Summary
Basic Information
Immunogen
Purified recombinant fragment of human BCL2 (AA: 1-239) expressed in E. Coli.
Clonality
Monoclonal Antibody
Application Notes
Application | Note |
WB | 1:500-1:2,000 |
FC | 1:200-1:400 |
ELISA | 1:10,000 |
Formulations & Storage [For reference only, actual COA shall prevail!]
Concentration
Batch dependent
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.
Target
Full Name
BCL2, Apoptosis Regulator
Alternative Names
BCL2, Apoptosis Regulator; Protein Phosphatase 1, Regulatory Subunit 50; B-Cell CLL/Lymphoma 2; Apoptosis Regulator Bcl-2; PPP1R50; Bcl-2;
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 (PubMed:17418785).
Biological Process
Actin filament organization Source: Ensembl
Apoptotic process Source: MGI
Axonogenesis Source: Ensembl
Axon regeneration Source: Ensembl
B cell homeostasis Source: Ensembl
B cell lineage commitment Source: Ensembl
B cell proliferation Source: MGI
B cell receptor signaling pathway Source: UniProtKB
Behavioral fear response Source: Ensembl
Branching involved in ureteric bud morphogenesis Source: Ensembl
CD8-positive, alpha-beta T cell lineage commitment Source: Ensembl
Cell aging Source: Ensembl
Cell-cell adhesion Source: Ensembl
Cellular response to DNA damage stimulus Source: UniProtKB
Cellular response to glucose starvation Source: Ensembl
Cellular response to hypoxia Source: Ensembl
Cochlear nucleus development Source: Ensembl
Cytokine-mediated signaling pathway Source: Reactome
Defense response to virus Source: UniProtKB
Digestive tract morphogenesis Source: Ensembl
Ear development Source: Ensembl
Endoplasmic reticulum calcium ion homeostasis Source: UniProtKB
Extrinsic apoptotic signaling pathway in absence of ligand Source: GO_Central
Extrinsic apoptotic signaling pathway via death domain receptors Source: MGI
Female pregnancy Source: UniProtKB
Focal adhesion assembly Source: Ensembl
Gland morphogenesis Source: Ensembl
Glomerulus development Source: Ensembl
Hair follicle morphogenesis Source: Ensembl
Homeostasis of number of cells within a tissue Source: Ensembl
Humoral immune response Source: UniProtKB
Intrinsic apoptotic signaling pathway in response to DNA damage Source: GO_Central
Intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stress Source: MGI
Intrinsic apoptotic signaling pathway in response to oxidative stress Source: Ensembl
Lymphoid progenitor cell differentiation Source: Ensembl
Male gonad development Source: Ensembl
Melanin metabolic process Source: Ensembl
Melanocyte differentiation Source: Ensembl
Mesenchymal cell development Source: Ensembl
Metanephros development Source: Ensembl
Negative regulation of anoikis Source: UniProtKB
Negative regulation of apoptotic process Source: UniProtKB
Negative regulation of apoptotic signaling pathway Source: UniProtKB
Negative regulation of autophagy Source: UniProtKB
Negative regulation of calcium ion transport into cytosol Source: Ensembl
Negative regulation of cell growth Source: Ensembl
Negative regulation of cell migration Source: Ensembl
Negative regulation of cellular pH reduction Source: UniProtKB
Negative regulation of extrinsic apoptotic signaling pathway in absence of ligand Source: MGI
Negative regulation of G1/S transition of mitotic cell cycle Source: Ensembl
Negative regulation of intrinsic apoptotic signaling pathway Source: UniProtKB
Negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator Source: BHF-UCL
Negative regulation of mitochondrial depolarization Source: UniProtKB
Negative regulation of myeloid cell apoptotic process Source: Ensembl
Negative regulation of neuron apoptotic process Source: MGI
Negative regulation of ossification Source: Ensembl
Negative regulation of osteoblast proliferation Source: Ensembl
Negative regulation of reactive oxygen species metabolic process Source: Ensembl
Negative regulation of retinal cell programmed cell death Source: Ensembl
Neuron apoptotic process Source: HGNC-UCL
Oocyte development Source: Ensembl
Organ growth Source: Ensembl
Ossification Source: Ensembl
Ovarian follicle development Source: Ensembl
Peptidyl-serine phosphorylation Source: Ensembl
Peptidyl-threonine phosphorylation Source: Ensembl
Pigment granule organization Source: Ensembl
Positive regulation of B cell proliferation Source: UniProtKB
Positive regulation of catalytic activity Source: Ensembl
Positive regulation of cell growth Source: MGI
Positive regulation of cell population proliferation Source: ARUK-UCL
Positive regulation of intrinsic apoptotic signaling pathway Source: Reactome
Positive regulation of melanocyte differentiation Source: Ensembl
Positive regulation of multicellular organism growth Source: Ensembl
Positive regulation of neuron maturation Source: Ensembl
Positive regulation of peptidyl-serine phosphorylation Source: Ensembl
Positive regulation of protein insertion into mitochondrial membrane involved in apoptotic signaling pathway Source: Reactome
Positive regulation of skeletal muscle fiber development Source: Ensembl
Positive regulation of smooth muscle cell migration Source: Ensembl
Post-embryonic development Source: Ensembl
Protein dephosphorylation Source: Ensembl
Protein polyubiquitination Source: MGI
Reactive oxygen species metabolic process Source: Ensembl
Regulation of calcium ion transport Source: MGI
Regulation of cell-matrix adhesion Source: Ensembl
Regulation of gene expression Source: Ensembl
Regulation of glycoprotein biosynthetic process Source: Ensembl
Regulation of mitochondrial membrane permeability Source: HGNC-UCL
Regulation of mitochondrial membrane potential Source: HGNC-UCL
Regulation of nitrogen utilization Source: Ensembl
Regulation of protein stability Source: Ensembl
Regulation of transmembrane transporter activity Source: BHF-UCL
Regulation of viral genome replication Source: Ensembl
Release of cytochrome c from mitochondria Source: HGNC-UCL
Renal system process Source: Ensembl
Response to cytokine Source: MGI
Response to drug Source: MGI
Response to gamma radiation Source: Ensembl
Response to glucocorticoid Source: Ensembl
Response to hydrogen peroxide Source: Ensembl
Response to iron ion Source: UniProtKB
Response to ischemia Source: Ensembl
Response to nicotine Source: UniProtKB
Response to radiation Source: UniProtKB
Response to toxic substance Source: HGNC-UCL
Response to UV-B Source: Ensembl
Spleen development Source: Ensembl
T cell differentiation in thymus Source: Ensembl
T cell homeostasis Source: Ensembl
Thymus development Source: Ensembl
Cellular Location
Endoplasmic reticulum membrane; Nucleus membrane; Mitochondrion outer membrane
Involvement in disease
A chromosomal aberration involving BCL2 has been found in chronic lymphatic leukemia. Translocation t(14;18)(q32;q21) with immunoglobulin gene regions. BCL2 mutations found in non-Hodgkin lymphomas carrying the chromosomal translocation could be attributed to the Ig somatic hypermutation mechanism resulting in nucleotide transitions.
Topology
Helical: 212- 233 aa
PTM
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.