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Mouse Anti-Bcl-2/PE-Cy5.5 Conjugated antibody (bsm-10846M-PE-Cy5.5)
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產(chǎn)品編號 bsm-10846M-PE-Cy5.5
英文名稱1 Mouse Anti-Bcl-2/PE-Cy5.5 Conjugated antibody
中文名稱 PE-Cy5.5標(biāo)記的Bcl-2抗體
別    名 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.  
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領(lǐng)域 細(xì)胞生物  信號轉(zhuǎn)導(dǎo)  細(xì)胞凋亡  腫瘤細(xì)胞生物標(biāo)志物  新陳代謝  線粒體  
抗體來源 Mouse
克隆類型 Monoclonal
克 隆 號 1A5
交叉反應(yīng) Human, 
產(chǎn)品應(yīng)用 ICC=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
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 Recombinant human Bcl-2 protein
亞    型 IgG
純化方法 affinity purified by Protein G
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 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.
產(chǎn)品介紹 background:
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).

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 (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.

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

Omim: 151430 Human

SwissProt: P10415 Human

Unigene: 150749 Human



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

Bcl-2基因是指B-cell lymphoma gene。人體濾泡B細(xì)胞淋巴瘤中過量表達(dá)的原癌基因。由于染色體t(14;18)易位,將Bcl-2基因置于免疫球蛋白重鏈的轉(zhuǎn)錄調(diào)控下,使其表達(dá)失控。在細(xì)胞系中其過量表達(dá)能延長細(xì)胞存活期而不誘導(dǎo)細(xì)胞增殖。它是哺乳動物中細(xì)胞調(diào)亡的抑制基因。參與細(xì)胞凋亡的調(diào)控。腫瘤中的Bcl-2基因可提高侵潤性瘤細(xì)胞的生存能力。主要用于濾胞型淋巴瘤、毛細(xì)管性白血病及細(xì)胞凋亡等方面的研究。
目前研究認(rèn)為:Bcl-2也是細(xì)胞凋亡的一種抑制因子、參與細(xì)胞凋亡調(diào)控,可以用于各種惡性腫瘤的細(xì)胞凋亡的研究。
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