Gene interactions and pathways from curated databases and text-mining

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IL1A — MAPK7

Text-mined interactions from Literome

Itoh et al., J Immunol 1999 (Melanoma) : In both cells, p38 MAPK was activated by IL-1
Palsson et al., J Biol Chem 2000 : Our studies therefore provide clear evidence using multiple approaches for Ras as a signaling component in the activation of p38 MAPK by IL-1 , with Rap having an inhibitory effect
Kumar et al., J Cell Physiol 2001 (Bone Resorption) : IL-1- and TNF induced bone resorption is mediated by p38 mitogen activated protein kinase ... In addition, IL-1 and TNF also activated p38 MAPK in fetal rat long bones and p38 MAPK inhibitors inhibited IL-1- and TNF stimulated bone resorption in vitro in a dose dependent manner ( IC ( 50 ) s 0.3 -- 1 microM )
Surapisitchat et al., Proc Natl Acad Sci U S A 2001 (MAP Kinase Signaling System) : TNF-alpha and IL-1 regulate gene expression in ECs, in part, by stimulating mitogen activated protein kinases ( MAPK ), which phosphorylate transcription factors
Dreikhausen et al., Eur J Immunol 2001 (MAP Kinase Signaling System) : The recombinant C3-like chimeric toxin, which consists of the C3 toxin of Clostridium limosum and the N-terminal part of Clostridium botulinum C2 toxin ( C2IN-C3 ) interacting with the C2II binding subunit to facilitate uptake into cells, and selectively inactivates Rho A by ADP-ribosylation, prevented IL-1 stimulated activation of Jun-NH2-terminal-kinases (JNK) and p38 mitogen-activated-protein kinases ( MAPK ) ... UDP-monoglucosylation and concomitant inactivation of Rho A and of Rac-2 by Clostridium difficile toxin B also inhibited IL-1 induced activation of JNK and p38 MAPK , but additionally inhibited activation of the extracellular-regulated-kinase pathway and DNA binding of the transcription factor NFkappaB
Sheng et al., Neurochem Int 2001 (Alzheimer Disease) : This, together with findings showing that IL-1 activates MAPK-p38 in vitro and is markedly overexpressed in Alzheimer brain, suggest a role for IL-1 induced MAPK-p38 activation in the genesis of neurofibrillary pathology in Alzheimer 's disease
McDermott et al., J Biol Chem 2002 : Here we have further investigated the role of Ras and Rap in p38 MAPK activation by IL-1 ... Dominant negative forms of these were found to inhibit activation of p38 MAPK by IL-1 ... In addition we found a role for TAK-1 in the activation of p38 MAPK by IL-1 , with TAK-1 also associating with active Ras ... Our study suggests that upon activation Ras becomes associated with IRAK, Traf-6, and TAK-1, possibly aiding the assembly of this multiprotein signaling complex required for p38 MAPK activation by IL-1
Thomas et al., Biochem J 2002 : Interestingly, IL-1beta induced p38 MAPK activity was greatly enhanced in ( alg+ ) compared with ( alg- ) cells
Mifflin et al., Am J Physiol Cell Physiol 2002 (Colitis) : In contrast to what occurs in other cell types, including other myofibroblasts such as renal mesangial cells, PKC inhibition did not prevent IL-1 induced NF-kappaB or mitogen activated protein kinase/ stress activated protein kinase activation, suggesting a novel role for PKC isoforms during this process
Li et al., Endocrinology 2002 : Phosphorylation of p38 MAPK was induced by RANKL, IL-1 , TNFalpha, and LPS in osteoclast precursors but not in osteoclasts
Vela et al., Mol Cell Neurosci 2002 : Regarding intracellular signaling, IL-1beta activated the p38 mitogen activated protein kinase ( MAPK ) but not the p42/p44 MAPK and, when combined with growth factors, intensified p38 activation but inhibited the growth-factor induced p42/p44 activation
