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CASP4 — 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