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CASP6 — DIABLO

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Du et al., Cell 2000 : Smac promotes caspase-9 activation by binding to inhibitor of apoptosis proteins, IAPs, and removing their inhibitory activity
Chai et al., Nature 2000 : Here we show that Smac/DIABLO promotes not only the proteolytic activation of procaspase-3 but also the enzymatic activity of mature caspase-3 , both of which depend upon its ability to interact physically with IAPs
Chauhan et al., J Biol Chem 2001 (Multiple Myeloma) : Smac , a second mitochondria derived activator of caspases, promotes caspase activation in the cytochrome c ( cyto-c ) /Apaf-1/caspase-9 pathway
Yoshikawa et al., J Immunol 2001 : Inhibition of DIABLO expression by antisense oligonucleotide is sufficient to decrease caspase activities and DNA fragmentation, but not cytochrome c release from mitochondria, suggesting that DIABLO plays a critical role in promoting apoptotic signals downstream of mitochondrial events
Suzuki et al., Mol Cell 2001 : Smac/DIABLO , an inhibitor of XIAP, is released from mitochondria upon receiving apoptotic stimuli and binds to the BIR2 and BIR3 domains of XIAP, thereby inhibiting its caspase-inhibitory activity
Adrain et al., EMBO J 2001 : However, whereas cell stress associated mitochondrial cytochrome c release was largely caspase independent, release of Smac/DIABLO in response to the same stimuli was blocked by a broad-spectrum caspase inhibitor
Sun et al., J Biol Chem 2002 : However, since Smac alone was sufficient to promote caspase-3 activity in vitro by inactivating XIAP, we proposed the existence of a death receptor induced, Smac dependent and apoptosome independent pathway
Yu et al., Clin Cancer Res 2002 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : STI571/flavopiridol mediated apoptosis was associated with the caspase independent down-regulation of Bcl-x ( L ) and Mcl-1, activation of extracellular signal regulated kinase and c-Jun NH ( 2 ) -terminal kinase, and the caspase dependent release of Smac/DIABLO and loss of deltapsi ( m )
Paris et al., J Biol Chem 2002 (Carcinoma, Hepatocellular...) : Furthermore, the combination of GD3 plus ionizing radiation stimulated the formation of reactive species followed by the mitochondrial release of cytochrome c and Smac/Diablo and caspase 3 activation
Kominsky et al., J Virol 2002 : Taken together, these results are consistent with a model in which Smac/DIABLO mediated inhibition of IAPs, rather than cytochrome c-mediated activation of caspase-9 , is the key event responsible for mitochondrial augmentation of reovirus induced apoptosis
Wang et al., Mol Pharmacol 2003 (Leukemia, Myeloid) : Whereas bryostatin 1 and UCN-01 both markedly enhanced ara-C induced mitochondrial injury ( e.g., cytochrome c and Smac/DIABLO release, loss of mitochondrial membrane potential ), caspase activation , and apoptosis, ectopic expression of an N-terminal loop deleted Bcl-2 mutant protein protected cells from ara-C/UCN-01- but not ara-C/bryostatin 1-mediated lethality
Yamaguchi et al., Cancer Res 2003 (Colonic Neoplasms) : Treating HCT116 cells with THG results in caspase-8 activation ; Bid cleavage ; Bax conformational change and mitochondrial translocation ; the release of cytochrome c, Smac/Diablo , and Omi/HtrA2 into the cytosol ; caspase-3 activation ; and apoptosis ... Taken together, our results indicate that Bax dependent Smac and Omi release plays an essential role in caspase-3 activation and apoptosis induced by THG in human colon cancer HCT116 cells
Tillman et al., Cancer Res 2003 (Colonic Neoplasms) : In RKO, rottlerin induced the release of cytochrome c, HtrA2/Omi, Smac/DIABLO , and AIF from the mitochondria, potentiated in combination with TRAIL, with concomitant caspase activation and down-regulation of XIAP
Saito et al., J Cereb Blood Flow Metab 2003 (Ischemic Attack, Transient) : Neither XIAP nor Smac/DIABLO expression was affected by caspase inhibition
Altznauer et al., J Biol Chem 2004 (Cystic Fibrosis) : Calpain-1 regulates Bax and subsequent Smac dependent caspase-3 activation in neutrophil apoptosis
