BID 蛋白
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- 抗原 See all BID 蛋白
- BID (BH3 Interacting Domain Death Agonist (BID))
- 蛋白类型
- Recombinant
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宿主
- 人
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资源
- 大肠杆菌（E. Coli）
- 原理
- Recombinant Human BID Protein
- 序列
- Met 1-Asp195
- 产品特性
- Recombinant Human BH3-Interacting Domain Death Agonist is produced by our E.coli expression system and the target gene encoding Met1-Asp195 is expressed.
- 纯度
- > 95 % as determined by reducing SDS-PAGE.
- 内毒素水平
- < 1.0 EU per μg as determined by the LAL method.
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- Discover our top product BID 蛋白
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BH3 Interacting Domain Death Agonist (BID) (AA 1-195) protein (GST tag)
BID 宿主: 人 宿主: 小麦胚 Recombinant WB, ELISA, AA, AP
BH3 Interacting Domain Death Agonist (BID) (Active) protein (GST tag,His tag)BID 宿主: 小鼠 宿主: 大肠杆菌（E. Coli） Recombinant > 95 % as determined by SDS-PAGE Active
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- 限制
- 仅限研究用
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- 状态
- Frozen, Liquid
- 缓冲液
- Supplied as a 0.2 μm filtered solution of 20 mM PB, 100 mM KCl, pH 7.4.
- 储存条件
- -20 °C
- 储存方法
- Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles.
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- 抗原
- BID (BH3 Interacting Domain Death Agonist (BID))
- 别名
- BID (BID 产品)
- 别名
- FP497 Protein, 2700049M22Rik Protein, AI875481 Protein, AU022477 Protein, BID Protein, bid Protein, si:ch211-238n5.6 Protein, fp497 Protein, xbid Protein, DKFZp469E066 Protein, BH3 interacting domain death agonist Protein, BH3 interacting domain death agonist S homeolog Protein, BID Protein, Bid Protein, bida Protein, bid.S Protein, bid Protein
- 背景
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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.
Synonym: BH3-Interacting Domain Death Agonist, p22 BID, BID
- 分子量
- 22.0 kDa
- 途径
- Apoptosis, Caspase Cascade in Apoptosis, Positive Regulation of Endopeptidase Activity
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