◀ Back to MAPK1
IL18 — MAPK1
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
MAPK1
→
IL18
(increases, IL18 Activity)
Morel et al., J Biol Chem 2002*
Evidence: Using phosphoinositide 3-kinase (PI3-kinase) inhibitor LY294002 and Src inhibitor PP2, we show that interleukin (IL)-18-induced ERK1/2 activation is Src kinase-dependent.
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KEGG Tuberculosis:
MAPK1/MAPK3
→
IL18
(gene expression, expression)
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
Lee et al., Proc Natl Acad Sci U S A 2004
(Fever...) :
Five minutes after exposure to either cytokine, phosphorylation of mitogen activated protein kinase ( MAPK ) p38 was present ; specific inhibition of p38
MAPK reduced
IL-18 activity to background levels
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
Elbim et al., Clin Diagn Lab Immunol 2005
:
Flow cytometric analysis of intact PMNs in whole blood showed that
IL-18 increased
p38MAPK phosphorylation and tyrosine phosphorylation
Park et al., J Invest Dermatol 2005
(MAP Kinase Signaling System) :
In order to investigate whether the mitogen activated protein kinase (
MAPK ) signaling pathway is
involved in the downregulation of
IL-18 production, cells were pre treated with SB203580, an inhibitor of p38 MAPK, prior to the addition of CRH
Niyonsaba et al., J Immunol 2005
(MAP Kinase Signaling System) :
The human beta-defensins ( -1, -2, -3, -4 ) and cathelicidin LL-37
induce IL-18 secretion through p38 and ERK
MAPK activation in primary human keratinocytes
Sekiyama et al., J Med Invest 2005
:
Inhibitors of caspase-1, reactive oxygen species and P38
MAPK prevented stress induced accumulation of plasma
IL-18
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
Hewins et al., Kidney Int 2006
(Autoimmune Diseases...) :
Furthermore, TNFalpha and IL-18 phosphorylated neutrophil p38 mitogen activated protein kinase ( MAPK ), but
IL-18 mediated p38
MAPK phosphorylation was unaffected by anti-TNFalpha antibody
Kanda et al., Eur J Immunol 2007
:
Inhibitors of PI3 K, p38
MAPK , and MEK
suppressed IL-18 plus IFN-gamma induced CXCL9, CXCL10, and CXCL11 production and NF-kappaB, STAT1, and IRF-1 activities ...
IL-18 induced phosphorylation of ERK and Akt, while IFN-gamma induced phosphorylation of p38
MAPK
Amin et al., Arthritis Rheum 2007
(Arthritis, Rheumatoid) :
IL-18 induced phosphorylation of JNK, PKCdelta, p38
MAPK , and activating transcription factor 2 ( ATF-2 ) in RA ST fibroblasts in a time dependent manner, with JNK-2 being upstream of PKCdelta, ATF-2, and NFkappaB
Zabalgoitia et al., Free Radic Biol Med 2008
:
IL-18 induced p38alpha
MAPK activation, and suppressed p38beta isoform expression
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
Galbiati et al., Toxicol In Vitro 2011
(Dermatitis, Allergic Contact) :
Regarding the signal transduction pathway, we could demonstrate using selective inhibitors a
role for oxidative stress, NF-?B and p38
MAPK activation in PPD induced
IL-18 production
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
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