Chen et al., Circ Res 2004 : Ox-LDL also decreased expression of antiapoptotic proteins Bcl-2 and c-IAP ( inhibitory apoptotic protein ) -1, which are involved in the release of cytochrome c and Smac and activation of caspase-9 , in a concentration- and time dependent manner ... This is followed by activation of apoptotic signaling pathway, involving release of cytochrome c and Smac and activation of caspase-9 and then caspase-3
Hasenjäger et al., Oncogene 2004 (Breast Neoplasms...) : Smac induces cytochrome c release and apoptosis independently from Bax/Bcl-x ( L ) in a strictly caspase-3 dependent manner in human carcinoma cells
Bartling et al., Exp Cell Res 2004 (Carcinoma...) : Unexpectedly, pan-caspase inhibition had no effect on Smac release
Doyle et al., Apoptosis 2004 : In contrast, the release of Smac/DIABLO was partially inhibited by caspase inhibition indicating differential release pathways for these mitochondrial pro-apoptotic factors
Chae et al., Life Sci 2004 (Calcium Signaling) : The treatment of BAPTA-AM, permeable endogenous calcium chelator, inhibited GJBRH induced caspase-3 and -9 activations, the release of cytochrome c and Smac/DIABLO into cytoplasm and the resultant cell death in HeLa human cervical carcinoma cells
Enoksson et al., J Biol Chem 2004 : In particular, we have shown previously that fully processed caspase-2 can permeabilize the outer mitochondrial membrane and cause cytochrome c and Smac/DIABLO release from these organelles
Qiu et al., J Biol Chem 2005 : Through these associations, BRUCE promotes the degradation of Smac and inhibits the activity of caspase-9 but not the effector caspase , caspase-3
Kumar et al., Curr Pharm Biotechnol 2004 (Neoplasms) : Upon apoptotic stimulus Smac/DIABLO is released from the mitochondria, which binds to IAPs and inhibits their caspase binding activity
Wu et al., Clin Exp Pharmacol Physiol 2004 : 3. The apoptotic effect induced by cinnamaldehyde could be further supported by the release of cytochrome c, Smac/Diablo and Omi/HtrA2 from mitochondria to the cytosol and activation of caspase 3
Gao et al., J Cereb Blood Flow Metab 2005 (Brain Ischemia...) : In strong support of a role for JNK in promoting the mitochondrial apoptosis signaling pathway, JNK inhibition prevented ischemia induced mitochondrial translocation of Bax and Bim, release of cytochrome c and Smac , and activation of caspase-9 and caspase-3
Choi et al., Cancer Res 2005 (Prostatic Neoplasms) : This conclusion is based on the following observations : ( a ) sulforaphane treatment caused a dose- and time dependent increase in the protein levels of both Bax and Bak and conformational change and mitochondrial translocation of Bax in SV40 transformed mouse embryonic fibroblasts (MEF) derived from wild-type mice to trigger cytosolic release of apoptogenic molecules ( cytochrome c and Smac/DIABLO ), activation of caspase-9 and caspase-3, and ultimately cell death ; ( b ) MEFs derived from Bax or Bak knockout mice resisted cell death by sulforaphane, and ( c ) MEFs derived from Bax and Bak double knockout mice exhibited even greater protection against sulforaphane induced cytochrome c release, caspase activation, and apoptosis compared with wild-type or single knockout cells
Lee et al., Biol Pharm Bull 2005 : Taken together, our data indicate that codonoposide 1c is a potent inducer of apoptosis and facilates its activity via Bid cleavage and translocation to mitochondria, Bax reduction in cytosol, release of cytochrome c and Smac/DIABLO into the cytosol, and subsequently caspase activation , providing a potential mechanism for the cytotoxic activity of codonoposide 1c
Jiang et al., Zhong Nan Da Xue Xue Bao Yi Xue Ban 2005 : H2O2 ( 0.5 mmol/L ) activated caspase-3 , caspase-9 8 h after the treatment and specific morphological changes of apoptosis 12 h after the treatment, and overexpression of Smac significantly promoted H2O2 induced activation of caspase-3, caspase-9 and apoptosis in C2C12 myogenic cells
Wu et al., Prostaglandins Leukot Essent Fatty Acids 2005 : Transfection of calpain 10 or Smac antisense oligodeoxynucleotide into the cells inhibited the LXA4 induced apoptosis, activity of caspase-3
