Product Name: Bik Antibody
Species Reactivity: Human, Mouse
Tested Applications: ELISA, ICC, IF, WB
Applications: BIK antibody can be used for the detection of BIK by Western blot at 1 – 2 μg/mL. Antibody can also be used for immunocytochemistry starting at 1 μg/mL. For immunofluorescence start at 10 μg/mL.
User Note: Optimal dilutions for each application to be determined by the researcher.
Predicted Molecular Weight: Predicted: 18 kDa Observed: 22 kDa
Immunogen: BIK antibody was raised against a 15 amino acid synthetic peptide from near the amino terminus of human BIK.The immunogen is located within the first 50 amino acids of Bik.
Host Species: Rabbit
Purification: Bik Antibody is affinity chromatography purified via peptide column.
Physical State: Liquid
CAS NO.: 4773-96-0
Product: Mangiferin
Buffer: Bik Antibody is supplied in PBS containing 0.02% sodium azide.
Concentration: 1 mg/mL
Storage Conditions: Bik antibody can be stored at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Clonality: Polyclonal
Conjugate: Unconjugated
Alternate Names: Bik Antibody: BP4, NBK, BIP1, Bcl-2-interacting killer, Apoptosis inducer NBK
Accession NO.: CAG30276
Protein Ino: 47678311
Official Symbol: BIK
Geneid: 638
Background: Bik Antibody: 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.
PubMed ID:http://aac.asm.org/content/42/2/468.abstract
