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CASP5 — JUN

Text-mined interactions from Literome

Harada et al., Jpn J Pharmacol 1999 : These results suggest that activation of c-Jun by p38 and/or JNK mediates the activation of caspase in the low KCl induced apoptosis in cerebellar granule neurons
Chen et al., Oncogene 1999 : Activation of c-Jun N-terminal kinase (JNK) by Fas ligation is caspase dependent , suggesting that caspases may regulate activators of the JNK pathway
Hossain et al., J Immunol 2000 (MAP Kinase Signaling System) : We demonstrated that NaAsO ( 2 ) -induced caspase activation is dependent on curcumin-sensitive c-Jun amino-terminal kinase and barely dependent on SB203580-sensitive p38 kinase or PD98059-sensitive extracellular signal regulated kinase
Ginham et al., Neurosci Lett 2001 : Elevated levels of caspase 3, c-Jun, and Fas ligand were found, in addition to a corresponding increase in c-Jun protein and activation of caspase-3
Suhara et al., Mol Cell Biol 2002 : Suppression of Akt signaling induces Fas ligand expression : involvement of caspase and Jun kinase activation in Akt mediated Fas ligand regulation
Liu et al., Hepatology 2002 : Inhibition of c-Jun function blocked mitochondrial cytochrome c release and activation of caspase-3 and -7
Tomicic et al., Mol Pharmacol 2003 (Necrosis) : The findings also show that the drug causes the induction of c-Jun and the activation of activator protein-1 resulting in increased level of Fas ligand (FasL) and caspase-8/-3 activation
Belmokhtar et al., J Biol Chem 2003 : Here we show that this defect in caspase activation is not due to mechanisms such as an absence of cytochrome c release, the expression of non-functional caspases, or the presence of an endogenous inhibitor but results from the loss of apoptosis protease activator protein-1 ( APAF-1 ) expression
Chen et al., J Neural Transm 2003 (Neuroblastoma) : During the apoptosis, production of reactive oxygen species ( ROS ), activation of c-Jun N-terminal kinase (JNK) and activation of caspase-3 were observed
Zhang et al., J Biol Chem 2003 (Insulinoma) : However, selective JNK inhibition had no effect on caspase-8 activation, and selective caspase-8 inhibition only partially suppressed apoptosis and c-Jun activation, indicating that caspase-8 may partially act upstream of the JNK pathway
Romashko et al., Free Radic Biol Med 2003 (Hyperoxia...) : Interestingly, hydrogen peroxide induced oxidative apoptosis of MLE-12 cells, with a shrinking nuclear morphology and activated caspase-3 activity, is also mediated by AP-1 , JNK, and p38
Peng et al., J Biol Chem 2004 : Our data show that paraquat induces the sequential phosphorylation of c-Jun N-terminal kinase (JNK) and c-Jun and the activation of caspase-3 and sequential neuronal death both in vitro and in vivo
Matsui et al., J Neurobiol 2004 : To examine the possible role of these events in the survival and death of the sensory receptors of the inner ear, we examined the effects of neomycin treatment on cytoplasmic calcium, activation of c-Jun-N-Terminal kinases (JNKs) , cytochrome c release, and caspase-3 activation in cultured vestibular hair cells
Yip et al., J Bone Miner Res 2005 (Calcium Signaling) : In this study, we showed a biphasic effect of TG on osteoclast formation and apoptosis through the regulation of ROS production, caspase-3 activity, cytosolic Ca2+, and RANKL induced activation of NF-kappaB and AP-1 activities
Hui et al., Brain Res 2005 (Brain Ischemia) : Furthermore, LY294002 significantly strengthened both peaks of JNK1/2 activation, c-Jun activation , Bcl-2 phosphorylation, and the activation of caspase-3 during reperfusion ... In contrast, insulin, a PI3K agonist, not only obviously activated Akt1 during early and later reperfusion, but also inhibited phosphorylation of JNK1/2, c-Jun , and Bcl-2 and attenuated the activation of caspase-3
Levkovitz et al., J Mol Neurosci 2005 (Glioma...) : These apoptotic changes were preceded by rapid increase in p-c-Jun levels, Cyt c release from mitochondria, and increased caspase-3-like activity
Andersson et al., Mol Cancer Ther 2006 (Breast Neoplasms) : An immunotoxin induced activation of c-Jun NH2-terminal kinase (JNK) preceded and overlapped caspase mediated cleavage of the alpha-subunit of AMPK in a time- and dose dependent manner
Nawaz et al., Toxicological sciences : an official journal of the Society of Toxicology 2006 (Necrosis) : Inhibition of the ERK activator MEK, as well as of p38, significantly reduced caspase activation and necrosis, whereas c-Jun N-terminal kinase (JNK) inhibition diminished only caspase activity
