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Merck
CN
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AB3609

Sigma-Aldrich

Anti-Smac/Diablo Antibody

Chemicon®, from rabbit

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UNSPSC代码:
12352203
eCl@ss:
32160702
NACRES:
NA.41

生物来源

rabbit

质量水平

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

种属反应性

human, mouse, rat

制造商/商品名称

Chemicon®

技术

western blot: suitable

UniProt登记号

运输

wet ice

靶向翻译后修饰

unmodified

基因信息

human ... DIABLO(56616)

一般描述

The inhibitor of apoptosis (IAP) proteins regulate programmed cell death by inhibiting members of the caspase family of enzymes. A novel mammalian protein that binds to IAPs and neutralizes their inhibitory effect on caspases has been designated Smac/DIABLO. This is a mitochondrial protein that is released along with cytochrome c during apoptosis and activates the cytochrome c/Apaf-1/caspase-9 pathway. Analysis of the structural basis of Smac/DIABLO reveals that the N-terminal amino acids are required for binding of Smac/DIABLO to IAPs and activation of caspases. Smac/DIABLO is expressed in a variety of human and mouse tissues.

特异性

Detects Smac/DIABLO in an approximately 25 kDa band by western blot.

免疫原

Peptide corresponding to aa 225-239 (EERAESEQEAYLRED) of human Smac/DIABLO.

应用

This Anti-Smac/Diablo Antibody is validated for use in WB for the detection of Smac/Diablo.
Western blot: 1:500 to 1:1000

Human heart tissue lysate can be used as a positive control.

Optimal working dilutions must be determined by end user.

外形

Format: Purified

其他说明

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

法律信息

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

WGK

WGK 2

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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APOLLON protein promotes early mitotic CYCLIN A degradation independent of the spindle assembly checkpoint.
Kikuchi, R; Ohata, H; Ohoka, N; Kawabata, A; Naito, M
The Journal of Biological Chemistry null
Zhaoqing Yang et al.
Journal of vascular research, 44(6), 483-494 (2007-07-28)
The inappropriate survival of cells in the neointima contributes to atherosclerotic plaque progression, while apoptosis in the fibrous cap of lesions contributes to myocardial infarction and stroke. Prior genomic-scale transcript profiling of human carotid artery plaque cells with known sensitivity
Zhaoqing Yang et al.
Arteriosclerosis, thrombosis, and vascular biology, 29(8), 1213-1219 (2009-05-16)
Increasing evidence suggests that chronic inflammation contributes to atherogenesis, and that acute inflammatory events cause plaque rupture, thrombosis, and myocardial infarction. The present studies examined how inflammatory factors, such as interferon-gamma (IFNgamma), cause increased sensitivity to apoptosis in vascular lesion

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