GAD1 / Unconjugated / GAD1/2563

Product Details
Supplier Biotium
Catalog #: BNUM2563-50 (View supplier product page)
Size 50 μl
Price $410.00
Antigen GAD1
Clone GAD1/2563
Host Mouse
Isotype IgG2b κ
Conjugate Unconjugated
Target Species Human
Applications FC, ICS
Description This MAb recognizes a protein of 67 kDa, which is identified as glutamic acid decarboxylase 1 (GDA1). There are two forms of glutamic acid decarboxylases (GADs) that are found in the brain: GAD65 (also known as GAD2) and GAD67 (also known as GAD1. GAD65 and GAD67 are members of the group II decarboxylase family of proteins and are responsible for catalyzing the rate-limiting step in the production of GABA (ÃŽ³-aminobutyric acid) from L-glutamic acid. Although both GAD s are found in the brain, GAD65 localizes to synaptic vesicle membranes in nerve terminals, while GAD67 is distributed throughout the cell. GAD67 is responsible for the basal levels of GABA synthesis. In the case of a heightened demand for GABA in neurotransmission, GAD65 will transiently activate to assist in GABA production. The loss of GAD65 is detrimental and can impair GABA neurotransmission, however the loss of GAD67 is lethal. Primary antibodies are available purified, or with a selection of fluorescent CF Dyes and other labels. CF Dyes offer exceptional brightness and photostability. Note: Conjugates of blue fluorescent dyes like CF405S and CF405M are not recommended for detecting low abundance targets, because blue dyes have lower fluorescence and can give higher non-specific background than other dye colors.
About GAD1 and Purified
GAD1 This gene encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes. The enzyme encoded is responsible for catalyzing the production of gamma-aminobutyric acid from L-glutamic acid. A pathogenic role for this enzyme has been identified in the human pancreas since it has been identified as an autoantigen and an autoreactive T cell target in insulin-dependent diabetes. This gene may also play a role in the stiff man syndrome. Deficiency in this enzyme has been shown to lead to pyridoxine dependency with seizures. Alternative splicing of this gene results in two products, the predominant 67-kD form and a less-frequent 25-kD form. [provided by RefSeq, Jul 2008]
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Purified Excitation and Emission Spectra