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FOS — TNFSF11

Text-mined interactions from Literome

Matsuo et al., Nat Genet 2000 : The osteoclast differentiation factor Rankl ( also known as TRANCE, ODF and OPGL ; refs 8-11 ) induces transcription of Fosl1 in a c-Fos dependent manner, thereby establishing a link between Rank signalling and the expression of Ap-1 proteins in osteoclast differentiation
Takayanagi et al., Nature 2002 (Bone Diseases, Metabolic) : Here we show that RANKL induces the interferon-beta (IFN-beta) gene in osteoclast precursor cells, and that IFN-beta inhibits the differentiation by interfering with the RANKL induced expression of c-Fos , an essential transcription factor for the formation of osteoclasts ... Thus an autoregulatory mechanism operates-the RANKL induced c-Fos induces its own inhibitor
Takayanagi et al., Arthritis Res 2002 (Arthritis...) : Second, RANKL induces the IFN-beta gene but not IFN-alpha genes, in osteoclast precursor cells, and that IFN-beta strongly inhibits the osteoclast differentiation by interfering with the RANKL induced expression of c-Fos
Lean et al., Biochem Biophys Res Commun 2004 (Bone Resorption) : We found that AP-1 , NFkappaB, and NFAT-reporter gene expression was enhanced more greatly by RANKL in RAW cells transfected with the Trx-expression construct
Kamel Mohamed et al., Biochem Biophys Res Commun 2005 : Interleukin-4 inhibits RANKL induced expression of NFATc1 and c-Fos : a possible mechanism for downregulation of osteoclastogenesis ... In addition, IL-4 inhibited the RANKL induced expression of NFATc1 and c-Fos in murine bone marrow cells
Takayanagi et al., J Mol Med (Berl) 2005 : RANKL activates TRAF6, c-Fos , and calcium signaling pathways, all of which are indispensable for the induction and activation of nuclear factor of activated T cells ( NFAT) c1, the master transcription factor for osteoclastogenesis
Yip et al., J Bone Miner Res 2005 (Calcium Signaling) : In this study, we showed a biphasic effect of TG on osteoclast formation and apoptosis through the regulation of ROS production, caspase-3 activity, cytosolic Ca2+, and RANKL induced activation of NF-kappaB and AP-1 activities ... At these lower concentrations, TG potentiated ROS production and RANKL induced NF-kappaB activity, but suppressed RANKL induced AP-1 activity and had little effect on ERK phosphorylation
Fujimura et al., Infect Immun 2006 : HbR inhibited RANKL mediated induction of c-Fos and NFATc1
Kwak et al., Exp Mol Med 2006 : Tanshinone IIA suppressed the expression levels of c-Fos and NFATc1 induced by RANKL
Yamashita et al., J Biol Chem 2007 : We report that RANKL and TNF can induce osteoclast formation directly from NF-kappaB p50/p52 double knockout ( dKO ) osteoclast precursors when either c-Fos or NFATc1 is expressed ... c-Fos expression requires concomitant RANKL or TNF treatment to induce NFATc1 activation in the dKO cells
Mohamed et al., Bone 2007 : IL-10 potently reduced the RANKL induced expression of NFATc1, c-Jun and c-Fos , which are known to be essential for osteoclastogenesis, in time- and dose dependent manners
Park et al., Int Immunopharmacol 2007 (Bone Resorption) : SKE suppressed the induction of c-Fos and NFATc1 by RANKL
Ha et al., J Immunol 2008 : Flagellin suppressed RANKL induction of c-Fos protein expression in bone marrow derived macrophages without affecting c-Fos mRNA expression
Park et al., Biochem Pharmacol 2008 (Bone Resorption) : The induction of c-Fos and NFATc1, key transcription factors for osteoclastogenesis, by RANKL was also suppressed by bavachalcone
Yamanaka et al., J Orthop Res 2008 (MAP Kinase Signaling System...) : We have previously determined that RANKL is an essential cytokine mediator of particle induced osteoclastogenesis, and that PMMA particles activate JNK and c-jun/AP-1 in bone marrow macrophages ( osteoclast precursors )
