| 產(chǎn)品編號(hào) | bs-1302R |
| 英文名稱 | Rabbit Anti-GAD67 antibody |
| 中文名稱 | 谷氨酸脫羧酶67抗體 |
| 別 名 | glutamate decarboxylase 67; decarboxylase 1; 67 kDa glutamic acid decarboxylase; Glutamate decarboxylase 67 kDa isoform; GAD1; GAD; GAD-67; GAD 67. |
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Specific References (1) | bs-1302R has been referenced in 1 publications.
[IF=2.378] Lin XY et al. Chronic exercise buffers the cognitive dysfunction and decreases the susceptibility to seizures in PTZ-treated rats. Epilepsy Behav. 2019 Aug 1;98(Pt A):173-187. WB ; Rat.
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| 研究領(lǐng)域 | 腫瘤 細(xì)胞生物 免疫學(xué) 神經(jīng)生物學(xué) 新陳代謝 |
| 抗體來源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | Human,Mouse (predicted: Rat) |
| 產(chǎn)品應(yīng)用 | WB=1:500-2000,IHC-P=1:100-500,IHC-F=1:100-500,Flow-Cyt=1ug/Test,IF=1:100-500,ELISA=1:5000-10000
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 理論分子量 | 67kDa |
| 細(xì)胞定位 | 細(xì)胞漿 細(xì)胞膜 |
| 性 狀 | Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human GAD67: 455-594/594 |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 緩 沖 液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| 保存條件 | Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
| 注意事項(xiàng) | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| PubMed | PubMed |
| 產(chǎn)品介紹 |
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. Function: Catalyzes the production of GABA. Subcellular Location: Mitochondrion; Plasma Membrane; Tissue Specificity: Isoform 3 is expressed in pancreatic islets, testis, adrenal cortex, and perhaps other endocrine tissues, but not in brain. 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 symmetrical, non-progressive spasticity and no adverse perinatal history or obvious underlying alternative diagnosis. Developmental delay, mental retardation and sometimes epilepsy can be part of the clinical picture. Similarity: Belongs to the group II decarboxylase family. SWISS: Q99259 Gene ID: 2571 Database links: Entrez Gene: 2571 Human Entrez Gene: 14415 Mouse Omim: 605363 Human SwissProt: Q99259 Human SwissProt: P48318 Mouse Unigene: 420036 Human Unigene: 272120 Mouse Unigene: 91245 Rat GAD67谷氨酸脫羧酶-67 是用于I II型糖尿病研究的很重要的蛋白。GAD67的大多數(shù)表位位于蛋白中部或C末端1／3蛋白，與GAD65有高度的同源性。 |
| 產(chǎn)品圖片 |
Sample:
Raji(Human) Cell Lysate at 40 ug
Primary: Anti-GAD67 (bs-1302R) at 1/300 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 67 kD
Observed band size: 67 kD
Paraformaldehyde-fixed, paraffin embedded (Mouse brain); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Antibody incubation with (GAD67) Polyclonal Antibody, Unconjugated (bs-1302R) at 1:400 overnight at 4°C, followed by operating according to SP Kit(Rabbit) (sp-0023) instructionsand DAB staining.
Blank control:K562.
Primary Antibody (green line): Rabbit Anti-GAD67 antibody (bs-1302R)
Dilution: 1μg /10^6 cells;
Isotype Control Antibody (orange line): Rabbit IgG .
Secondary Antibody : Goat anti-rabbit IgG-FITC
Dilution: 0.5μg /test.
Protocol
The cells were incubated in 5%BSA to block non-specific protein-protein interactions for 30 min at room temperature .Cells stained with Primary Antibody for 30 min at room temperature. The secondary antibody used for 40 min at room temperature. Acquisition of 20,000 events was performed.
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