磷酸化BH3结构域凋亡诱导蛋白抗体

参考价:¥1580
供货周期: 现货
品牌: LMAI Bio
规格: 50ul/100ul/200ul
货号: LM5231R
CAS号:
上海联迈生物工程有限公司
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磷酸化BH3结构域凋亡诱导蛋白抗体

 

英文名称    phospho-Bid (Ser61)    

中文名称    磷酸化BH3结构域凋亡诱导蛋白抗体    

别    名    Bid (phospho S61); p-Bid (phospho S61); BH3 interacting domain death agonist; p22 BID; BID;) BH3-interacting domain death agonist; AltName: BH3-interacting domain death agonist p15; BH3-interacting domain death agonist p13; p13 BID; BH3-interacting domain death agonist p11; p11 BID.      

产品类型    磷酸化抗体     

研究领域    肿瘤  细胞生物  免疫学  信号转导  细胞凋亡      

抗体来源    Rabbit    

克隆类型    Polyclonal    

交叉反应    Human, Mouse,     

产品应用    WB=1:500-2000 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=0.2μg/Test IF=1:100-500 (石蜡切片需做抗原修复) 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.    

分 子 量    21kDa    

细胞定位    细胞浆 细胞膜     

性    状    Lyophilized or Liquid    

浓    度    1mg/ml    

免 疫 原    KLH conjugated Synthesised phosphopeptide derived from mouse Bid around the phosphorylation site of Ser61:DG(p-S)QA     

亚    型    IgG    

纯化方法    affinity purified by Protein A    

储 存 液    0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.    

保存条件    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.    

PubMed    PubMed    

产品介绍    Bid, a BH3 domain containing proapoptotic Bcl2 family member, is localized in the cytosolic fraction of cells as an inactive precursor. Its active form is generated upon proteolytic cleavage by caspase 8 in the Fas signaling pathway. Cleaved Bid translocates to mitochondria and releases its potent proapoptotic activity, which in turn induces cytochrome c release and mitochondrial damage. The cytochrome c releasing activity of Bid was antagonized by Bcl2. Mutation in the SH3 domain can diminish the cytochrome c releasing activity. In animal model studies, Bid deficient mice are found resistant to the lethal effects of death factor signals relayed through Fas.    


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