货号 |
bs-1302R-1 |
品牌 |
|
浓度 |
|
货期 |
现货 |
英文名称 |
Rabbit Anti-GAD67 antibody |
中文名称 |
Rabbit Anti-GAD67 antibody |
研究领域 |
肿瘤,细胞生物,免疫学,神经生物学,新陈代谢, |
英文别名 |
glutamate decarboxylase 67; decarboxylase 1; 67 kDa glutamic acid decarboxylase; Glutamate decarboxylase 67 kDa isoform; GAD1; GAD; GAD-67; GAD 67. |
反应物种(已验证) |
Human,Mouse |
反应物种(预测) |
Rat |
产品应用(已验证) |
WB,IHC,FCM |
产品应用(可推荐) |
IF,ELISA |
推荐稀释比例 |
WB=1:500-2000,Elisa=1:5000-10000,IHC-P=1:100-500,IHC-F=1:100-500,Flow Cyt=1ug/Test,IF=1:100-500, |
克隆类型 |
多克隆 |
抗体来源 |
Rabbit |
理论分子量 |
67 |
细胞定位 |
细胞浆,细胞膜 |
性状 |
Liquid |
免疫原 |
KLH conjugated synthetic peptide derived from human GAD67 |
抗原表位 |
455-594/594 |
亚型 |
IgG |
纯化方法 |
affinity purified by Protein A |
SUBCELLULAR |
Mitochondrion; Plasma Membrane; |
Tissue |
Isoform 3 is expressed in pancreatic islets, testis, adrenal cortex, and perhaps other endocrine tissues, but not in brain. |
SIMILARITY |
Belongs to the group II decarboxylase family. |
Function |
Catalyzes the production of GABA. |
DISEASE |
Defects in GAD1 are the cause of cerebral palsy spastic quadriplegic type 1 (CPSQ1) [MIM:603513]. A non-progressive disorder of movement and/or posture resulting from defects in the developing central nervous system. Affected individuals manifest symmetri |
SWISS |
Q99259 |
Gene ID |
2571 |
保存条件 |
Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. |
Important Note |
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
英文介绍 |
Glutamic Acid Decarboxylase (GAD) catalyzes the conversion of L glutamate to g-aminobutyric acid (GABA), the principal inhibitory neurotransmitter in the brain, and a putative paracrine signal molecule in pancreatic islets. GAD has a restricted tissue distribution. It is highly expressed in the cytoplasm of GABAergic neurons in the central nervous system (CNS) and pancreatic beta cells. It is also present in other non-neuronal tissues such as testis, oviduct and ovary. GAD is also transiently expressed in non-GABAergic cells of the embryonic and adult nervous system, suggesting its involvement in development and plasticity.
GAD exists as two isoforms, GAD65 and GAD67 (molecular masses of 65 and 67 kD, respectively) that are encoded by two different genes. GAD65 is an ampiphilic, membraneanchored protein, (585 amino acid residues) and is encoded on human chromosome 10. GAD67 is a cytoplasmic protein (594 amino acid residues) and is encoded on chromosome 2. There is 64% amino acid identity between the two isoforms, with the highest diversity located at the N terminus, which in GAD65 is required for targeting the enzyme to GABA-containing secretory vesicles. The two isoforms appear to have distinct intraneuronal distribution in the brain. GAD65 has been identified as an autoantigen in insulindependent diabetes mellitus (IDDM) and stiff-man syndrome (SMS), IDDM is an autoimmune disease that results from T cell mediated destruction of pancreatic insulin-secreting beta cells. Islet-reactive T cells and antibodies primarily to GAD65 (also named beta cell autoantigen) can be detected in peripheral blood of 80% of recent-onset IDD patients and in pre-diabetic high-risk subjects before onset of clinical symptoms. This suggests that GAD may be an important marker in the early stages of the disease. Also, autoantibodies to GAD65 and GAD67 are detected in animal models of IDDM, including the non-obese diabetes (NOD) mouse. In the NOD mouse, T cell reactivity is initially restricted to the C terminal regions of GAD65, but later spreads to other parts of GAD65. Stiff-man syndrome (SMS), a rare disorder of the CNS, is characterized by progressive rigidity of the body musculature with painful spasms, due to impairment of the GABAergic neurotransmission. |