◀ Back to JUN
IL17A — JUN
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Benderdour et al., J Rheumatol 2002
(Osteoarthritis) :
Of note, in OA chondrocytes,
IL-17 and IL-1beta
induced collagenase-3 production through
AP-1 occurred with differential protein complexes : IL-17 stimulation resulted in FosB activation, while IL-1beta stimulated c-Fos ... We demonstrated that
IL-17 and IL-1beta
induced collagenase-3 production in OA chondrocytes mainly through
AP-1 mediated transcriptional activity but with differential protein complexes, suggesting that some AP-1 proteins play a pivotal role in the different cytokine responses in terms of collagenase-3 production
Sylvester et al., Cell Signal 2004
:
IL-17 stimulated phosphorylation of extracellular signal regulated kinase ( ERK ), protein 38 (p38) and
c-Jun N-terminal kinase (JNK)
Faour et al., J Biol Chem 2005
(Arthritis, Rheumatoid) :
PGE2 suppression of
IL-17 induced
ATF-2/c-Jun transactivation and DNA binding was dependent on Egr-1 mediated inhibition of induced c-Jun expression
Kim et al., Arthritis Res Ther 2005
(Arthritis, Rheumatoid...) :
However, inhibition of
activator protein-1 and extracellular signal regulated kinase 1/2 did not
affect IL-17 production
Yagi et al., J Gastroenterol 2007
(Colitis) :
IL-17A and IL-17F rapidly
induced phosphorylation of extracellular signal regulated kinases ( ERK ) 1/2, p38 MAPKs, and
c-Jun-NH ( 2 ) -terminal kinase ( JNK ) as early as 15 min after stimulation
Cortez et al., Am J Physiol Heart Circ Physiol 2007
:
IL-17 stimulated
activator protein-1 [ AP-1 ( c-Fos, c-Jun, and Fra-1 ) ], NF-kappaB ( p50 and p65 ), and CCAAT enhancer binding protein (C/EBP)-beta DNA binding and reporter gene activities, effects attenuated by antisense oligonucleotides, siRNA mediated knockdown, or expression of dominant negative signaling proteins