Chen et al., J Biol Chem 2008 : The lack of PLCgamma2 markedly diminished RANKL induced activation of NF-kappaB, AP-1 , and NFATc1
Lee et al., J Biol Chem 2009 : We found that Trolox down-regulated the induction by RANKL of c-Fos protein by suppressing its translation
Kim et al., Eur J Pharmacol 2009 (Bone Neoplasms...) : Trichostatin A inhibits osteoclastogenesis and bone resorption by suppressing the induction of c-Fos by RANKL ... This effect was accompanied by a significant decrease in the RANKL stimulated induction of c-Fos and NFATc1, which are key transcription factors during early osteoclastogenesis
Kwak et al., Bone 2010 (Bone Resorption) : Inhibition of osteoclast differentiation and bone resorption by rotenone, through down-regulation of RANKL induced c-Fos and NFATc1 expression ... Further, RANKL induced c-Fos and NFATc1 protein expression was suppressed by rotenone
Hasegawa et al., Biol Pharm Bull 2010 (Bone Resorption) : The RANKL induced expressions of c-Fos and nuclear factor of activated T cells-c1 ( NFATc1 ), which are crucial transcriptional factors for osteoclastogenesis, were also reduced by treatment with honokiol
Sugatani et al., Blood 2011 : In addition, RANKL induced c-Fos up-regulates miR-21 gene expression
Kim et al., Arthritis Res Ther 2011 (Arthritis, Rheumatoid...) : Blocking of PI3 kinase, p38 MAP kinase, JAK-2, NF-?B, and AP-1 also led to a marked reduction in RANKL expression and osteoclastogenesis
Bishop et al., J Biol Chem 2011 (Calcium Signaling) : Mouse Rankl expression is regulated in T cells by c-Fos through a cluster of distal regulatory enhancers designated the T cell control region
Cheng et al., Food Chem Toxicol 2012 (MAP Kinase Signaling System) : Pretreatment with ginsenoside Rb1 significantly inhibited RANKL induced the gene expression of c-Fos and nuclear factor of activated T-cells c1 ( NFATc1 ), which are two essential and crucial transcription factors for osteoclast formation ... Taken together, our data suggest that ginsenoside Rb1 is one of the effective components of GSS for the anti-osteoporosis activity and can inhibit osteoclastogenesis by suppressing RANKL induced activation of both JNK and p38 MAPKs and NF-?B pathways, and consequently down regulating the gene expression of c-Fos and NFATc1 in osteoclast precursors
Kim et al., Eur J Pharmacol 2012 (Bone Resorption) : MS-275 inhibited RANKL mediated osteoclast differentiation from its precursors by suppressing RANKL induced expression of c-Fos , a crucial transcription factor for osteoclastogenesis
Kim et al., Exp Cell Res 2013 : These findings suggest that ApoE plays an inhibitory role in osteoclast differentiation via the suppression of RANKL dependent activation of NF-?B and induction of c-Fos and NFATc1
Kim et al., J Immunol 2013 (Bone Resorption...) : LC8 inhibited RANKL induced phosphorylation and subsequent degradation of I?Ba, the expression of c-Fos , and the consequent activation of NFATc1, which is a pivotal determinant of osteoclastogenesis
Im et al., Biol Pharm Bull 2013 : Mechanistically, DMF inhibited RANKL induced expression of nuclear factor of activatied T-cells, cytoplasmic, calcineurin dependent 1 ( NFATc1 ) and c-Fos via inhibition of mitogen activated protein kinases ( MAPKs ) pathway
Zheng et al., Biol Pharm Bull 2013 : In experiments to elucidate its mechanism of action, CPC was found to suppress RANKL induced expression of c-Fos and nuclear factor of activated T cells ( NFATc1 ), transcription factors that are essential for osteoclast differentiation
Kong et al., PloS one 2013 (Osteolysis) : Moreover, RANKL induced c-Fos and NFATc1 protein expression was suppressed by PQQ
Ha et al., J Mol Med (Berl) 2013 (Bone Resorption) : An MSK1 inhibitor efficiently prevented the induction of c-Fos and NFATc1 and CREB phosphorylation by RANKL