癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
Rabbit Anti-Bcl-2 (Ser70) Polyclonal Antibody
Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
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- 实验流程
- 背景知识
Application 
| IHC-P, IHC-F, IF, E |
|---|---|
| Primary Accession | P49950 |
| Reactivity | Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 26622 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated Synthesised phosphopeptide derived from rat Bcl-2 around the phosphorylation site of Ser70 |
| Epitope Specificity | RT(p-S)PL |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Mitochondrion outer membrane; Single-pass membrane protein. Nucleus membrane; Single-pass membrane protein. Endoplasmic reticulum membrane; Single-pass membrane protein. |
| 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. 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. |
| 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. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | 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). |
| Gene ID | 24224 |
|---|---|
| Other Names | Bcl-2; Apoptosis regulator Bcl-2; Bcl2 |
| Target/Specificity | Expressed in a variety of tissues. |
| Dilution | IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,Flow-Cyt=1ug/test,ELISA=1:5000-10000 |
| Format | 0.01M TBS(pH7.4) with 1% BSA, 0.09% (W/V) sodium azide and 50% Glyce |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. 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. |
| Name | Bcl2 |
|---|---|
| Synonyms | Bcl-2 |
| 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). Also acts as an inhibitor of autophagy: interacts with BECN1 and AMBRA1 during non-starvation conditions and inhibits their autophagy function. May attenuate inflammation by impairing NLRP1- inflammasome activation, hence CASP1 activation and IL1B release. |
| Cellular Location | Mitochondrion outer membrane {ECO:0000250|UniProtKB:P10415}; Single-pass membrane protein. Nucleus membrane {ECO:0000250|UniProtKB:P10415}; Single- pass membrane protein. Endoplasmic reticulum membrane {ECO:0000250|UniProtKB:P10415}; Single-pass membrane protein. Cytoplasm {ECO:0000250|UniProtKB:P10417} |
| Tissue Location | Expressed in a variety of tissues, with highest levels in reproductive tissues. In the adult brain, expression is localized in mitral cells of the olfactory bulb, granule and pyramidal neurons of hippocampus, pontine nuclei, cerebellar granule neurons, and in ependymal cells. In prenatal brain, expression is higher and localized in the neuroepithelium and in the cortical plate |
Research Areas
For Research Use Only. Not For Use In Diagnostic Procedures.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
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).
REFERENCES
Sato T.,et al.Gene 140:291-292(1994).
Tilly J.L.,et al.Endocrinology 136:232-241(1995).
Castren E.,et al.Neuroscience 61:165-177(1994).
Eliseev R.A.,et al.J. Biol. Chem. 284:9692-9699(2009).
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