Lane 1: Jurkat cell lysate
Lane 2: U937 cell lysate
Lane 3: THP-1 cell lysate
Recombinant Rabbit monoclonal primary
Bcl-2 Recombinant Rabbit Monoclonal Antibody [SZ10-03] (ET1603-11)
Synthetic peptide within human bcl-2 aa 40-90.
Jurkat cell lysate, U937 cell lysate, THP-1 cell lysate, A549, MCF-7, SH-SY5Y, human kidney tissue, human breast carcinoma tissue, Jurkat.
Store at +4C after thawing. Aliquot store at -20C or -80C. Avoid repeated freeze / thaw cycles.
1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
Protein A affinity purified.
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
Belongs to the Bcl-2 family.
Expressed in a variety of tissues.
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.
Mitochondrion outer membrane, Nucleus membrane, Endoplasmic reticulum membrane.
Apoptosis is defined as a set of cascades which, when initiated, programs the cell to undergo lethal changes such as membrane blebbing, mitochondrial break down and DNA fragmentation. Bcl-2 is one among many key regulators of apoptosis, which are essential for proper development, tissue homeostasis, and protection against foreign pathogens. Human Bcl-2 is an anti-apoptotic, membrane-associated oncoprotein that can promote cell survival through protein-protein interactions with other Bcl-2 related family members, such as the death suppressors Bcl-xl, Mcl-1, Bcl-w, and A1 or the death agonists Bax, Bak, Bik, Bad, and Bid. The anti-apoptotic function of Bcl-2 can also be regulated through proteolytic processing and phospho-rylation. Bcl-2 may promote cell survival by interfering with the activation of the cytochrome c/Apaf-1 pathway through stabilization of the mitochondrial membrane. Mutations in the Bcl-2 gene can contribute to cancers where normal physiological cell death mechanisms are compromised by deregulation of the anti-apoptotic influence of Bcl-2.
Li, Xiaotong et al.
Silkworm Pupa Protein Hydrolysate Induces Mitochondria-Dependent Apoptosis and S Phase Cell Cycle Arrest in Human Gastric Cancer SGC-7901 Cells. | International Journal of Molecular Sciences 
Yang, Yanfang et al.
SAE1 promotes human glioma progression through activating AKT SUMOylation-mediated signaling pathways. | Cell Communication and Signaling : Ccs