Overview |
bs-5220R-PE |
Bcl-2(Thr129) Polyclonal Antibody, PE Conjugated |
WB, FCM |
Human, Mouse, Rat, Others |
Dog, Cow, Sheep, Pig, Horse |
Specifications |
PE |
Rabbit |
KLH conjugated synthetic phosphopeptide derived from rat Bcl-2 around the phosphorylation site of Thr129 |
Thr129 |
Polyclonal |
IgG |
1ug/ul |
Purified by Protein A. |
Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles. |
Target |
24224 |
Cytoplasm, Nucleus, Cell membrane |
Bcl-2 phospho T129; Bcl-2 phospho Thr129; p-Bcl-2 Thr129; Apoptosis regulator Bcl 2; Apoptosis regulator Bcl2; AW986256; B cell CLL/lymphoma 2; B cell leukemia/lymphoma 2; B cell lymphoma 2; Bcl 2; Bcl-2; Bcl2; BCL2 protein; C430015F12Rik; D630044D05Rik; D830018M01Rik; Leukemia/lymphoma, B-cell, 2; Oncogene B-cell leukemia 2; BCL2_HUMAN. |
BCL2 is 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. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. |
Application Dilution |
WB |
1:300-5000 |
FCM |
1:20-100 |