Bcl-2 Mouse Monoclonal Antibody [9F1] (EM1701-82)

UNIPROT #

P10415

PROTEIN NAME

Bcl-2

SYNONYMS

Apoptosis regulator Bcl 2 antibody;Apoptosis regulator Bcl-2 antibody;Apoptosis regulator Bcl2 antibody;AW986256 antibody;B cell CLL/lymphoma 2 antibody;B cell leukemia/lymphoma 2 antibody;Bcl-2 antibody;Bcl2 antibody;BCL2_HUMAN antibody;C430015F12Rik antibody;D630044D05Rik antibody;D830018M01Rik antibody;Leukemia/lymphoma, B-cell, 2 antibody;Oncogene B-cell leukemia 2 antibody;PPP1R50 antibody;Protein phosphatase 1, regulatory subunit 50 antibody;Bcl 2 antibody

SEQUENCE SIMILARITIES

Belongs to the Bcl-2 family.

TISSUE SPECIFICITY

Expressed in a variety of tissues.

POST-TRANSLATIONAL MODIFICATION

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-87, wich stimulates starvation-induced autophagy. Dephosphorylated by protein phosphatase 2A (PP2A) (By similarity).; 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 increase its stability. Ubiquitinated by SCF(FBXO10), leading to its degradation by the proteasome.

SUBCELLULAR LOCATION

Mitochondrion outer membrane, Nucleus membrane, Endoplasmic reticulum membrane, Cytoplasm.

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). May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release.