重组
expressed in E. coli
质量水平
方案
≥95% (SDS-PAGE)
表单
buffered aqueous solution
分子量
22 kDa by SDS-PAGE (reducing)
UniProt登记号
运输
dry ice
储存温度
−20°C
基因信息
mouse ... Bid(12122)
生化/生理作用
Regulates outer mitochondrial membrane permeability, pro-apoptotic, causes release of cytochrome c from mitochondrial intermembrane space to cytosol.
外形
Solution, 0.2 μm filtered, in 25 mM HEPES, pH 7.5, and 0.1 M KCl.
分析说明
Measured by its ability to induce cytochrome c release from isolated mouse liver mitochondria.
储存分类代码
10 - Combustible liquids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
新产品
此项目有
J Zha et al.
Science (New York, N.Y.), 290(5497), 1761-1765 (2000-12-02)
Many apoptotic molecules relocate subcellularly in cells undergoing apoptosis. The pro-apoptotic protein BID underwent posttranslational (rather than classic cotranslational) N-myristoylation when cleavage by caspase 8 caused exposure of a glycine residue. N-myristoylation enabled the targeting of a complex of p7
M C Wei et al.
Genes & development, 14(16), 2060-2071 (2000-08-19)
TNFR1/Fas engagement results in the cleavage of cytosolic BID to truncated tBID, which translocates to mitochondria. Immunodepletion and gene disruption indicate BID is required for cytochrome c release. Surprisingly, the three-dimensional structure of this BH3 domain-only molecule revealed two hydrophobic
H Li et al.
Cell, 94(4), 491-501 (1998-09-04)
We report here that BID, a BH3 domain-containing proapoptotic Bcl2 family member, is a specific proximal substrate of Casp8 in the Fas apoptotic signaling pathway. While full-length BID is localized in cytosol, truncated BID (tBID) translocates to mitochondria and thus
X Luo et al.
Cell, 94(4), 481-490 (1998-09-04)
We report here the purification of a cytosolic protein that induces cytochrome c release from mitochondria in response to caspase-8, the apical caspase activated by cell surface death receptors such as Fas and TNF. Peptide mass fingerprinting identified this protein
BCL-2 family members and the mitochondria in apoptosis.
A Gross et al.
Genes & development, 13(15), 1899-1911 (1999-08-13)
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