- CITATIONS: 0
|Application ||WB, IHC|
|Calculated MW||27131 Da|
|Other Names||Diablo homolog, mitochondrial, Direct IAP-binding protein with low pI, Second mitochondria-derived activator of caspase, Smac, DIABLO, SMAC|
|Target/Specificity||A synthetic peptide corresponding to C-terminal residues human Smac/DIABLO was used as immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Function||Promotes apoptosis by activating caspases in the cytochrome c/Apaf-1/caspase-9 pathway. Acts by opposing the inhibitory activity of inhibitor of apoptosis proteins (IAP). Inhibits the activity of BIRC6/bruce by inhibiting its binding to caspases. Isoform 3 attenuates the stability and apoptosis- inhibiting activity of XIAP/BIRC4 by promoting XIAP/BIRC4 ubiquitination and degradation through the ubiquitin-proteasome pathway. Isoform 3 also disrupts XIAP/BIRC4 interacting with processed caspase-9 and promotes caspase-3 activation. Isoform 1 is defective in the capacity to down-regulate the XIAP/BIRC4 abundance.|
|Cellular Location||Mitochondrion. Note=Released into the cytosol when cells undergo apoptosis|
|Tissue Location||Ubiquitously expressed with highest expression in testis. Expression is also high in heart, liver, kidney, spleen, prostate and ovary. Low in brain, lung, thymus and peripheral blood leukocytes. Isoform 3 is ubiquitously expressed|
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Provided below are standard protocols that you may find useful for product applications.
Smac/Diablo (Second Mitochondria-derived Activator of Caspases/Direct IAP Binding Protein with Low PI) is localized to the mitochondria and involved in activating programmed cell death, or apoptosis (1). In response to apoptotic stimuli, Smac/Diablo is released from the mitochondria and binds anti-apoptotic IAP proteins, supressing their inhibitory activity and promoting caspase activation (1,2). This interaction involves primarily the amino-terminal residues of Smac/Diablo with the BIR3 region of the IAP protein (3,4).
1. Du, C. et al. Cell 102:33-42 (2000)
2. Verhagen, A.M. et al. Cell 102: 43-53 (2000)
3. Liu, Z. et al. Nature 408: 1004-1007 (2000)
4. Wu, G. et al. Nature 408, 1008-1012 (2000)
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