Apoptosis plays a major role in normal organism development, tissue homeostasis, and removal of damaged cells and is caused by the activation of proteolytic enzymes termed caspases. Proteins that comprise the Bcl-2 family appear to control the activation of these enzymes. One such protein BIK was recently identified as an endoplasmic reticulum (ER)-residing pro-apoptotic member of the Bcl-2 homology domain-3 (BH3)-only group of the Bcl-2 family that stimulates mitochondrial release of cytochrome c following p53 induction of apoptosis. A significant fraction of BIK is found as an ER transmembrane protein, with most of the protein facing the cytosol. Restricting BIK to the ER membrane by replacing the transmembrane region with that of the ER-selective membrane anchor of cytochrome b resulted in a decreased cytochrome c release from mitochondria and a corresponding drop in cell death. Recent evidence suggests that BIK cooperates with NOXA, another BH3-only protein, to somehow enhance the activation of Bax to stimulate the rapid release of cytochrome c from mitochondria.
应用类型
ELISA,IF Microscopy,Western Blot,
免疫原
Anti-BIK antibody was prepared from whole rabbit serum produced by repeated immunizations with a 15 amino acid synthetic peptide from near the N-terminus of human BIK.
来源宿主
Rabbit
反应性
H. sapiens (Human); Mus musculus (Mouse)
保存建议
Store vial at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use.