Yan et al., J Biol Chem 2002 : This model probiotic also inhibits activation of the pro-apoptotic p38/mitogen activated protein kinase by tumor necrosis factor, interleukin-1alpha , or gamma-interferon
Weber et al., Am J Physiol Endocrinol Metab 2004 : In addition, these ligands impair IL-1 induced NF-kappaB and MAPK as well as IFN-gamma stimulated signal transducer and activator of transcription ( STAT ) 1 activation in beta-cells
Wang et al., Mol Psychiatry 2004 : Interleukin 1alpha (IL-1alpha) induced activation of p38 mitogen activated protein kinase inhibits glucocorticoid receptor function
Ling et al., Biochem J 2004 (Inflammation) : Stimulation of human skin fibroblasts or articular chondrocytes with IL-1 or TNF-alpha in the presence of HC-gp39 resulted in a marked reduction of both p38 mitogen activated protein kinase and stress activated protein kinase/Jun N-terminal kinase phosphorylation, whereas nuclear translocation of nuclear factor kappaB proceeded unimpeded
Kim et al., J Neurochem 2004 : IFNbeta enhanced IL-1 induced phosphorylation of p38 MAPK , but was not effective alone
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
Wu et al., J Neurochem 2004 (Translocation, Genetic) : In accordance with these findings, IL-1beta stimulated phosphorylation of p42/p44 MAPK , p38, and c-Jun N-terminal kinase (JNK), which was attenuated by U0126, SB202190, or SP600125, respectively
Wang et al., Am J Physiol Endocrinol Metab 2005 (Reperfusion Injury) : After I/R, myocardium was assessed for expression of TNF-alpha, IL-1beta , and IL-6 ( RT-PCR, ELISA ) ; IL-1alpha and IL-10 mRNA ( RT-PCR ) ; and activation of p38 MAPK ( Western blot )
Chi et al., BMC immunology 2004 (Arteriosclerosis...) : MAPK dependent regulation of IL-1- and beta-adrenoreceptor induced inflammatory cytokine production from mast cells : implications for the stress response
Wang et al., Am J Physiol Lung Cell Mol Physiol 2005 : Consistently, IL-1beta stimulated phosphorylation of p42/p44 MAPK , p38, and JNK was attenuated by pretreatment with U0126, SB-202190, or SP-600125, respectively
Petersen et al., Cytokine 2005 (MAP Kinase Signaling System) : Western blotting revealed that IL-1alpha activated p38 MAPK and JNK/SAPK, but not ERK, in Sertoli cells from 8- or 9-day-old rat
Görtz et al., Arthritis Res Ther 2005 (Arthritis...) : Systemic blockade of TNF reduced activation of p38MAPKalpha and ERK, whereas inhibition of IL-1 only affected p38MAPKalpha and blockade of RANK ligand did not result in any decrease in MAPK activation in the synovial membrane
Wang et al., Int J Mol Med 2005 : In this study, we first investigated the effect of IL-1 on MAPK activity, c-Jun and c-Fos mRNA expression, and MMP-1 and MMP-2 production in UVA irradiated human dermal fibroblasts
Cherla et al., J Leukoc Biol 2006 (MAP Kinase Signaling System) : The MAPK inhibitors or Mnk1 inhibitor blocked soluble interleukin (IL)-1beta and IL-8 production or release by 73-96 %
Sawai et al., Oncogene 2006 (Disease Progression...) : Alteration of ILK kinase activity controlled IL-1alpha induced p38 MAPK phosphorylation and its downstream AP-1 activation with subsequent regulation of pancreatic cancer cell adhesion and invasion ... Overexpressed ILK enhances the IL-1alpha induced p38 MAPK phosphorylation more strongly through glycogen synthase kinase 3 ( GSK-3 ) activation, and subsequently induces AP-1 activation, which promotes aggressive capabilities of pancreatic cancer cells
