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We report that an Smac-mimetic selectively induces TNF-alpha (show TNF ELISA Kits)-dependent cystic renal epithelial cell death, leading to the removal of cystic epithelial cells from renal tissues and delaying cyst formation.
Results demonstrate an essential and apoptosis-independent function of SMAC in tumor suppression and provide new insights into the biology and targeting of colon cancer.
Identification of a novel anti-apoptotic E3 ubiquitin ligase that ubiquitinates antagonists of inhibitor of apoptosis proteins SMAC, HtrA2 (show HTRA2 ELISA Kits), and ARTS.
Loss of Smac/DIABLO alters both caspase (show CASP3 ELISA Kits)-dependent and caspase (show CASP3 ELISA Kits)-independent intrinsic programmed cell death.
Membrane-associated XIAP (show XIAP ELISA Kits) induces mitochondrial outer membrane permeabilization leading to cytochrome c (show CYCS ELISA Kits) and Smac release, which is dependent on Bax (show BAX ELISA Kits) and Bak (show BAK1 ELISA Kits).
data suggest the existence of a redundant molecule or molecules capable of compensating for a loss of Smac/DIABLO function.
mitochondrial activation by Bid (show BID ELISA Kits) is required for reversing the inhibitor-of-apoptosis proteins inhibition through Smac release
Diablo was present within the mitochondria of healthy cells, but released into the cytosol following the induction of apoptosis by UV.
Transient focal ischemia was produced for 1 hour in mice. Mitochondrial levels of DIABLO increased after 2-11 h reperfusion. DIABLO increased in the cytosol after 5 h reperfusion, implying the translocation of DIABLO into the cytosol.
Bax (show BAX ELISA Kits) and Bak (show BAK1 ELISA Kits) differentially regulate the release of cytochrome c (show CYCS ELISA Kits) and Smac/DIABLO from mitochondria, and Smac/DIABLO can be used to sensitize cells that are deficient in Bax (show BAX ELISA Kits) and Bak (show BAK1 ELISA Kits) genes, or resistant to TRAIL.
Expressions of SDF-1 (show CXCL12 ELISA Kits), survivin (show BIRC5 ELISA Kits) and smac were significantly higher in epithelial ovarian cancer tissue than those in normal tissue.
Results indicate that Smac plays an important role in reticulum stress-induced apoptosis in human lens epithelial cells, suggesting its close association with cataract development.
Smac mimetic APG (show SMAD1 ELISA Kits)-1387 exerts a potent antitumor effect on nasopharyngeal carcinoma cells by inducing apoptosis.
These results reveal a pro-apoptotic function of PARL (show PARL ELISA Kits) and identify PARL (show PARL ELISA Kits)-mediated Smac processing and cytochrome c (show CYCS ELISA Kits) release facilitated by OPA1 (show OPA1 ELISA Kits)-dependent cristae remodelling as two independent pro-apoptotic pathways in mitochondria.
Study found a negative correlation between Smac and XIAP (show XIAP ELISA Kits) at the level of protein but not mRNA in non-small cell lung carcinoma (NSCLC) patients. Overexpressed XIAP (show XIAP ELISA Kits) could degrade through ubiquitination, the mature Smac inhibiting NSCLC apoptosis.
Report role of RIP1 in Smac mimetic mediated chemosensitization of neuroblastoma (show ARHGEF16 ELISA Kits) cells.
This review discusses the promise as well as some challenges at the translational interface of exploiting Smac mimetics as cancer therapeutics.
Data indicate that Smac/DIABLO showed an inverse correlation with inhibitor of apoptosis proteins XIAP (show XIAP ELISA Kits), cIAP-1 (show BIRC2 ELISA Kits) and cIAP-2 (show BIRC3 ELISA Kits).
Data show that mitochondrial X-linked inhibitor of apoptosis protein (XIAP (show XIAP ELISA Kits)) entry requires apoptosis regulatory proteins Bax (show BAX ELISA Kits) or Bak (show BAK1 ELISA Kits) through mitochondrial permeabilization and Smac/DIABLO protein degradation.
SapC-DOPS acts through a mitochondria-mediated pathway accompanied by an early release of Smac and Bax (show BAX ELISA Kits).
hyperosmotic shock induces rapid calpain activation and high levels of Smac/DIABLO release from the mitochondria before significant amounts of cytochrome c (show CYCS ELISA Kits) are released to promote caspase-3 (show CASP3 ELISA Kits) activation
Identification of the third vertebrate homologue of Smac/DIABLO.
This gene encodes an inhibitor of apoptosis protein (IAP)-binding protein. The encoded mitochondrial protein enters the cytosol when cells undergo apoptosis, and it moderates the caspase inhibition of IAPs. Multiple polyadenylation sites have been found for this gene. Four alternatively spliced transcript variants have been described for this gene, with two of them encoding different isoforms and the other two probably not encoding a protein.
Direct IAP-binding protein with low pI
, diablo homolog, mitochondrial
, second mitochondria-derived activator of caspase
, direct IAP binding protein with low PI
, direct IAP-binding protein with low pI
, diablo homolog
, mitochondrial diablo-like protein
, mitochondrial diablo
, second mitochondrial derived activator of caspases
, Second mitochondria-derived activator of caspase