| Tissue Specificity | Expressed in a variety of tissues. |
| Post Translational Modifications | Phosphorylation/dephosphorylation on Ser-70 regulates anti-apoptotic activity. Growth factor-stimulated phosphorylation on Ser-70 by PKC is required for the anti-apoptosis activity and occurs during the G2/M phase of the cell cycle. In the absence of growth factors, BCL2 appears to be phosphorylated by other protein kinases such as ERKs and stress-activated kinases. Phosphorylated by MAPK8/JNK1 at Thr-69, Ser-70 and Ser-84, which stimulates starvation-induced autophagy. Dephosphorylated by protein phosphatase 2A (PP2A). Proteolytically cleaved by caspases during apoptosis. The cleaved protein, lacking the BH4 motif, has pro-apoptotic activity, causes the release of cytochrome c into the cytosol promoting further caspase activity. Monoubiquitinated by PRKN, leading to an increase in its stability. Ubiquitinated by SCF(FBXO10), leading to its degradation by the proteasome. |
| Function | Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1). Also acts as an inhibitor of autophagy: interacts with BECN1 and AMBRA1 during non-starvation conditions and inhibits their autophagy function. May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release. |
| Protein Name | Apoptosis Regulator Bcl-2 |
| Database Links | Reactome: R-MMU-111447Reactome: -MMU-111453Reactome: -MMU-844455 |
| Cellular Localisation | Mitochondrion Outer MembraneSingle-Pass Membrane ProteinNucleus MembraneEndoplasmic Reticulum MembraneCytoplasm |
| Alternative Antibody Names | Anti-Apoptosis Regulator Bcl-2 antibodyAnti-Bcl2 antibodyAnti-Bcl-2 antibody |
Information sourced from Uniprot.org
