Bcl-2重组兔单抗

Rrmab®兔单抗
2026-01-04~2026-02-28,TR
Bcl-2重组兔单抗
货号:bsm-10846R
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概述

产品编号
bsm-10846R
产品类型
重组兔单抗
英文名称
Bcl-2 Recombinant Rabbit mAb
中文名称
Bcl-2重组兔单抗
英文别名
Bcl-2; PPP1R50; BCL2_HUMAN; BCL2;
抗体来源
Rabbit
免疫原
Recombinant human Bcl-2 protein: 1-211/239
亚型
IgG
性状
Liquid
纯化方法
affinity purified by Protein A
克隆类型
Recombinant
克隆号
3E3
理论分子量
26 kDa
SWISS
Gene ID
保存条件
Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles
注意事项
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
产品介绍
Bcl-2基因是指B-cell lymphoma gene。人体滤泡B细胞淋巴瘤中过量表达的原癌基因。由于染色体t(14;18)易位,将Bcl-2基因置于免疫球蛋白重链的转录调控下,使其表达失控。在细胞系中其过量表达能延长细胞存活期而不诱导细胞增殖。它是哺乳动物中细胞调亡的抑制基因。参与细胞凋亡的调控。肿瘤中的Bcl-2基因可提高侵润性瘤细胞的生存能力。主要用于滤胞型淋巴瘤、毛细管性白血病及细胞凋亡等方面的研究。
目前研究认为:Bcl-2也是细胞凋亡的一种抑制因子、参与细胞凋亡调控,可以用于各种恶性肿瘤的细胞凋亡的研究。
背景资料
The Bcl-2 gene was isolated at the chromosomal breakpoint of t(14;18)-bearing follicular B cell lymphomas(1,2).Bcl-2 blocks cell death following a variety of stimuli and confers a death-sparing effect to certain hematopoietic cell lines following growth factor withdrawal (3,5).Bcl-2 appears to function in several subcellular locations yet lacks any known motifs that would confer insight into its mechanism of action (6,7).A more recently identified protein,designated Bax p21(i.e., Bcl-associated X protein ),has extensive amino acid homology with Bcl-2 and both homodimerizes and forms heterodimers with Bcl-2(8). Overexpression of Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3 dependent cell line and Bax also counters the death repressor activty of Bcl-2(8).
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产品应用

应用已检合格种属预测种属推荐稀释比例
WBHuman1:1000-5000
IHC-PHuman1:200-500
IHC-FHuman1:200-500
IFHuman1:200-500
Flow-CytHuman1μg/Test
ICC/IFHuman1:50-200

交叉反应

交叉反应: Human

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靶标

基因名
BCL2
蛋白名
Apoptosis regulator Bcl-2
亚基
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. Interacts with EI24 (By similarity). Also interacts with APAF1, BBC3, BCL2L1, BNIPL, MRPL41 and TP53BP2. Binding to FKBP8 seems to target BCL2 to the mitochondria and probably interferes with the binding of BCL2 to its targets. Interacts with BAG1 in an ATP-dependent manner. Interacts with RAF1 (the 'Ser-338' and 'Ser-339' phosphorylated form). Interacts (via the BH4 domain) with EGLN3; the interaction prevents the formation of the BAX-BCL2 complex and inhibits the anti-apoptotic activity of BCL2. Interacts with G0S2; this interaction also prevents the formation of the anti-apoptotic BAX-BCL2 complex.
亚细胞定位
Mitochondrion outer membrane; Single-pass membrane protein. Nucleus membrane; Single-pass membrane protein. Endoplasmic reticulum membrane; Single-pass membrane protein.
组织特异性
Expressed in a variety of tissues.
翻译后修饰
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).
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 PARK2, leading to increase its stability.
疾病
Note=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.
相似性
Belongs to the Bcl-2 family.
功能
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).

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