Chan et al., Ann N Y Acad Sci 2005 (Stroke) : Recent studies have shown that mitochondrially formed oxidants are mediators of molecular signaling and have implicated mitochondria dependent apoptosis involving pro- and antiapoptotic protein binding, the release of cytochrome c and Smac , the activation of downstream caspase-9 and -3, and the fragmentation of DNA
Redlak et al., Am J Physiol Gastrointest Liver Physiol 2005 : We conclude that Bcl-2 protein family members and Smac regulate the apoptotic pathway in a caspase dependent manner
Bockbrader et al., Oncogene 2005 (Breast Neoplasms) : During apoptosis the caspase inhibition by IAPs can be negatively regulated by a mitochondrial protein second mitochondrial derived activator of caspase ( Smac )
Jiang et al., Free Radic Biol Med 2005 : The results showed that : ( 1 ) H ( 2 ) O ( 2 ) ( 0.5 mmol/L ) resulted in a marked release of Smac/DIABLO from mitochondria to cytoplasm 1 h after treatment, activation of caspase-3 and caspase-9 4 h after treatment, and specific morphological changes of apoptosis 24 h after treatment ; ( 2 ) overexpression of Smac/DIABLO in C2C12 cells significantly enhanced H ( 2 ) O ( 2 ) -induced apoptosis and the activation of caspase-3 and caspase-9 ( P < 0.05 )
Izeradjene et al., Cancer Res 2005 (Colonic Neoplasms) : Data suggest that in the presence of mitochondrial derived ROS, TRAIL induced mitochondrial release of Smac/DIABLO and inactivation of X-linked inhibitor of apoptosis through caspase-9 independent activation of caspase 3
Dasmahapatra et al., Mol Pharmacol 2006 (Leukemia) : Coadministration of flavopiridol with HDAC inhibitors synergistically potentiated mitochondrial damage ( cytochrome c, second mitochondria derived activator of caspases/direct IAP binding protein with low pI , and apoptosis inducing factor release ), caspase activation , poly ( ADP-ribose ) polymerase degradation, and cell death in both wild type and Bcl-2- or Bcl-x ( L ) -overexpressing cells and induced a pronounced loss of clonogenicity
Giagkousiklidis et al., Cancer Res 2005 (Glioblastoma...) : Smac enhanced activation of caspase-2 , caspase-3, caspase-8, and caspase-9, loss of mitochondrial membrane potential, and cytochrome c release on gamma-irradiation
Amano et al., Biosci Biotechnol Biochem 2005 : Upon treatment of the Jurkat cells with p29 at a lower concentration, translocation of phosphatidylserine to the external cell surface, release of cytochrome c and Smac/DIABLO from the mitochondria, and activation of caspase-9 were induced
Yang et al., Cancer Res 2006 (Ovarian Neoplasms) : Apoptotic stimuli induce second mitochondria derived activator of caspase ( Smac ) release from mitochondria into the cytosol, where it attenuates inhibitor of apoptosis protein mediated caspase inhibition
Liu et al., J Invest Dermatol 2006 : These responses were associated with Bid cleavage, caspase activation ( caspases 3, 8, and 9 ), mitochondrial depolarization and release of cytochrome c, Smac/DIABLO , and apoptosis inducing factor ( AIF ), but not endonuclease G
Tian et al., Zhonghua Xue Ye Xue Za Zhi 2006 : Apoptosis induced by bufalin is related to downregulation of expressions of bcl-2 and survivin, decrease of Bcl-2/Bax ratio, mitochondrial release of Smac/DIABLO , and activation of caspase-3
Li et al., Brain Res 2006 (Seizures) : In the present study, we explored the effect of an inhibitor of caspase-8 ( z-IETD-fmk ) on the release of Smac/DIABLO and cytochrome c from mitochondria
Morales et al., Oncogene 2007 (Carcinoma, Hepatocellular) : DNR plus NOE or acid CDase siRNA induced cell death was preceded by ultrastructural changes in mitochondria, stimulation of reactive oxygen species generation, release of Smac/DIABLO and cytochrome c and caspase-3 activation
Kashkar et al., Blood 2006 (Hodgkin Disease) : In HL cells, grzB induced mitochondrial release of proapoptotic Smac is blocked, which results in complete abrogation of cytotoxicity mediated by CTLs. Cytosolic expression of recombinant mature Smac enhanced caspase activity induced by grzB and restored the apoptotic response of HL cells
Nagy et al., Pathol Oncol Res 2006 (Colonic Neoplasms) : These results are consistent with a model where the full activation of caspase-3 by caspase-8 is dependent on the release of Smac/DIABLO in response to the combined treatment
