FITC标记的磷酸化Bcl-2抗体
产品名称： FITC标记的磷酸化Bcl-2抗体
英文名称： Anti-Phospho-Bcl-2 (Ser70)/FITC
产品编号： HZ-3052R-FITC
产品价格： null
产品产地： 中国/上海
品牌商标： HZbscience
更新时间： 2023-08-17T10:24:20
使用范围： Flow-Cyt=1:50-200 IF=1:50-200
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Rabbit Anti-Phospho-Bcl-2 (Ser70)/FITC Conjugated antibody
FITC标记的磷酸化Bcl-2抗体
| 英文名称 | Anti-Phospho-Bcl-2 (Ser70)/FITC |
| 中文名称 | FITC标记的磷酸化Bcl-2抗体 |
| 别 名 | Bcl2 (phospho S70); p-Bcl2 (phospho S70); 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. |
| 规格价格 | 100ul/2980元 购买 大包装/询价 |
| 说 明 书 | 100ul |
| 产品类型 | 磷酸化抗体 |
| 研究领域 | 肿瘤 细胞生物 神经生物学 信号转导 细胞凋亡 线粒体 |
| 抗体来源 | Rabbit |
| 克隆类型 | Polyclonal |
| 交叉反应 | Human, Mouse, Rat, Dog, Rabbit, |
| 产品应用 | Flow-Cyt=1:50-200 IF=1:50-200 not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 26kDa |
| 细胞定位 | 细胞膜 线粒体 |
| 性 状 | Lyophilized or Liquid |
| 浓 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated Synthesised phosphopeptide derived from rat Bcl-2 around the phosphorylation site of Ser70 |
| 亚 型 | IgG |
| 纯化方法 | affinity purified by Protein A |
| 储 存 液 | 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| 保存条件 | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| 产品介绍 | background: 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. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL. 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). 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. Interacts with EI24. 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. Subcellular Location: Mitochondrion outer membrane; Single-pass membrane protein. Nucleus membrane; Single-pass membrane protein. Endoplasmic reticulum membrane; Single-pass membrane protein. Tissue Specificity: Expressed in a variety of tissues. Post-translational modifications: 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. DISEASE: 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. Similarity: Belongs to the Bcl-2 family. Database links: Entrez Gene: 596 Human Entrez Gene: 12043 Mouse Entrez Gene: 24224 Rat Omim: 151430 Human SwissProt: O02718 Cow SwissProt: P10415 Human SwissProt: P10417 Mouse SwissProt: P49950 Rat Unigene: 150749 Human Unigene: 257460 Mouse Unigene: 9996 Rat
Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications |
BCL2是一种完整的线粒体外膜蛋白，阻断某些细胞如淋巴细胞的凋亡死亡。BCL2的组成型表达，如在BC2易位到Ig重链基因座的情况下，被认为是滤泡性淋巴瘤的原因。由交替剪接产生的两个转录变体（α和β），它们的C-末端不同。BCL2抑制多种细胞系统中的凋亡，包括依赖于因子的淋巴造血和神经细胞。它通过控制线粒体膜通透性来调节细胞死亡。它似乎在具有半胱氨酸天冬氨酸蛋白酶的反馈回路系统中起作用。BCL2通过抑制细胞色素C从线粒体释放和/或结合凋亡活化因子（APAF1）来抑制caspase活性。它可以形成同源二聚体，并具有Bax、BAD、BAK和BclX（L）的异源二聚体。Bax的异源二聚需要完整的BH1和BH2结构域，是抗凋亡活性所必需的。还与APAF1、RAF1、TP53BP2、BBC3、BCL2L1和BNIPL相互作用。