BID抗体

BID抗体产品信息

免疫原 :
Recombinant Human BID protein (Catalog#10468-HNCE)
Antibody Type : Mouse Monoclonal Antibody ( Mouse mAb Service Platform )
Clone ID :
10
抗体宿主 :
Mouse IgG1
缓冲液 : 0.2 μm filtered solution in PBS, 5% trehalose may be added in some batches. Please read the hardcopy of COA or contact our customer service to confirm the formulation.
制备方法 :
This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human BID (rh BID; Catalog#10468-HNCE; P55957-1; Met 1-Asp 195). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
BID抗体Background
BID, BH3-interacting domain death agonist, is a member of the Bcl-2 protein family. BID contains only the BH3 domain, which is required for its interaction with the Bcl-2 family proteins and for its pro-death activity. BID is susceptible to proteolytic cleavage by caspases, calpains, Granzyme B and cathepsins. It is an integrating key regulator of the intrinsic death pathway that amplifies caspase-dependent and caspase-independent execution of neuronal apoptosis. Therefore pharmacological inhibition of BID provides a promising therapeutic strategy in neurological diseases where programmed cell death is prominent, and also offer a new strategy for the treatment of acute renal failure associated with ischemia-reperfusion. BID receives direct inputs from a key regulator of the cell cycle arrest/DNA repair machinery (ATM), and therefore is an excellent candidate to coordinate genotoxic stress responses and apoptotic cell death. BID is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Activated BID is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. Recent studies further indicate that BID may be more than just a killer molecule. Deletion of BID inhibits carcinogenesis in the liver, although this genetic alteration promotes tumorigenesis in the myeloid cells. This is likely related to the function of BID to promote cell cycle progression into S phase. BID could be also involved in the maintenance of genomic stability by engaging at mitosis checkpoint.
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