Su et al., Food Chem Toxicol 2007 (Carcinoma, Hepatocellular...) : SC-1 also activated intrinsic pathway via increase of pro-apoptotic ( tBid, Bak and Bax ) and decrease of anti-apoptotic ( Bcl-2 and Bcl-x ( L ) ) proteins on mitochondria, disruption of mitochondrial membrane potential, release of cytochrome c and Smac ( second mitochondria derived activator of caspase/direct IAP binding protein with low PI ) from mitochondria, and activation of caspase 9
Taghiyev et al., Cancer Biol Ther 2006 (Prostatic Neoplasms) : TSA treatment resulted in the release of cytochrome c and Smac/DIABLO from mitochondria in DU145, and activation of caspase-9 in both cell lines
Zhang et al., Acta Biochim Biophys Sin (Shanghai) 2007 : Smac/DIABLO acts as a dimer and it contributes to caspase activation by sequestering the inhibitor of apoptosis proteins ( IAPs )
Turner et al., Ann Surg 2007 : Smac prevented the inhibitory effect of bile salts on caspase-3 activation
Rajalingam et al., Apoptosis 2007 : Smac/DIABLO is required for effector caspase activation during apoptosis in human cells
Luo et al., Cornea 2007 (MAP Kinase Signaling System) : The 90 mM NaCl high saline medium notably increased release of cytochrome c and Smac/DIABLO from mitochondria ; activated caspase-3 , JNK and ERK ; stimulated mRNA expression of interleukin-1 converting enzyme and Bax ; and reduced Bcl2 expression
Coll et al., J Lipid Res 2007 : In contrast, bSMase microinjection, which increased ceramide levels in a time- and dose dependent manner, resulted in oocyte apoptosis characterized by reactive oxygen species ( ROS ) generation, reduced glutathione ( GSH ) depletion in cytosol and mitochondria, release of cytochrome c and Smac/Diablo from mitochondria, and caspase-3 activation
Poh et al., Cell Death Differ 2007 : This increase in TRAIL sensitivity involved mitochondrial membrane permeabilization resulting in the egress of cytochrome c and second mitochondrial activator of caspase/direct IAP binding protein with low PI , cleavage of X-linked inhibitor of apoptosis protein, and activation of caspase 9
Das et al., Cancer 2007 (Glioblastoma) : Other events in apoptosis included overexpression of Bax, down-regulation of Bcl-2 and some BIRC proteins, mitochondrial release of cytochrome c and Smac into the cytosol, and activation of calpain, caspase-9 , and caspase-3
Das et al., J Neurooncol 2008 (Brain Neoplasms...) : The events of apoptosis included increase in expression of Bax, down regulation of Bcl-2 and baculoviral inhibitor-of-apoptosis protein (IAP) repeat containing ( BIRC ) proteins, mitochondrial release of cytochrome c and Smac into the cytosol, increase in intracellular free [ Ca ( 2+ ) ], and activation of calpain, caspase-9 , and caspase-3
Zhang et al., Sci China C Life Sci 2008 : The release of Cyt c, HtrA2 and Smac from mitochondria did not occur via the same mechanism, the release of Cyt c and HtrA2 was caspase independent and the release of Smac was caspase dependent
Miyawaki et al., Proc Natl Acad Sci U S A 2008 (Brain Ischemia...) : Here we show that preconditioning acts via PI3K/Akt signaling to block the ischemia induced cascade involving mitochondrial translocation of Bad, assembly of Bad with Bcl-x ( L ), cleavage of Bcl-x ( L ) to form its prodeath fragment, DeltaN-Bcl-x ( L ), activation of large-conductance channels in the mitochondrial outer membrane, mitochondrial release of cytochrome c and Smac/DIABLO ( second mitochondria derived activator of caspases/direct IAP binding protein with low pI ), caspase activation , and neuronal death
Lee et al., Biochem Biophys Res Commun 2008 (Colorectal Neoplasms) : In addition, activation of caspase-8, change of mitochondrial membrane potential, release of cytochrome c and Smac/DIABLO , and activation of caspase-9 and -3 were observed at the early time point
Das et al., Brain Res 2008 (Brain Neoplasms...) : Besides, apoptosis was associated with alterations in expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins resulting in an increase in Bax : Bcl-2 ratio, mitochondrial release of cytochrome c and Smac , downregulation of selective baculoviral inhibitor-of-apoptosis repeat containing ( BIRC ) molecules, an increase in intracellular free [Ca2+ ], and activation of calpain and caspase-3
