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CRK — IL6

Text-mined interactions from Literome

Tokunou et al., Arterioscler Thromb Vasc Biol 2001 : Pharmacological inhibition of extracellular signal regulated protein kinase ( ERK ), p38 mitogen activated protein kinase ( MAPK ), or epidermal growth factor receptor (EGF-R) suppressed the thrombin induced IL-6 expression
Banerjee et al., J Virol 2002 : Experiments with a specific inhibitor of p38 MAPK, SB 203580, demonstrated that MHV induced p38 MAPK activation resulted in the accumulation of interleukin-6 (IL-6) mRNAs and an increase in the production of IL-6 , regardless of MHV induced general host protein synthesis inhibition
Ahmed et al., J Leukoc Biol 2002 (MAP Kinase Signaling System) : IL-1 induced inhibition of IL-6 signaling was not mediated by the activation of tyrosine phosphatases or by p38 dependent activation of phospholipase A ( 2 ) or cyclooxygenases, which could lead to indirect inhibition via production of prostaglandins
Pinteaux et al., J Neurochem 2002 : Bacterial lipopolysaccharide (LPS) caused increased expression of IL-1RI, IL-1RII and IL-1RAcP mRNAs, induced the release of IL-1beta, IL-6 and prostaglandin-E2 ( PGE2 ), and activated nuclear factor kappaB (NF-kappaB) and the mitogen activated protein kinases ( MAPKs ) p38 , and extracellular signal regulated protein kinase ( ERK1/2 ), but not c-Jun N-terminal kinase (JNK) in microglial cultures
Sengul et al., American journal of physiology. Renal physiology 2003 : Inhibitors of ERK, JNK, and p38 reduced LC-induced IL-6 and MCP-1 production
Garcia-Cao et al., EMBO Rep 2003 (MAP Kinase Signaling System) : Consistent with recent reports demonstrating the antagonistic actions of NF-kappaB and c-Jun amino-terminal kinase (JNK) signalling, we have found that Par4 ( -/- ) cells show a reduced activation of the sustained phase of JNK and p38 stimulation by TNF-alpha and interleukin 1
Kim et al., Pharmacol Res 2004 : Results indicated that both p38 and ERK pathways are involved in LPS stimulated NO synthesis and the expression of IL-1beta and IL-6
Zvalova et al., Glia 2004 : Therefore, interleukin-1beta (IL-1beta), which contributes to stroke induced brain injury and activates p38/SAPK2 , and hyperosmolarity induced by sorbitol, a potent stimulus of p38/SAPK2 in non-neuronal cells, were used to investigate a possible involvement of p38/SAPK2 in GJC modulation in mouse cultured astrocytes
Goral et al., J Immunol 2005 (Inflammation) : Specifically, the study focused on the proinflammatory cytokines IL-6 and TNF-alpha and activation of p38 and ERK1/2 MAPKs after a single in vivo exposure to physiologically relevant level of ethanol followed by ex vivo stimulation with specific TLR ligands
Obara et al., Mol Pharmacol 2005 (Astrocytoma) : Furthermore, both CREB and IL-6 promoter activities were suppressed by SB203580 [ 4- ( 4-fluorophenyl ) -2- ( 4-methylsulfinylphenyl ) -5- ( 4-pyridyl ) -1H-imidazole ], a p38 mitogen activated protein kinase ( MAPK ) inhibitor, and H89 [ N- [ 2- ( 4-bromocinnamylamino ) -ethyl ] -5-isoquinoline ], a protein kinase A (PKA) inhibitor, indicating involvements of p38 MAPK and PKA in CREB activation and IL-6 expression
Thobe et al., Am J Physiol Cell Physiol 2006 (Anoxia...) : Furthermore, administration of PP1 prevented the hypoxia induced increase in IL-6 but not MCP-1 release by KC. Additional in vitro results suggest that p38 but not ERK1/2 or JNK are critical for KC IL-6 production
Fabisiak et al., Am J Physiol Lung Cell Mol Physiol 2006 (Lung Diseases...) : Application of specific inhibitors of various MAPKs suggested that p38 and JNK/stress activated protein kinase were involved in early IL-6 release after exposure to TNF-beta and M. fermentans, respectively
Thirunavukkarasu et al., Hepatology 2006 (Disease Models, Animal...) : In conclusion, endotoxin induced synthesis of NO, TNF-alpha, and IL-6 in HSCs is mediated by p38 and NF-kappaB, with involvement of H ( 2 ) O ( 2 ) in TNF-alpha production
