Recombinant Human GAD1GAD/GAD67 protein (His Tag) (PDEH101044)
For research use only.
| Synonyms | CPSQ1, GAD, SCP |
| Species | Human |
| Expression Host | E.coli |
| Sequence | Met1-Try350 |
| Accession | Q99259-1 |
| Calculated Molecular Weight | 38.4 kDa |
| Observed Molecular Weight | 39 kDa |
| Tag | N-His & C-His |
| Bio-activity | Not validated for activity |
| Purity | > 95% as determined by reducing SDS-PAGE. |
| Endotoxin | < 10 EU/mg 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 a 0.2 μm filtered solution in PBS with 5% Trehalose and 5% Mannitol. |
| Reconstitution | It is recommended that sterile water be added to the vial to prepare a stock solution of 0.5 mg/mL. Concentration is measured by UV-Vis. |
| 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. |
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