产品货号：
JN1912
中文名称：
重组人BH3结构域凋亡诱导蛋白(BID)
英文名称：
Recombinant Human BH3-Interacting Domain Death Agonist
产品规格：
10μg|50μg|500μg|1mg
发货周期：
1～3天
产品价格：
询价
本品由我们的大肠杆菌表达系统制备而成，目的基因编码的Met1-Asp195表达纯化得来。
BID/BH3-interacting domain death agonist质量控制：＞95%(还原性SDS-PAGE)
BID/BH3-interacting domain death agonist制剂：液体
BID/BH3-interacting domain death agonist保存：收到货后请置于-20℃，可保存6个月，避免反复冻融。
关于BID/BH3-interacting domain death agonist：
BH3-Interacting Domain Death Agonist (BID) is a member of the Bcl-2 protein family which regulates outer mitochondrial membrane permeability. BID is a pro-apoptotic member that causes cytochrome c to be released from the mitochondria intermembrane space into the cytosol. Interaction of Bid with Bak causes altered mitochondrial membrane permeability. 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. 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.
相关搜索：重组人BH3结构域凋亡诱导蛋白(BID)
BID/BH3-interacting domain death agonist质量控制：＞95%(还原性SDS-PAGE)
BID/BH3-interacting domain death agonist制剂：液体
BID/BH3-interacting domain death agonist保存：收到货后请置于-20℃，可保存6个月，避免反复冻融。
关于BID/BH3-interacting domain death agonist：
BH3-Interacting Domain Death Agonist (BID) is a member of the Bcl-2 protein family which regulates outer mitochondrial membrane permeability. BID is a pro-apoptotic member that causes cytochrome c to be released from the mitochondria intermembrane space into the cytosol. Interaction of Bid with Bak causes altered mitochondrial membrane permeability. 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. 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.
相关搜索：重组人BH3结构域凋亡诱导蛋白(BID)