Human CellExp™ GAD1, human recombinant

Catalog #: 7250 | abID:

Product Details

Cat # +Size 7250-10
Size 10 μg
Alternate Name GAD1, CPSQ1, GAD, SCP, GAD-1, CPSQ-1, GAD67, GAD-67
Gene Symbol GAD1
Gene ID 2571
Accession # Q99259
Source HEK 293 cells
Appearance Lyophilized powder
Physical Form Description Lyophilized from 0.22 μm filtered solution in PBS, pH 7.4, 1 mM EDTA with some stabilizer. Generally 5-8% Mannitol or trehalose is added as a protectant before lyophilization.
Molecular Weight This protein is fused with 6×his tag at C-terminus, has a calculated MW of 67 kDa expressed. The predicted N-terminus is Met1. Protein migrates as the predominant 64 kDa form and a less-frequent 24-kDa form in reduced SDS-PAGE resulting from alternative s
Purity by SDS-PAGE ≥92%
Endotoxin Level < 0.1 ng/μg of protein (<1EU/μg).
Reconstitution Instructions Centrifuge the vial prior to opening. Reconstitute in sterile PBS, pH 7.4 to a concentration of 50 µg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 month. For extended storage, it is recommended to store at -20°C.
Handling Centrifuge the vial prior to opening.
Storage Conditions -20°C
Shipping Conditions Gel Pack
USAGE For Research Use Only! Not For Use in Humans.

Details

Glutamate decarboxylase 1 (GAD1), also known as 67 kDa glutamic acid decarboxylase and Glutamate decarboxylase 67 kDa isoform, is a member of the group II decarboxylase family. GAD1 is expressed in benign and malignant prostatic tissue and may serve as a highly prostate-specific tissue biomarker. GAD1 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. GAD1 may also play a role in the stiff man syndrome. Defects in GAD1 are the cause of cerebral palsy spastic quadriplegic type 1 (CPSQ1) which is a non-progressive disorder of movement and/or posture resulting from defects in the developing central nervous system. GAD1 has been shown to interact with GAD2. Affected individuals manifest symmetrical, non-progressive spasticity and no adverse perinatal history or obvious underlying alternative diagnosis.


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