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產(chǎn)品名稱：Anti-GAD67/GAD1*,*脫羧酶67抗體
中文名稱：*脫羧酶67抗體
英文名稱：Anti-GAD67/GAD1
產(chǎn)品編號：BYK-1302R
產(chǎn)品別名：glutamate decarboxylase 67; decarboxylase 1; 67 kDa glutamic acid decarboxylase; Glutamate decarboxylase 67 kDa isoform; GAD1; GAD; GAD-67; GAD 67.

本公司另供應(yīng)“*脫羧酶67抗體”的標(biāo)記有：Alexa Fluor 350 Alexa Fluor 488 Alexa Fluor 555 Alexa Fluor 647 AP APC Biotin Cy3 Cy5 Cy5.5 Cy7 FITC Gold HRP PE PE-Cy3 PE-CY5 PE-CY5.5 PE-CY7 RBITC.
產(chǎn)品規(guī)格：100ug/200ug
產(chǎn)品濃度： 1mg/1ml
抗體來源：兔源、鼠源、山羊
克 ?。簡慰寺】贵w、多克隆抗體
抗體類型：一抗
性 狀： 凍干粉或液體
保存條件：Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.

Anti-GAD67/GAD1*,*脫羧酶67抗體技術(shù)說明，產(chǎn)品*，由于篇幅原因，更多信息請：

Anti-SYT3/FITC  熒光素標(biāo)記突觸結(jié)合蛋白3抗體IgG
Anti-Synaptophysin（SAP-1）/FITC  熒光素標(biāo)記抗突觸素抗體IgG
Anti-alpha-Synuclein/FITC  熒光素標(biāo)記核突觸蛋白-α抗體（C端）IgG
Anti-α-Synuclein/FITC  熒光素標(biāo)記核突觸蛋白-α抗體IgG
Anti-SYPH1/FITC  熒光素標(biāo)記synphilin-1抗體IgG
Anti-SYVN1/FITC  熒光素標(biāo)記滑膜細(xì)胞凋亡抑制物1抗體IgG
Anti-TNF-α /Biotin  *標(biāo)記 腫瘤壞死因子抗體
Anti-T3/FITC  熒光素標(biāo)記三碘甲狀腺素T3抗體IgG
Anti-TACR3/NK-3 receptor /FITC  熒光素標(biāo)記速激肽受體3抗體IgG
Anti-Tanis/SELS /FITC  熒光素標(biāo)記炎癥負(fù)調(diào)控因子蛋白抗體IgG
Anti-TANK/FITC  熒光素標(biāo)記TANK抗體IgG
Anti-STAT2/FITC  熒光素標(biāo)記信號轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子2（STAT2）抗體IgG
Anti-STAT3 /FITC  熒光素標(biāo)記信號轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子3抗體IgG
Anti-STAT4 /FITC  熒光素標(biāo)記信號轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子4抗體IgG
Anti-STAT5/FITC  熒光素標(biāo)記信號轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子5（STAT5）抗體IgG
Anti-STAT6 /FITC  熒光素標(biāo)記信號轉(zhuǎn)導(dǎo)和轉(zhuǎn)錄激活因子6抗體IgG
Anti-STEAP1/FITC  熒光素標(biāo)記前列腺跨膜上皮抗原1抗體IgG
Anti-Stra8/FITC  熒光素標(biāo)記*激活基因8抗體IgG
Anti-STRO-1/FITC  熒光素標(biāo)記STRO-1抗體IgG
Anti-SULT1E1/FITC  熒光素標(biāo)記雌激素硫酸轉(zhuǎn)移酶抗體IgG
Anti-SUMO/FITC  熒光素標(biāo)記類泛素蛋白抗體IgG
Anti-Survivin/FITC  綠色熒光素標(biāo)記Survivin蛋白抗體IgG
Anti-SYK/FITC  熒光素標(biāo)記非受體型*蛋白激酶抗體IgG

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.