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CASP12 — HLA-DRB1

Text-mined interactions from Literome

Choi et al., Mol Cell Biol 2002 (Astrocytoma...) : We demonstrate that DR5 ligation by either TRAIL or TRA-8 induces two functional outcomes, apoptosis and expression of the chemokine interleukin-8 (IL-8) ; the nonspecific caspase inhibitor Boc-D-Fmk blocks both TRAIL mediated cell death and IL-8 production ; the caspase 3-specific inhibitor z-DEVD-Fmk suppresses TRAIL mediated apoptosis but not IL-8 induction ; caspase 1- and 8-specific inhibitors block both TRAIL mediated cell death and IL-8 production ; and DR5 ligation by TRAIL mediates AP-1 and NF-kappaB activation, which can be inhibited by caspase 1- and 8-specific inhibitors
Liu et al., J Natl Cancer Inst 2004 (Carcinoma, Non-Small-Cell Lung...) : Overexpression of a dominant negative Fas associated death domain mutant, but not of BCL2, reduced the level of celecoxib induced apoptosis, and silencing of DR5 expression by DR5 siRNA suppressed celecoxib induced caspase 8 activation and apoptosis
Xia et al., Mol Cancer Ther 2005 (Leukemia, Myeloid) : These data taken together suggest that boswellic acid acetate induces myeloid leukemia cell apoptosis through activation of caspase-8 by induced expression of DR4 and DR5, and that the activated caspase-8 either directly activates caspase-3 by cleavage or indirectly by cleaving Bid, which in turn decreases mitochondria membrane potential
Zanchi et al., Cancer Res 2005 (Carcinoma, Squamous Cell...) : The results indicated a synergistic interaction between the two drugs associated with a dramatic enhancement of apoptotic response, up-regulation of the cell death receptor DR5 , and caspase 8 activation
Beurel et al., Int J Oncol 2005 (Carcinoma, Hepatocellular) : LY294002 increased Hep3B cell susceptibility to chemotherapy induced apoptosis by enhancing the expression of DR4 and DR5 and the activation of caspase-8 and -3
Horinaka et al., Oncogene 2005 (Prostatic Neoplasms) : In addition, suppression of DR5 expression with siRNA efficiently reduced luteolin induced caspase activation and apoptosis
Kosakowska-Cholody et al., Mol Cancer Ther 2005 (Colonic Neoplasms) : The recruitment of the p53 dependent apoptosis pathway was suggested by the up-regulation of p53, p21, Bax, DR-4 , DR-5, and p53 phosphorylated on Ser15 ; down-regulation of Bcl-2 ; and activation of caspase-8 , -9, -7, and -3 in cells treated with 100 nmol/L WMC-79
Nagane et al., J Neurosurg 2007 (Glioma) : Synergistic cell death was suppressed by TRAIL neutralizing DR5-Fc , caspase inhibitors , expression of dominant negative Fas associated protein with death domain and CrmA, which selectively blocks caspase-8, and overexpression of Bcl-X ( L )
Hussain et al., Cancer Res 2007 (Lymphoma, B-Cell) : Finally, N-acetylcysteine, an inhibitor of ROS, inhibits sanguinarine induced generation of ROS, up-regulation of DR5 , Bax conformational changes, activation of caspase-3 , and down-regulation of IAPs
Lee et al., Cell Microbiol 2008 : Collectively, these data suggest that Shiga toxins trigger monocytic cell apoptosis through the ER stress response, the increased expression of DR5 and TRAIL, and activation of caspase-8 via a calpain dependent mechanism
Chattergoon et al., Mol Ther 2008 : DR5 activation of caspase-8 induces DC maturation and immune enhancement in vivo
Portanova et al., Int J Oncol 2008 (Adenocarcinoma...) : In addition, SAHA up-regulated the death receptor DR5 , inducing the activation of caspase-8 with the consequent cleavage of Bid
Zhang et al., Cancer Biol Ther 2009 (Breast Neoplasms) : The internalized DR4 , but not DR5, is cleaved in a caspase dependent manner
Lokeshwar et al., Cancer Res 2010 (Neoplasm Invasiveness...) : 4-MU induced caspase-8, caspase-9, and caspase-3 activation , PARP cleavage, upregulation of Fas-L, Fas, FADD and DR4 , and downregulation of bcl-2, phosphorylated bad, bcl-XL, phosphorylated Akt, phosphorylated IKB, phosphorylated ErbB2, and phosphorylated epidermal growth factor receptor
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
Guo et al., J Control Release 2011 (Glioblastoma) : This sensitization was accompanied by up-regulation of death receptor 5 (DR5) expression and caspase activation
Cazanave et al., J Biol Chem 2011 (Fatty Liver) : Finally, knockdown of CHOP, an ER stress mediated transcription factor, reduced DR5 up-regulation and DR5 mediated caspase-8 activation upon palmitate treatment
Lu et al., J Urol 2011 (Prostatic Neoplasms) : Data suggest that paclitaxel induces nuclear translocation and activation of PKC-d, which in turn causes Golgi-Cdk1 activation, leading to Golgi associated DR5 up-regulation, and caspase-8 and 3 activation
Guo et al., Int J Nanomedicine 2012 (Carcinoma, Non-Small-Cell Lung...) : The mechanism behind this combination treatment includes both increased expression of DR5 and caspase activation