Sheryanna et al., J Am Soc Nephrol 2007 (Glomerulonephritis) : In the in vitro study, the p38 MAPKalpha/beta inhibitor reduced production of MCP-1 and IL-6 by TNF-alpha-or IL-1beta stimulated mesangial cells without any effect on cell viability or apoptosis
Kiu et al., Growth Factors 2007 : In addition, p38 mitogen activated protein kinase ( p38 ) activation also negatively regulates IL-6 signaling independent of its parallel and necessary action to induce SOCS3 expression
Wijagkanalan et al., Mol Pharmacol 2008 (Pneumonia) : DPML significantly inhibited tumor necrosis factor alpha, interleukin-1beta , and cytokine induced neutrophil chemoattractant-1 levels, suppressed neutrophil infiltration and myeloperoxidase activity, and inhibited NFkappaB and p38 mitogen activated protein kinase activation in the lung
Huang et al., J Mol Endocrinol 2009 : Finally, the CRH-R antagonists alpha-helical ( 9-41 ) CRH and astressin-2B completely inhibit Ucn induced IL-6 release, as well as activation of ERK, p38 , and NF-kappaB
Kitatani et al., J Biol Chem 2009 (Breast Neoplasms) : Acid beta-glucosidase 1 counteracts p38delta dependent induction of interleukin-6 : possible role for ceramide as an anti-inflammatory lipid
Noguchi et al., J Endod 2009 : After the pretreatment of LPS with O ( 3 ) aq, effects of LPS and O ( 3 ) aq-treated LPS on cell viability ; calcification ability ; expression of cyclooxygenase 2 (COX-2), interleukin 6 (IL-6) , and tumor necrosis factor alpha (TNF-alpha) ; and activation of p38 of KN-3 cells were examined
Cuong et al., Life Sci 2009 (Inflammation...) : Pre-treatment with C-K significantly inhibited zymosan mediated secretion of tumor necrosis factor-alpha, interleukin (IL)-6 , and IL-12 p40, and the activation of ERK1/2 and p38
Lee et al., Eur J Pain 2010 : These results suggest a new mechanism of neuropathic pain, in which IL-6 induces microglial CX3CR1 expression in the spinal cord through p38 MAPK activation, enhancing the responsiveness of microglia to fractalkine in the spinal cord, thus playing an important role in neuropathic pain after peripheral nerve injury
Zhou et al., Proc Natl Acad Sci U S A 2010 (Tuberculosis) : We uncovered that mPTPB subverts the innate immune responses by blocking the ERK1/2 and p38 mediated IL-6 production and promoting host cell survival by activating the Akt pathway
Kloesch et al., Immunol Lett 2012 (Arthritis, Rheumatoid...) : H ( 2 ) S-induced expression of IL-6 , IL-8 and COX-2 was completely blocked by specific inhibitors of p38 and ERK1/2 MAPK and NF-?B
Byun et al., Biochem Biophys Res Commun 2012 (Inflammation) : In addition, EGCG treated DCs inhibited lipopolysaccharide (LPS) induced production of pro-inflammatory cytokines ( tumor necrosis factor [TNF ] -a, interleukin [ IL]-1ß, and IL-6 ) and activation of mitogen activated protein kinases ( MAPKs ), e.g., extracellular signal regulated kinase 1/2 ( ERK1/2 ), p38 , c-Jun N-terminal kinase (JNK), and nuclear factor ?B ( NF-?B ) p65 translocation through 67LR
Frey et al., Ann Rheum Dis 2013 (Arthritis, Psoriatic...) : Functionally, IL-36a induced the expression of IL-6 and IL-8 in FLS through p38/NFkB activation
Tsai et al., PloS one 2013 : Bla g 2 can stimulate up-regulation of inflammatory cytokines including TNF-alpha and IL-6 and activation of nuclear factor kappa B ( NF-kB/p65 ), p38 mitogen activated protein kinase ( p38 ), ERK, and JNK in cultured fibrocytes
Lai et al., PloS one 2013 : Additionally, IL-6 mediated angiotensinogen expression through the Janus kinase ( JAK ) /signal transducer and activator of transcription 3 ( STAT3 ) and JAK/p38 signaling ... IL-6 mediated signaling, JAK2, STAT3 and p38 inhibitors reduced angiotensinogen expression in the partially hepatectomized mice
De Cesaris et al., J Biol Chem 1998 : Our data strongly support the hypothesis that, in response to TNF-alpha, activation of p38 leads to IL-6 production, whereas ICAM-1 and VCAM-1 expression could be induced by activation of the c-Jun N-terminal protein kinase/stress activated protein kinase pathway