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产品名称
起订量
单价(含增值税)
库存(PCS)
起订数量
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Recombinant Human BID/BH3-interacting domain deathGV-P00730-10ug￥ 956.001
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Recombinant Human BID/BH3-interacting domain deathGV-P00730-50ug￥ 3000.001
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Recombinant Human BID/BH3-interacting domain deathGV-P00730-500ug￥ 13520.001
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Recombinant Human BID/BH3-interacting domain deathGV-P00730-1mg￥ 18800.001
产品简介
| 中文名称 | Recombinant Human BID/BH3-interacting domain death agonist |
| Known as | BH3-Interacting Domain Death Agonist; p22 BID; BID |
| Derived from | E.coli |
| Purity | Greater than 95% as determined by reducing SDS-PAGE. |
| Formulation | Supplied as a 0.2 μm filtered solution of 20mM PB, 100mM KCl, pH 7.4. |
| Storage | Store at ≤-70°C, stable for 6 months after receipt.Store at ≤-70°C, stable for 3 months under sterile conditions after opening.Please minimize freeze-thaw cycles. |
| Endotoxin | Less than 0.1 ng/ug (1 EU/ug) as determined by LAL test. |
| Background | 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. |
| 规格 | 10ug50ug500ug1mg |
注意：
1.本产品仅供科研使用。请勿用于医药、临床诊断或治疗，食品及化妆品等用途。请勿存放于普通住宅区。
2.为了您的安全和健康，请穿好实验服并佩戴一次性手套和口罩操作。
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