Rudy et al., Cell Death Differ 2008 : We also show that Smac is critically involved in caspase-9 activation as evidenced by gene silencing experiments
Kadohara et al., J Biol Chem 2009 : Jurkat cells deficient in caspase-8 were more resistant to Ac-CHX than wild-type Jurkat cells and manifested decreased apoptosis induction and caspase activation as well as inefficient release of cytochrome c, Smac/DIABLO , and AIF into the cytosol
Lee et al., Cancer Sci 2009 : The apoptotic signaling cascades may proceed via proteolytic activation of caspase-2, change of mitochondrial membrane potential ( Deltapsi ( m ) ), release of cytochrome c and second mitochondria derived activator of caspase/direct IAP binding protein with low pI ( Smac/DIABLO ), activation of caspase-9 and -3, and cleavage of poly ( ADP-ribose ) polymerase ( PARP )
Karmakar et al., Neuroscience 2009 (Body Weight...) : Combination of 4-HPR and GST increased Bax : Bcl-2 ratio, mitochondrial release of Smac , downregulation of baculovirus inhibitor-of-apoptosis repeat containing ( BIRC ) proteins including BIRC-2 and BIRC-3, and activation of caspase-3 and apoptosis inducing factor ( AIF )
Shawgo et al., J Biol Chem 2009 : By comparison, Apaf-1-deficient Jurkat cells were sensitive to anti-Fas, exhibiting Bid cleavage, Bak activation, the release of cytochrome c and Smac , and activation of executioner caspase-3
Das et al., Cancer 2010 (Brain Neoplasms...) : Other events in apoptosis included overexpression of Bax, loss of DeltaPsi ( m ), mitochondrial release of cytochrome c and Smac into the cytosol, down-regulation of baculoviral inhibitor-of-apoptosis repeat containing proteins, and activation of calpain, caspase-9 , and caspase-3
Shakibaei et al., Antioxid Redox Signal 2010 : Since pan-caspase inhibitor z-VAD-fmk abolished the TNF-alpha induced mitochondrial changes, z-DEVD-fmk, an inhibitor of caspase-3 had no effect, suggesting that TNF-alpha induced mitochondrial changes or cytochrome c and Smac release requires caspase-8 but not caspase-3 activation
Moon et al., Cancer research and treatment : official journal of Korean Cancer Association 2004 : The CDCA derivatives demonstrated various apoptosis hallmarks, such as mitochondrial changes ( reduction of MMP, cytochrome c release, and Smac/ DIABLO translocation ), activation of caspase-3 ( resulting in the degradation of PARP and DFF45 ), DNA fragmentation and nuclear condensation
Li et al., Apoptosis 2010 : Smac/DIABLO release could not be blocked by these caspase inhibitors, indicating that it is an event upstream of caspase activation
Sun et al., Clin Cancer Res 2011 (Head and Neck Neoplasms) : Second mitochondria derived activator of caspase ( Smac ) promotes caspase activation by binding to IAPs upon release from the mitochondria
Flanagan et al., Cell death & disease 2010 : The Smac binding capacity of XIAP, but not caspase inhibition , was central for mitochondrial Smac retention, as evidenced in experiments using XIAP mutants that can not bind to Smac or effector caspases
Laukens et al., Neoplasia (New York, N.Y.) 2011 : By comparison, Smac mimetic and TNFa trigger activation of caspase-8 , -9, and -3 and DNA fragmentation in wild-type cells
Zhao et al., Asian Pac J Cancer Prev 2011 (Pancreatic Neoplasms) : The mechanism of the apoptosis-sensitization effect appeared associated with significant up-regulation of Smac/DIABLO and cytochrome C, down-regulation of XIAP, and activation of caspase-3
Cristofanon et al., Cell death & disease 2012 (Glioblastoma) : Coinciding with tBid accumulation, the activation of Bcl2 associated X protein (Bax), loss of mitochondrial membrane potential, release of cytochrome-c and second mitochondria derived activator of caspase ( Smac ) into the cytosol and caspase activation are strongly increased in cotreated cells
Liu et al., Int J Mol Med 2013 : Furthermore, we found that the silencing of Smac with siRNA in the HSFBs induced a noticeable decrease in caspase-3 and -9 activity, leading to a significant reduction in apoptosis