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MAPK10 — TNFSF11

Text-mined interactions from Literome

Wei et al., J Biol Chem 2002 (MAP Kinase Signaling System) : Consistent with this observation, the inhibitory effects of IL-4 on RANKL induced NF-kappa B and mitogen activated protein kinase activation are STAT6 dependent
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
Park et al., Biochem Biophys Res Commun 2004 (MAP Kinase Signaling System) : Taken together, these results demonstrate that naturally occurring furosin has an inhibitory activity on both osteoclast differentiation and function through mechanisms involving inhibition of the RANKL induced p38MAPK and JNK/AP-1 activation as well as actin ring formation
Kobayashi et al., J Biol Chem 2005 : RANKL induced degradation of I kappa B alpha and phosphorylation of p38 MAPK and c-Jun N-terminal kinase in RAW264.7 cells were up-regulated by PGE2 in a cAMP dependent protein kinase A (PKA) dependent manner, suggesting that EP2 and EP4 signals cross-talk with RANK signals
Takami et al., FEBS Lett 2005 : Induction of TRANCE expression by IBMX was partially suppressed by the inhibitors of protein kinase A (PKA), ERK, and p38 MAPK, suggesting that activation of ERK and p38 MAPK , as well as PKA, is involved in TRANCE expression by IBMX
Lee et al., Arthritis Rheum 2006 (Arthritis, Rheumatoid) : However, specific inhibitors of MAPK/ERK-1/2 and p38 MAPK partially blocked the induction of RANKL expression and osteoclastogenesis
Itoh et al., J Periodontal Res 2006 : Our results indicate that EMD induces the formation of osteoclasts through interaction with RANKL , while ERK and p38 MAPK may play a critical role in the enhancement of osteoclast formation in RAW 264.7 cells
Rossa et al., J Interferon Cytokine Res 2006 (MAP Kinase Signaling System) : MKK3/6-p38 MAPK signaling is required for IL-1beta and TNF-alpha induced RANKL expression in bone marrow stromal cells
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
Oikawa et al., J Periodontal Res 2007 : In addition, extracellular signal regulated kinase, p38 MAPK , and c-Jun N-terminal kinase signals may co-operatively mediate interleukin-1beta stimulated RANKL expression and its activity in those cells
Cheng et al., J Cell Biochem 2011 : Previous studies have shown that IL-4 selectively blocks RANKL induced activation of NF-?B and mitogen activated protein kinase ( MAPK ) pathway molecules, suggesting that the cytokine arrests osteoclastogenesis by blockade of these signaling cascades
Kim et al., Arthritis Rheum 2012 (Arthritis, Rheumatoid) : IL-22 induced RANKL expression was down-regulated significantly by the inhibition of p38 MAPK/NF-?B or JAK-2/STAT-3 signaling
Moon et al., Phytother Res 2012 : The SSE thereafter suppressed RANKL induced p38 mitogen activated protein kinase and I?Ba kinase signalling activities which were activated by ROS generation for osteoclastogenesis
Kim et al., Exp Cell Res 2013 : While ApoE did not affect the activation of ERK, JNK, and p38 MAPK signaling pathways by RANKL , the phosphorylation of p65 trans-activation domain on serine 536 and transcription activity of NF-?B were reduced by ApoE overexpression
Sung et al., PloS one 2013 : Furthermore, cardamonin also downregulated RANKL induced phosphorylation of MAPK including ERK and p38 MAPK