Didierlaurent et al., Mol Cell Biol 2006 : Activation of interleukin-1 (IL-1) receptor ( IL-1R ), Toll-like receptor 2 (TLR2), and TLR4 triggers NF-kappaB and mitogen activated protein kinase ( MAPK ) -dependent signaling, thereby initiating immune responses
Besse et al., J Biol Chem 2007 : A green fluorescent protein fusion protein containing the last 100 residues of TAK1 ( TAK1-C100 ) abolished the interaction of endogenous TAB2/TAB3 with TAK1, the phosphorylation of TAK1, and prevented the activation of IKK and MAPK induced by IL-1 , TNF, and RANKL
Hayer et al., Arthritis Rheum 2007 (Arthritis...) : Early lesions were associated with up-regulation of interleukin-1 (IL-1) and IL-6 as well as activation of p38 MAPK and ERK
Studer et al., Spine (Phila Pa 1976) 2007 (Spinal Diseases) : Blocking cytokine activation of p38 MAPK reduced IL-1 and TNF-alpha induced PGE2 and IL-6 accumulation
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
Rønn et al., Diabetologia 2008 (Diabetes Mellitus, Experimental) : Rat islet cultures transduced with Socs3-adenovirus displayed reduced cytokine induced nitric oxide and apoptosis associated with inhibition of the IL-1 induced nuclear factor-kappaB and mitogen activated protein kinase ( MAPK ) pathways
Kidd et al., Neurogastroenterol Motil 2009 (Crohn Disease) : We examined whether interleukin (IL)1beta and Escherichia coli lipopolysaccharide (LPS) induced EC cell 5HT release through Toll-like/IL-1 (TIL) receptor activation, nuclear factor kappa B (NFkappaB) and mitogen activated protein kinase ( MAPK ) phosphorylation and evaluated whether somatostatin could inhibit this phenomenon
Brereton et al., J Immunol 2009 (Autoimmune Diseases) : Inhibition of ERK MAPK suppresses IL-23- and IL-1-driven IL-17 production and attenuates autoimmune disease
Grzelkowska-Kowalczyk et al., Cell Mol Biol Lett 2010 : The aim of this study was to compare the effects of TNF-alpha, IL-1beta and IFN-gamma on the activation of protein kinase B (PKB), p70 ( S6k ), mitogen activated protein kinase ( MAPK ) and p90 ( rsk ), and on IGF-I stimulated glucose uptake and protein synthesis in mouse C2C12 myotubes
Ralay Ranaivo et al., Brain Res 2010 (MAP Kinase Signaling System) : Albumin activated ERK1/2, p38 MAPK and JNK signaling pathways in astrocytes, and induced the production of interleukin (IL)-1beta , inducible nitric oxide (NO) synthase, the NO metabolite nitrite, and the chemokine CX3CL1 while reducing the level of S100B
Suzuki et al., Cytokine 2010 (MAP Kinase Signaling System) : Finally, IL-6+sIL-6R induced IL-1RI expression was inhibited by a STAT pathway inhibitor, but not a MAPK pathway inhibitor
Galán et al., J Hypertens 2011 : IL-1ß activated p38 mitogen activated protein kinase ( MAPK ) and extracellular signal regulated kinase ( ERK ) 1/2 pathways, and coincubation with Ang II resulted in a higher and more sustained phosphorylation of both MAPK
Eda et al., Rheumatol Int 2011 (MAP Kinase Signaling System) : IL-1ß and TNF-a activated the intracellular mitogen activated protein kinases ( MAPKs ) : p44/42 MAPK , p38, and c-Jun N-terminal kinase (JNK) as well as nuclear factor-?B ( NF-?B ) in osteoblasts
Hu et al., Invest Ophthalmol Vis Sci 2011 : IL-1ß ( 0.1-10 ng/mL ) increased IL-6 transcript and protein levels in a dose- and time dependent manner up to sixfold, accompanied by a significant increase of NF-?B in nuclear extracts and phosphorylated p38 MAPK in cell lysates
