anti-Glutamate Decarboxylase, 65kDa isoform, Clone: GAD-6, Millipore™ (Chemicon™)

Manufacturer: EMD Millipore MAB351DEL

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Catalog No. 50-175-315


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    Antigen Glutamate Decarboxylase, 65kDa isoform
    Conjugate Unlabeled
    Cross Reactivity Human,Rat
    Format Semi-purified
    Host Species Mouse
    Immunogen Purified rat brain glutamic acid decarboxylase.
    Isotype IgG2a
    Quantity 100μg
    Regulatory Status RUO
    Research Discipline Neuroscience
    Primary or Secondary Primary
    Monoclonal or Polyclonal Monoclonal

    Gutamic acid decarboxylase (GAD; E.C. is the enzyme responsible for the conversion of glutamic acid to gamma-aminobutyric acid (GABA), the major inhibitory transmitter in higher brain regions, and putative paracrine hormone in pancreatic islets. Two molecular forms of GAD (65kDa and 67kDa, 64% aa identity between forms) are highly conserved and both forms are expressed in the CNS, pancreatic islet cells, testis, oviduct and ovary. The isoforms are regionally distributed cytoplasmically in the brains of rats and mice (Sheikh, S. et al. 1999). GAD65 is an ampiphilic, membrane-anchored protein (585aa), encoded on human chromosome 10, and is responsible for vesicular GABA production. GAD67 is cytoplasmic (594aa.), encoded on chromosome 2, and seems to be responsible for significant cytoplasmic GABA production. GAD expression changes during neural development in rat spinal cord. GAD65 is expressed transiently in commissural axons around E13 but is down regulated the next day while GAD67 expression increases mostly in the somata of those neurons (Phelps, P. et al. 1999). In mature rat pancreas, GAD65 and GAD67 appear to be differentially localized, GAD65 primarily in insulin-containing beta cells and GAD67 in glucagon-containing (A) cells (Li, L. et al. 1995). GAD67 expression seems to be particularly plastic and can change in response to experimental manipulation (for example neuronal stimulation or transection) or disease progression and emergent disorders like schizophrenia (Volk et al., 2000). Colocalization of the two GAD isoforms also shows changes in GAD65/GAD67 distributions correlated with certain disease states such as IDDM and SMS.

    Immunohistochemistry, Western Blotting

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