Oh et al., J Biomed Sci 2007 : HeLa cells treated with phytoglycoprotein ( 150 kDa ) were killed by activation of caspase 3 via inhibitory activities of NF-kappaB and AP-1
Kanamori et al., Am J Physiol Heart Circ Physiol 2007 (Myocardial Infarction...) : Ten days post-MI, apoptosis among granulation tissue cells was significantly suppressed in the olmesartan treated hearts, where expression of Fas, Bax, procaspase-3, and Daxx and activation of caspase-3 , c-Jun NH ( 2 ) -terminal kinase, and c-Jun were all significantly attenuated
Repici et al., Neuroscience 2007 (Disease Models, Animal...) : D-JNKI1 markedly prevented the increase of P-c-Jun in both core and penumbra and powerfully inhibited caspase-3 activation in the core
Vauzour et al., J Neurochem 2007 (MAP Kinase Signaling System) : Exposure of cortical neurons to hydrogen peroxide led to the activation of apoptosis signal regulating kinase 1 via its de-phosphorylation at Ser963, the phosphorylation of c-jun N-terminal kinase and c-Jun ( Ser73 ) and the activation of caspase 3 and caspase 9
Chan et al., IUBMB Life 2008 : Experiments with the embryonic stem cell line, ESC-B5, disclose that CTN induces apoptosis via several mechanisms, including ROS generation, increased cytoplasmic free calcium levels, intracellular nitric oxide production, enhanced Bax/Bcl-2 ratio, loss of mitochondrial membrane potential, cytochrome c release, activation of caspase-9 and caspase-3, and p21 activated protein kinase 2 and c-Jun N-terminal protein kinase activation
Barone et al., J Neurochem 2008 : Developing neurons deprived of trophic support undergo apoptosis mediated by activation of c-Jun N-terminal kinases (JNK) and c-Jun , induction of the Bcl-2 homology 3-only protein Bim ( EL ), Bax dependent loss of mitochondrial cytochrome c, and caspase activation
Ballaun et al., Biochem Biophys Res Commun 2008 : Transcription of the caspase-14 gene in human epidermal keratinocytes requires AP-1 and NFkappaB ... Our data reveal the basic organization of the human caspase-14 promoter and suggest an important role of AP-1 and NFkappaB in the transcriptional control of caspase-14
Mao et al., Cell Res 2008 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Treatment of K562 cells with shikonin ( e.g., 0.5 muM ) resulted in profound induction of apoptosis accompanied by rapid generation of reactive oxygen species ( ROS ), striking activation of c-Jun-N-terminal kinase (JNK) and p38, marked release of the mitochondrial proteins cytochrome c and Smac/DIABLO, activation of caspase-9 and -3 , and cleavage of PARP
Li et al., J Neuropathol Exp Neurol 2008 (Nerve Degeneration) : Here, we demonstrate that the proteasome inhibitor lactacystin induces phosphorylation of c-Jun N-terminal kinase (JNK) and c-Jun, the release of cytochrome c, activation of both caspase-9 and caspase-3, and sequential apoptosis of dopaminergic neurons in vitro
Rudolf et al., Toxicol Lett 2009 : We show that initially exposure of fibroblasts to Cr ( III ) induced membrane dependent signaling including activation of Rac1 GTPase, Src and apoptosis signal regulating kinase 1 ( ASK-1 ) kinases leading to increased activities of p38 and particularly Jun N-terminal kinase (JNK) and subsequent activation of caspase-3
Hasegawa et al., J Immunol 2009 : ASC mediated AP-1 activation was inhibited by chemical or protein inhibitors for caspase-8, caspase-8 targeting small interfering RNA, and p38 and JNK inhibitors, but not by a caspase-1 inhibitor, caspase-9 or Fas associated death domain protein ( FADD ) dominant negative mutants, FADD- or RICK targeting small interfering RNAs, or a MEK inhibitor, indicating that the ASC induced AP-1 activation is mediated by caspase-8, p38, and JNK, but does not require caspase-1, caspase-9, FADD, RICK, or ERK
Henrotin et al., Osteoarthritis Cartilage 2010 (Inflammation...) : Curcumin blocks IL-1beta induced proteoglycan degradation, AP-1/NF-kappaB signalling, chondrocyte apoptosis and activation of caspase-3
Saxena et al., Gastroenterology 2010 (Carcinoma, Hepatocellular...) : Adiponectin increased phosphorylation of c-Jun-N-terminal kinase (JNK) and inhibition of c-Jun-N-terminal kinase-phosphorylation inhibited adiponectin induced apoptosis and caspase-3 activation
Xia et al., J Biol Chem 2013 (Mammary Neoplasms, Animal) : Here, we demonstrate that treatment with CDDP resulted in down-regulation of c-Jun expression via caspase-9 dependent cleavage of c-Jun at Asp-65 and MEKK1 mediated ubiquitylation and degradation of c-Jun in CDDP-sensitive cancer cells