Human GAD67 / GAD1 Protein (His Tag)
CPSQ1,GAD,SCP
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| Catalog Number | P12570-H08B |
|---|---|
| Organism Species | Human |
| Host | Baculovirus-Insect Cells |
| Synonyms | CPSQ1,GAD,SCP |
| Molecular Weight | The recombinant human GAD1 consists of 605 amino acids and predicts a molecular mass of 68.3 kDa. It migrates as an approximately 64 kDa band in SDS-PAGE in SDS-PAGE under reducing conditions. |
| predicted N | Met 1 |
| SDS-PAGE |  |
| Purity | > 92 % as determined by SDS-PAGE |
| 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. |
| Bio-activity | |
| Research Area | Signaling |Signal Transduction |Metabolism |Pathways and Processes |Metabolic signaling pathways |Amino acid metabolism | |
| Formulation | Lyophilized from sterile 20mM Tris, 500mM NaCl, 10% gly, pH 8.5 1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA. |
| 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. |
| Reference |