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Rabbit Anti-Phospho-Bcl2 (Thr69)/Gold Conjugated antibody (bs-12578R-Gold)
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說(shuō) 明 書(shū): 100ul(10nm  15nm  35nm
100ul/2980.00元
大包裝/詢(xún)價(jià)
產(chǎn)品編號(hào) bs-12578R-Gold
英文名稱(chēng) Rabbit Anti-Phospho-Bcl2 (Thr69)/Gold Conjugated antibody
中文名稱(chēng) 膠體金標(biāo)記的磷酸化Bcl-2抗體
別    名 Bcl2 (Phospho-Thr69); Bcl2 (Phospho-T69); Bcl2 (phospho T69); p-Bcl2 (phospho T69); 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; Apoptosis regulator Bcl-2.  
規(guī)格價(jià)格 100ul/2980元 購(gòu)買(mǎi)        大包裝/詢(xún)價(jià)
說(shuō) 明 書(shū) 100ul(10nm  15nm  35nm
產(chǎn)品類(lèi)型 磷酸化抗體 
研究領(lǐng)域 腫瘤  細(xì)胞生物  神經(jīng)生物學(xué)  信號(hào)轉(zhuǎn)導(dǎo)  細(xì)胞凋亡  新陳代謝  線(xiàn)粒體  
抗體來(lái)源 Rabbit
克隆類(lèi)型 Polyclonal
交叉反應(yīng) Human, Mouse, Rat, 
產(chǎn)品應(yīng)用 IEM=1:20-200 ICA=1:20-200 ChIP=1:20-200 
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 0.4mg/ml
免 疫 原 KLH conjugated Synthesised phosphopeptide derived from human Bcl-2 around the phosphorylation site of Thr69
亞    型 IgG
純化方法 affinity purified by Protein A
儲(chǔ) 存 液 0.02M TBS(pH8.2) with 1% BSA, 0.03% Proclin300.
保存條件 Store at 2-8 oC for 3-6 months. Avoid repeated freeze/thaw cycles.
產(chǎn)品介紹 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 (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.
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