Choe et al., Joint Bone Spine 2012 (Arthritis, Rheumatoid...) : This study demonstrates that tacrolimus inhibits the expressions of Ang-1, Tie-2, and VEGF by blocking the activations of the IL-1ß mediated JNK and p38 MAPK pathways in human FLS
Hedl et al., J Biol Chem 2011 : Our findings clarify mechanisms of IL-1ß contributions to Nod2 responses and elucidate the dominant role of IL-1ß in MDP initiated MAPK and cytokine secretion
Li et al., J Clin Endocrinol Metab 2011 (Inflammation...) : NF?B and MAPK ( MAPK kinase, JUN NH2-terminal kinase, p38 kinase ) pathways were activated by IL-1ß or TNF-a in first trimester decidual cells
Arai et al., Endocrinology 2011 (MAP Kinase Signaling System) : In summary, the present study indicates that the p38 MAPK , the MAPK/ERK kinase, the nuclear factor ?B pathway, and PGE ( 2 ) mediate the effects of IL-1ß on INHBA mRNA expression
Wilhelm et al., Neuropharmacology 2012 (Body Weight) : Within the hippocampus, IL-1ß reduced levels of p38 MAPK , but had no impact on levels of phospho-p38 MAPK except in the presence of DMP904
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
Zhou et al., Molecular vision 2011 : Both 17ß-estradiol and progesterone inhibited the IL-1ß induced phosphorylation of p38 MAPK without affecting that of the MAPKs extracellular Signal regulated Kinase ( ERK ) or c-jun N-terminal kinase ( JNK )
Akhtar et al., Ann Rheum Dis 2012 (Osteoarthritis) : IL-1ß induced activation of p38-MAPK correlates inversely with miR199a* expression levels
Herfs et al., Am J Respir Cell Mol Biol 2012 (Hyperplasia...) : Using immunohistological techniques, we showed a higher epithelial expression of TNF-a, IL-1ß , and IL-6, as well as an activation of NF-?B and activator protein-1/mitogen activated protein kinase signaling pathways in the respiratory tract of smoking patients, compared with the normal ciliated epithelium of nonsmoking patients
Jagielska et al., Arterioscler Thromb Vasc Biol 2012 (Disease Models, Animal...) : Accordingly, cellular cholesterol depletion ( cyclodextrin ) and silencing of caveolin-1 ( small interfering RNA ) inhibited IL-1ß induced activation of p38-MAPK and MK2, as well as IL-1ß induced tube formation and migration
Zhou et al., Invest Ophthalmol Vis Sci 2012 (Disease Models, Animal) : MPA inhibited the IL-1ß induced phosphorylation of p38 MAPK without affecting that of the MAPKs ERK or JNK
Liu et al., PloS one 2012 (Shock, Septic) : In the present study, we show that a novel chromone derivative, DCO-6, significantly reduced lipopolysaccharide (LPS) induced production of nitric oxide, IL-1ß and IL-6, decreased the levels of iNOS, IL-1ß and IL-6 mRNA expression in both RAW264.7 cells and mouse primary peritoneal macrophages, and inhibited LPS induced activation of p38 MAPK but not of JNK, ERK
Chen et al., Proc Natl Acad Sci U S A 2012 (Inflammation...) : Here, we identified the E3 ubiquitin ligase membrane associated RING-CH ( MARCH8 ) as a suppressor of IL-1ß induced NF-?B- and MAPK-activation pathways ... Overexpression of MARCH8 inhibits IL-1ß induced NF-?B and MAPK activation, whereas knockdown of MARCH8 has the opposite effect
Hedl et al., Gastroenterology 2012 : In response to PRR stimulation of macrophages, the level of MAPK signaling is regulated by autocrine IL-1 and determines whether production of inflammatory cytokines is inhibited or stimulated
Sung et al., Glia 2012 (Hyperalgesia...) : IL-1ß induced P-p38 MAPK and iNOS expression predominantly in microglia and less in astrocytes
