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IL1A — RNF19A

Text-mined interactions from Literome

Itoh et al., J Immunol 1999 (Melanoma) : Antiproliferative effect of IL-1 is mediated by p38 mitogen activated protein kinase in human melanoma cell A375
Salituro et al., Curr Med Chem 1999 (Cardiovascular Diseases) : Subsequent downstream events triggered by p38 activation result in the production of IL-1 and TNF-a, suggesting that inhibition of this enzyme may provide a useful therapeutic target for intervention in various diseases mediated by these cytokines
Paraskevas et al., Ann Surg 2001 (Cadaver) : In the cytokine stimulation studies, IL-1 beta stimulated p38 activation in a dose dependent manner, while JNK was relatively unaffected
Hattori et al., J Interferon Cytokine Res 2001 (Melanoma) : We have demonstrated previously that p38 mitrogen activated protein kinase ( MAPK ) mediated the antiproliferative effect of IL-1 partially through the downregulation of activity and protein level of ornithine decarboxylase (ODC)
Park et al., Mol Pharmacol 2002 : Moreover, IL-1 beta stimulation of the cells caused the phosphorylation of p38 and extracellular signal regulated kinase ( ERK ), and IL-1 beta induced COX-2 expression was inhibited by the pretreatment of WISH cells with a p38 inhibitor, in contrast ERK upstream inhibitor had no effect
Lasa et al., Mol Cell Biol 2002 : The proinflammatory cytokine interleukin 1 (IL-1) induced MKP-1 expression in a p38 dependent manner and acted synergistically with dexamethasone to induce MKP-1 expression
Pinteaux et al., J Neurochem 2002 : In comparison, IL-1beta induced the release of PGE2, IL-6 and activated NF-kappaB, p38 , JNK and ERK1/2 in mixed glial cultures, but failed to induce any of these responses in microglial cell cultures
Zhao et al., J Neuroimmunol 2004 (MAP Kinase Signaling System) : 15d-PGJ2 inhibited transactivation of NF-kappaB dependent promoters, as well as p38 and JNK MAPK phosphorylation induced by IL-1 , while having no inhibitory effect on IFN induced Stat signaling pathways
Itoh et al., J Anesth 2004 : In contrast, neither halothane nor isoflurane enhanced the p38 MAPK activation induced by IL-1
Netea et al., Proc Natl Acad Sci U S A 2008 : Whereas the induction of TNFalpha, IL-1beta , and IL-6 by IL-32 is mediated by p38-MAPK , IL-32 induced monocyte-to-macrophage differentiation is mediated through nonapoptotic, caspase-3 dependent mechanisms
Bachstetter et al., Journal of neuroinflammation 2011 : Increased IL-1ß and TNFa production by the BV-2 microglial cell line and by primary microglia cultures was inhibited in a concentration dependent manner by the p38a MAPK targeted inhibitor
Ryll et al., Molecular bioSystems 2011 (MAP Kinase Signaling System) : Our model based data analysis, for instance, suggested model modifications regarding ( i ) Akt contribution to IL-1 stimulated p38 MAPK activation and ( ii ) insignificant p38 MAPK activation in response to IL-6
Simões et al., Journal of neuroinflammation 2012 (MAP Kinase Signaling System) : The selective A ( 2A ) R antagonist, SCH58261 ( 50 nmol/l ), prevented both the IL-1ß induced phosphorylation of JNK and p38 , as well as the IL-1ß induced deregulation of calcium and the consequent enhanced neurotoxicity, whereas it had no effect on glutamate actions
Kim et al., Parasite Immunol 2013 : N. fowleri mediated IL-1ß and IL-6 expression requires ERK, JNK and p38 mitogen activated protein kinases ( MAPKs ) activation in astrocytes
Howard et al., Shock 2013 (Acute Lung Injury...) : Remarkably, IL-1ß dependent p38 activation 24 h after heat shock did not result in an inhibition of aENaC mRNA expression and channel function
Gotoh et al., Connect Tissue Res 2013 : ß-NAD ( + ) had no significant effect on the IL-1a induced phosphorylation of ERK1/2, JNK, and p38 and also had no effect on the IL-1a induced degradation of I?Ba relative to the control, suggesting that inhibition by ß-NAD ( + ) was independent of the MAP kinase and the nuclear factor-?B signaling pathways
Negoro et al., Scientific reports 2013 (Disease Models, Animal...) : In urothelial cells, IL-1ß stimulation increased Cx43 expression, dye coupling, and p38 MAPK phosphorylation but not ERK1/2 phosphorylation
Zhong et al., Int Immunopharmacol 2013 : Interestingly, vorinostat selectively inhibited IL-1ß induced p38 and ERK1/2 activation without affecting JNK activation
Geng et al., J Clin Invest 1996 : In contrast, JNK and p38 are only activated by IL-1 or TNF, suggesting that these kinases participate in the induction of the catabolic program in cartilage
Matsumoto et al., J Allergy Clin Immunol 1998 : The specific p38 MAP kinase inhibitor, SB 203580, completely inhibited TNF-alpha-, IL-1alpha- , or PAF induced IL-8 protein and mRNA expression in BECs