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This is a purified mouse anti-human BID Monoclonal Antibody, PE conjugate, that can be used in the validated application of flow cytometry. This BID Monoclonal 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, and conjugated with FITC under optimum conditions. The unreacted FITC was removed.
Antibody characteristics include:
Applications: This BID Monoclonal Antibody has been validated for use in flow cytometry Host species and isotype: This is a mouse Monoclonal IgG1 against human BID Clone ID of monoclonal antibody (mAb): The BID monoclonal antibody clone ID is 10 Immunogen: Recombinant human BID protein Product size: 100 Tests
As described by NCBI, 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.