Mao et al., J Trauma Acute Care Surg 2012 (MAP Kinase Signaling System) : IL-1ß induced dose- and time dependent activation of p38 MAPK in EPCs
Clarke et al., Mol Cell Proteomics 2013 (MAP Kinase Signaling System) : Mixed-effects modeling analysis of our data was vital for ascertaining that IL-1a and TGF-a treatment increased the activities of more pathways than IL-6 and TNF-a and that TGF-a and TNF-a increased p38 MAPK and c-Jun N-terminal kinase (JNK) phospho-protein levels in a synergistic manner
Akutsu et al., J Oral Pathol Med 2013 (Dislocations...) : In addition, the IL-1ß- and TNF-a stimulated MIP-3a production was potently reduced by the MAPK and NF?B signaling pathway inhibitors
Kataoka et al., Biochem Biophys Res Commun 2013 (Synovitis) : Western blotting analysis revealed that IL-1ß induced phosphorylation of p38 MAPK and JNK protein were diminished by HMW-HA
Tseng et al., PloS one 2013 : Moreover, IL-1ß markedly stimulated p42/p44 MAPK and JNK1/2 phosphorylation in SIRCs ... In addition, IL-1ß also enhanced p42/p44 MAPK translocation from the cytosol into the nucleus
Olajide et al., Eur J Med Chem 2013 (Neuroblastoma) : At 10 and 20 µM, CAS inhibited IL-1ß induced phosphorylation of p38 MAPK
Bando et al., Biochim Biophys Acta 2013 : Modeled using human epidermal keratinocytes ( HaCaT cells ), IL-1a stimulated the phosphorylation of p38 MAPK and induced S100A9 expression, which was blocked by IL-1 receptor antagonist, RNAi suppression of p38, or a p38 MAPK inhibitor
Park et al., Osteoarthritis Cartilage 2013 (Osteoarthritis, Knee) : IL-1ß induced activation of MAP kinase ( MAPK ) and nuclear factor-?B ( NF-?B ) decreased miR-558 expression and induced COX-2 expression in chondrocytes
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
Hosokawa et al., Cell Immunol 2013 (Periodontitis) : Polyinosinic-polycytidylic acid ( Poly I:C ), which is a TLR3 agonist, stimulation could moderately induce CCL20 production in HGFs. Poly I:C synergistically enhanced CCL20 expression from IL-1ß stimulated HGFs. Inhibitors of p38 MAPK , extracellular signal regulated kinase ( ERK ), c-Jun N terminal kinase (JNK), and NF-?B significantly inhibited CCL20 production in Poly I:C/IL-1ß stimulated HGFs. Western blot analysis disclosed phosphorylation of p38 MAPK, JNK, and I?B-a were enhanced in Poly I:C/IL-1ß treated HGFs
Bird et al., J Biol Chem 1994 : In KB epidermoid cells, we previously showed that interleukin-1 alpha (IL-1) and various mitogens activate the mitogen activated protein ( MAP ) kinases ERK1 and ERK2, which phosphorylate both myelin basic protein (MBP) and a peptide containing Thr669 of the epidermal growth factor receptor
Lee et al., J Biol Chem 1994 : IL-1 alpha did activate mitogen activated protein kinase ... Genistein, a tyrosine kinase inhibitor, blocked both IL-1 alpha induced mitogen activated protein kinase activation as well as IL-1 alpha mRNA expression
Lu et al., Neurochem Int 1997 (Neuroma) : The increases in MAPK induced by TNF-alpha and IL-1 were similar to the increases induced by PMA and PDGF-AB ... Our findings indicate that TNF-alpha and IL-1 activate parallel signal transduction pathways in human neuroma fibroblasts, and that they are relatively stronger activators of MAPK than of SAPK
Utal et al., Neurochem Res 1998 (Astrocytoma...) : Of these, IL-1 beta activated only MAPK ... In cultured rat astrocytes, IL-1 beta caused activation of MAPK without inducing proliferation
Bhat et al., J Neurochem 1999 : In contrast, IFN gamma neither activated on its own nor enhanced the activation of p38 MAPK in response to TNF alpha and IL-1