Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition.

By Chunying Du, M. Fang, Yucheng Li, Lily Y. Li, Xiaodong Wang. Cell, 2000

3,661 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/8ed6770ccd62bfeb1de2fc6f380eb4df3eeaad40

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Citations in the corpus

Smac agonists sensitize for Apo2L/TRAIL- or anticancer drug-induced apoptosis and induce regression of malignant glioma in vivo (2002, background): “Recently, Smac was identified as a protein that is released from mitochondria in response to apoptotic stimuli and promotes apoptosis by antagonizing IAPs (refs”
The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues. (2000, background): “These include AIF, which upon release appears to translocate to the nucleus and promote DNA degradation (Susin et al., 1999), and Smac/ DIABLO, which can block the ability of IAP proteins to act as caspase inhibitors (Du et al., 2000; Verhagen et al., 2000).”
Bcl-2-family proteins and the role of mitochondria in apoptosis. (2003, background): “Mitochondria play an important role in apoptotic cell death by releasing key effector proteins [1], including cytochrome c and Smac/DIABLO, from the mitochondrial intermembrane space (IMS).”
Mechanisms of resistance to TRAIL-induced apoptosis in cancer (2005, background): “The activity of IAPs can be blocked by Smac/Diablo, a mitochondrial protein that is released into the cytosol at some point during the apoptotic cascade, where it promotes cell death by eliminating IAP inhibition of caspases.(74,75) Smac/Diablo is thought to interact with the BIR regions on IAPs, th”
Elimination of Mcl-1 is required for the initiation of apoptosis following ultraviolet irradiation. (2003, background): “These include Smac/Diablo and Omi/ HtrA2, which antagonize the caspase-inhibitory IAP proteins, and AIF and EndoG, which cause apoptotic changes independent of caspase activity (Susin et al. 1999; Du et al. 2000; Verhagen et al. 2000; Li et al. 2001; Suzuki et al. 2001; Hegde et al. 2002; Martins et”
Apoptosis in development (2000, background): “Whether or not RPR, GRIM and HID have any direct homologues in mammals, they nonetheless interact with components of Drosophila cell death machinery that are conserved, in particular the evolutionarily conserved inhibitor-of-apoptosis protein (IAP) family that in mammals are targets of the pro-”
Potent activity of carfilzomib, a novel, irreversible inhibitor of the ubiquitin-proteasome pathway, against preclinical models of multiple myeloma. (2005, methodology): “A major characteristic of intrinsic caspase-stimulated apoptosis is the loss of mitochondrial trans-membrane potential (∆Ψm) and release of pro-apoptotic proteins, including cytochrome c and second mitochondrial activator of caspases (Smac/DIABLO).(24,25) To examine whether carfilzomib-mediated apop”
TRAIL and apoptosis induction by TNF-family death receptors (2003, background): “SMAC/DIABLO promotes apoptosis by binding to inhibitor of apoptosis (IAP) proteins and preventing these factors from attenuating caspase activation (Du et al., 2000; Verhagen et al., 2000) (Figure 2).”