- ￥832 - 21120
- Solarbio
- P00730
- 北京
- 2025年07月25日
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- 详细信息
- 技术资料
- 库存：
现询
- 供应商：
北京索莱宝科技有限公司
- 规格：
1mg/500ug/50ug/10ug
| 规格： | 1mg | 产品价格： | ￥21120.0 |
|---|---|---|---|
| 规格： | 500ug | 产品价格： | ￥14784.0 |
| 规格： | 50ug | 产品价格： | ￥2600.0 |
| 规格： | 10ug | 产品价格： | ￥832.0 |
| 基本信息 | |
| 基因名 | |
| 别名 | BH3-Interacting Domain Death Agonist;p22 BID;BID |
| 中文名称 | Recombinant Human BID/BH3-interacting domain death agonist |
| 外观(性状) | Supplied as a 0.2 μm filtered solution of 20mM PB, 100mM KCl, pH 7.4. |
| 纯度 | ≥95% as determined by reducing SDS-PAGE. |
| 储存条件 | 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. |
| 运输条件 | 干冰运输 |
| 背景说明 | 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. |
| 来源 | E.coli |
| 内毒素 | Less than 0.1 ng/ug(1 EU/ug)as determined by LAL test. |
| 单位 | 支 |
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P00730 Recombinant Human BID/BH3-interacting domain death agonist 细胞因子/蛋白
￥832 - 21120
