- 产品信息
商品描述
靶点-Target
Bcl-2
反应性
Human
应用
WB,IF,IP,ELISA
宿主物种-Host Species
Rabbit
同种型-Isotype
IgG,Kappa
MW(Calculated)
26kD
MW(Observed)
26kD
推荐稀释比
WB 1:2000-1:10000;IF 1:200-1:1000;ELISA 1:5000-1:20000;IP 1:50-1:200;
组成
PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA
纯化工艺
Protein A
储存
-15°C to -25°C/1 year(Do not lower than -25°C)
克隆性
Monoclonal
克隆号
PT1385R
特异性
Bcl-2 (Phospho Ser70) Antibody detects endogenous levels of Bcl-2 protein only when phosphorylated at S70.The name of modified sites may be influenced by many factors, such as species (the modified site was not originally found in human samples) and the change of protein sequence (the previous protein sequence is incomplete, and the protein sequence may be prolonged with the development of protein sequencing technology). When naming, we will use the "numbers" in historical reference to keep the sites consistent with the reports. The antibody binds to the following modification sequence (lowercase letters are modification sites):RTsPL
基因名称
BCL2
蛋白名称
Apoptosis regulator Bcl-2
别名
BCL2;Apoptosis regulator Bcl-2
Organism-1
Human
基因ID-1
596
SwissProt-1
P10415
Organism-2
Mouse
基因ID-2
12043
SwissProt-2
P10417
Organism-3
Rat
基因ID-3
24224
SwissProt-3
P49950
背景
BCL2, apoptosis regulator(BCL2) Homo sapiens 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. [provided by RefSeq, Feb 2016],
细胞定位
Disease:A chromosomal aberration involving BCL2 may be a cause of follicular lymphoma (FL) [MIM:151430]; also known as type II 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.,Domain:The BH4 motif is required for anti-apoptotic activity and for interaction with RAF-1.,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).,online information:Bcl-2 entry,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. Dephosphorylated by protein phosphatase 2A (PP2A).,PTM: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.,similarity:Belongs to the Bcl-2 family.,subunit:Forms homodimers, and heterodimers with BAX, BAD, BAK and Bcl-X(L). Heterodimerization with BAX requires intact BH1 and BH2 motifs, and is necessary for anti-apoptotic activity (By similarity). Also interacts with APAF1, RAF-1, TP53BP2, BBC3, BCL2L1, MRPL41 and BNIPL. Binding to FKBP8 seems to target BCL2 to the mitochondria and probably interferes with the binding of BCL2 to its targets.,tissue specificity:Expressed in a variety of tissues.,





