Mouse Anti-BCL2 Recombinant Antibody (EC86) (V2LY-0624-LY86)

Mouse

Human, Mouse, Rat

EC86

IgG

WB, IHC-P

Synthetic Peptide.

Mouse

Human, Mouse, Rat

IgG

Monoclonal Antibody

Liquid

PBS, pH 7.4, 50% glycerol

0.02% sodium azide

Batch dependent

>95% by SDS Page

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

BCL2, Apoptosis Regulator

This gene encodes an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Alternative splicing results in multiple transcript variants.

BCL2, Apoptosis Regulator; Protein Phosphatase 1, Regulatory Subunit 50; B-Cell CLL/Lymphoma 2; Apoptosis Regulator Bcl-2; PPP1R50; Bcl-2;

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).

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

Endoplasmic reticulum membrane; Nucleus membrane; Mitochondrion outer membrane

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.

Helical: 212- 233 aa

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.