with painful spasms, due to impairment of the GABAergic neurotransmission. High-titer autoantibodies directed against GAD 65 and GABAergic neurons (nerve terminals) have been detected in the serum and cerebrospinal fluid (CSF) in 60% of patients with the syndrome.14 Strikingly, many of the SMS patients also developed late-onset IDDM. Antibodies that react specifically with GAD 65 are useful for the study of the differential tissue expression and intracellular localization of this isoform in normal and disease conditions.

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

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Publication using NB110-41528	Applications	Species
Lee M, Suk K, Kang Y et al. Neurotoxic factors released by stimulated human monocytes and THP-1 cells. Brain Res. 11;1400:99-111. doi: 10.1016/j.brainres.2011.05.021. 2011-07-01 [PMID: 21640980]

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Enlarge	4 reviewed by: Verified Customer	IHC-P	Other	04/29/2014	View Summary Application Immunohistochemistry-Paraffin Sample Tested Brain Species Other Lot 028H4856

Array NB110-41528

• GAD2/GAD65 Antibodies
• GAD2/GAD65 ELISA Kits
• GAD2/GAD65 Lysates
• GAD2/GAD65 Proteins