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.
Especificidade
Detects Smac/DIABLO in an approximately 25 kDa band by western blot.
Imunogênio
Peptide corresponding to aa 225-239 (EERAESEQEAYLRED) of human Smac/DIABLO.
Aplicação
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.
forma física
Format: Purified
Outras notas
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Informações legais
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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Código de classe de armazenamento
10 - Combustible liquids
Classe de risco de água (WGK)
WGK 2
Ponto de fulgor (°F)
Not applicable
Ponto de fulgor (°C)
Not applicable
Certificados de análise (COA)
Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.
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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
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
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