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CASP14 — DDIT3

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Abdelrahim et al., Carcinogenesis 2006 (Pancreatic Neoplasms) : The subsequent downstream effects of DIM/DIM-C-pPhtBu- and Tg-induced ER stress included CHOP dependent induction of death receptor DR5 and subsequent cleavage of caspase 8, caspase 3, Bid and PARP
Chuang et al., Molecular cancer 2008 (Neoplasms) : The differential growth-inhibitory and apoptosis-stimulatory potency of these compounds in short-term assays did not at all correlate with their capacity to inhibit COX-2, but was closely aligned with their ability to trigger endoplasmic reticulum stress ( ERS ), as indicated by the induction of the ERS marker CHOP/GADD153 and activation of the ERS associated caspase 7
Mak et al., J Biol Chem 2008 : Tensile force induced caspase 3 cleavage, DNA fragmentation, depolarization of mitochondria, and induction of CHOP10 , all indicative of activation of apoptosis
Ling et al., Cancer Chemother Pharmacol 2009 (Carcinoma, Non-Small-Cell Lung...) : Moreover, the combination induced apoptosis in H1650 cells through induction of CHOP expression, activation of caspase-12 and caspase-3 , cleavage of PARP and bak, and down-regulation of anti-apoptotic proteins bcl-xL and survivin
Sánchez-Quiles et al., Proteomics 2010 (Carcinoma, Hepatocellular...) : In agreement, increased C/EBP homologous protein levels, poly-ADP ribose polymerase cleavage and activation of caspase 12 and downstream caspase 7 evidenced ER stress induced apoptosis
He et al., Int J Oncol 2010 (Laryngeal Neoplasms) : ROS induced by 9-HPbD-PDT directly led to downregulated expression of Bcl-2, loss of mitochondrial membrane potential, release of cytochrome c from mitochondria, elevation of intracellular calcium due to ER stress, as well as induction of CHOP and activation of caspase-3 , -8, -9 and -12
Lee et al., Infect Immun 2010 : Silencing of CHOP or DR5 expression selectively prevented caspase activation, loss of mitochondrial membrane potential, and Stx1 induced apoptosis of macrophage-like THP-1 cells
Tiwary et al., PloS one 2010 : Knockdown studies using siRNAs to TRAIL, DR5, JNK and CHOP as well as chemical inhibitors of ER stress and caspase-8 showed that : i ) alpha-TEA activation of DR5/caspase-8 induces an ER stress mediated JNK/CHOP/DR5 positive amplification loop ; ii ) alpha-TEA downregulation of c-FLIP ( L ) protein levels is mediated by JNK/CHOP/DR5 loop via a JNK dependent Itch E3 ligase ubiquitination that further serves to enhance the JNK/CHOP/DR5 amplification loop by preventing c-FLIP 's inhibition of caspase-8 ; and ( iii ) alpha-TEA downregulation of Bcl-2 is mediated by the ER stress dependent JNK/CHOP/DR5 signaling
Choi et al., Toxicol In Vitro 2011 (Carcinoma, Renal Cell...) : Furthermore, CHOP siRNA or inhibition of caspase-4 activity attenuated withaferin A-induced apoptosis
Pallepati et al., Biochim Biophys Acta 2011 : Longer exposure ( 1-3h ) to H ( 2 ) O ( 2 ) induced ER-mediated apoptosis, whereby CHOP expression increased, and enzymatic activity of calpain, caspase-7 , -4, -12 and -9 also increased
Gajate et al., Oncogene 2012 (Pancreatic Neoplasms) : Pancreatic cancer cells show a prominent ER and edelfosine accumulated in this subcellular structure, inducing a potent ER stress response, with caspase-4 , BAP31 and c-Jun NH ( 2 ) -terminal kinase ( JNK ) activation, CHOP/GADD153 upregulation and phosphorylation of eukaryotic translation initiation factor 2 a-subunit that eventually led to cell death
Wang et al., Nutr Cancer 2012 (Calcium Signaling...) : Exposure to DATS additionally induced endogenous endoplasmic reticulum stress markers and intracellular Ca2? mobilization, upregulation of Bip/GRP78 and CHOP/GADD153 , and activation of caspase-4
Yu et al., J Med Food 2012 (Breast Neoplasms) : This was supported by observations showing that treatment with PD induces phosphorylation of PKR-like ER kinase (PERK) and eukaryotic initiation factor 2 a ( eIF 2a ), up-regulating expression of glucose regulated protein 78/immunoglobulin heavy chain binding protein ( GRP78/Bip ) and CCAAT/enhancer binding protein homologous protein/growth arrest and DNA damage-inducible gene 153 ( CHOP/GADD153 ) and activation of caspase-4
Ou et al., Toxicol Lett 2012 : The results demonstrated that phycocyanin suppressed SRA01/04 cells ' morphologic changes and apoptosis induced by d-galactose, inhibited the expression and activation of caspase 3, alternated the Bax/Bcl-2 ratio, and down-regulated the level of p53, GRP78, and CHOP in d-galactose treated SRA01/04 cells
Němcová-Fürstová et al., Cell Physiol Biochem 2013 : Caspase-2 silencing had no effect on PARP as well as caspase-8 , -9 and -7 cleavage and the induction of CHOP expression, however, it also decreased the induction of BiP expression
Cui et al., PloS one 2013 (Diabetes Mellitus, Type 2) : Moreover, calpain-2 was required for FFA induced expression of CHOP and activation of caspase-12 and caspase-3 , thus promoting cell apoptosis in ß-TC3 cells