Gene interactions and pathways from curated databases and text-mining

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IL32 — MAPK3

Text-mined interactions from Literome

McDermott et al., J Biol Chem 2002 : Ras participates in the activation of p38 MAPK by interleukin-1 by associating with IRAK, IRAK2, TRAF6, and TAK-1
Ling et al., Crit Care Med 2002 : In contrast to its effects on the janus kinase/STAT pathways, interleukin-6 activation of MAP kinases ( extracellular signal regulated kinase-1 , extracellular signal regulated kinase-2, and p38 ) was unaffected by endotoxin
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
Jee et al., J Invest Dermatol 2002 (Carcinoma, Basal Cell...) : Next, interleukin-6 stimulation elicited extracellular signal regulated kinase activation in basal cell carcinoma cells, and the mitogen activated protein kinase inhibitor, PD98059, could affect this response without affecting the interleukin-6-medi ated Mcl-1 upregulation
Kotturi et al., J Biol Chem 2003 : We found that treatment of T lymphocytes with ( +/- ) Bay K 8644 increased intracellular Ca2+ and induced the activation of phosphoextracellular regulated kinase 1/2 ( Erk1/2 ), whereas nifedipine blocked Ca2+ influx, the activity of Erk1/2 and nuclear factor of activated T cells ( NFAT ), interleukin-2 (IL-2) production, and IL-2 receptor expression
Mason et al., Infect Immun 2004 : TRAF6 dependent mitogen activated protein kinase activation differentially regulates the production of interleukin-12 by macrophages in response to Toxoplasma gondii
Yang et al., Clin Exp Immunol 2006 (MAP Kinase Signaling System...) : Differential regulation of interleukin-12 and tumour necrosis factor-alpha by phosphatidylinositol 3-kinase and ERK 1/2 pathways during Mycobacterium tuberculosis infection
Hamdi et al., Biochim Biophys Acta 2008 (MAP Kinase Signaling System) : As a functional consequence of this PLD2 dependent MAPK activation, interleukin-2 production evoked by PMA/ionomycin stimulation or CD3/CD28 engagement was enhanced in the two T-cell lines overexpressing PLD2
Munitz et al., Gastroenterology 2010 (Colitis...) : In vitro analysis showed increased production of proinflammatory cytokines ( interleukin-6, interleukin-1beta , and tumor necrosis factor alpha ) and activation of MAPK and NF-kappaB in Pirb-/- macrophages following bacterial activation
Glossop et al., J Tissue Eng Regen Med 2010 : In a previous gene expression study, we reported a potentially important role for mitogen activated protein kinase kinase kinase 8 ( MAP3K8 ) and interleukin-1ß ( IL-1B ) in MAPK signalling in MSCs exposed to fluid shear stress
Rasheed et al., Arthritis Res Ther 2010 (Osteoarthritis) : Pomegranate extract inhibits the interleukin-1ß induced activation of MKK-3, p38a-MAPK and transcription factor RUNX-2 in human osteoarthritis chondrocytes
Dauphinee et al., Am J Physiol Heart Circ Physiol 2011 : We find that Ga ( i/o ) -mediated activation of the MAPK is independent of the canonical MyD88, interleukin-1 receptor associated kinase, and tumor necrosis factor receptor associated factor 6 signaling cascade in LPS stimulated cells
Nakayama et al., Arthritis Res Ther 2012 (Arthritis, Experimental...) : However, IL-32a alone induced TNFa production in RAW264.7 cells through phosphorylation of inhibitor kappa B ( I?B ) and ERK1/2 MAPK
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
Tormos et al., Hepatology 2013 (Chronic Disease...) : p38a mitogen activated protein kinases ( MAPK ) may be essential in the up-regulation of proinflammatory cytokines and can be activated by transforming growth factor ß, tumor necrosis factor-a, interleukin-1ß , and oxidative stress