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Recombinant Human GAD65/GAD2/GAD-2 Protein (GST Tag)

Uniprot : Q05329
  • Cat.No.:PKSH030280

  • Expression host: Baculovirus-Insect Cells

To Purchase PKSH030280

Size:
  • 100μg
Price: $998
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Description

Synonyms GAD65
Species Human
Expression_host Baculovirus-Insect Cells
Sequence Met 1-Leu 585
Accession NP_000809.1
Mol_Mass 92.6 kDa
Tag N-GST

Properties

Purity > 90 % as determined by reducing SDS-PAGE.
Endotoxin level < 1.0 EU per μg of the protein as determined by the LAL method.
Storage Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80℃. Reconstituted protein solution can be stored at 4-8℃ for 2-7 days. Aliquots of reconstituted samples are stable at < -20℃ for 3 months.
Shipping This product is provided as lyophilized powder which is shipped with ice packs.
Formulation Lyophilized from sterile 200 Tirs, 150 mM NaCl, pH 8.0, 10 % glycerol, 1 mM GSH
Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.
Please refer to the specific buffer information in the printe
Reconstitution Please refer to the printed manual for detailed information.

Background

Glutamate decarboxylase 2, also known as glutamate decarboxylase 65 kDa isoform, 65 kDa glutamic acid decarboxylase, GAD2 and GAD65, is a member of thegroup II decarboxylase family. GAD2 is identified as a major autoantigen in insulin-dependent diabetes. GAD2 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 autoantibody and an autoreactive T cell target in insulin-dependent diabetes. GAD2 may also play a role in the stiff man syndrome. GAD2 is implicated in the formation of the gamma-aminobutyric acid (GABA), a neurotransmitter involved in the regulation of food intake. GABA is synthesized in brain by two isoforms of glutamic acid decarboxylase (Gad), GAD1 and GAD2. GAD1 provides most of the GABA in brain, but GAD2 can be rapidly activated in times of high GABA demand. Mice lacking GAD2 are viable whereas deletion of GAD1 is lethal. Deletion of GAD2 increased ethanol palatability and intake and slightly reduced the severity of ethanol-induced withdrawal.

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