Description
Recombinant Human GAD67/GAD1 Protein (His Tag) | PKSH030814 | Gentaur US, UK & Europe Disrtribition
Synonyms: CPSQ1;GAD;SCP
Active Protein: N/A
Activity: A DNA sequence encoding the human GAD1 (Q99259-1) (Met 1-Leu 594) was fused with a polyhistidine tag at the C-terminus.
Protein Construction: A DNA sequence encoding the human GAD1 (Q99259-1) (Met 1-Leu 594) was fused with a polyhistidine tag at the C-terminus.
Fusion Tag: C-His
Species: Human
Expressed Host: Baculovirus-Insect Cells
Shipping: This product is provided as lyophilized powder which is shipped with ice packs.
Purity: > 92 % as determined by reducing SDS-PAGE.
Endotoxin: < 1.0 EU per µg as determined by the LAL method.
Stability and 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.
Molecular Mass: 68.3 kDa
Formulation: Lyophilized from sterile 20mM Tris, 500mM NaCl, 10% gly, pH 8.5
Reconstitution: Please refer to the printed manual for detailed information.
Background: Glutamate decarboxylase 1, also known as 67 kDa glutamic acid decarboxylase, Glutamate decarboxylase 67 kDa isoform and GAD1, 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 isoform 3 is expressed in pancreatic islets, testis, adrenal cortex, and perhaps other endocrine tissues, but not in brain. Tissue-specific markers are useful for identification of tumour type in advanced cancers of unknown origin. In plants, as in most eukaryotes, glutamate decarboxylase catalyses the synthesis of GABA. Root-specific calcium/calmodulin-regulated GAD1 plays a major role in GABA synthesis in plants under normal growth conditions and in response to stress. 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. Affected individuals manifest symmetrical, non-progressive spasticity and no adverse perinatal history or obvious underlying alternative diagnosis.
Research Area: N/A
