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JUN — TNFSF11

Text-mined interactions from Literome

Huber et al., Endocrinology 2001 : In RAW264.7 cells, androgens appear to block RANKL induced osteoclast formation through selective regulation of c-JUN : Accordingly, 5 alpha-dihydrotestosterone suppressed RANKL induced c-Jun N-terminal kinase activation and reduced c-Jun expression levels ... These effects resulted in a reduction in RANKL induced activator protein-1 DNA binding activity and a corresponding suppression in activator protein-1 mediated transcriptional activation
David et al., J Cell Sci 2002 : Moreover, JNK1 dependent c-Jun phosphorylation in response to RANKL is not involved in the anti-apoptotic function of JNK1
Wang et al., J Bone Miner Res 2003 : Assays for NF-kappaB nuclear translocation, NF-kappaB reporter gene activity, protein kinase activity, and Western blotting were used to examine the effects of TPA on RANKL induced NF-kappaB, c-Jun N-terminal kinase (JNK) , and MEK/ERK and p38 signal transduction pathways
Wattel et al., J Cell Biochem 2004 : Analysis of protein-DNA interaction by electrophoretic mobility shift assay ( EMSA ) performed on RAW cells showed that a pre-treatment with quercetin inhibited RANKL induced nuclear factor kB ( NF kappa B ) and activator protein 1 (AP-1) activation
Ikeda et al., J Clin Invest 2004 : We investigated the role of the transcription factor c-Jun , which is activated by RANKL , in osteoclastogenesis using transgenic mice expressing dominant negative c-Jun specifically in the osteoclast lineage
Takada et al., Blood 2004 : Deletion of both TNF receptors also potentiated RANKL induced c-Jun N-terminal kinase (JNK) , extracellular signal regulated kinase 1 and 2 ( ERK1/2 ), and p38 mitogen activated protein kinase ( MAPK ) activations in a dose- and time dependent manner
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
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
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
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
Xu et al., Antioxid Redox Signal 2010 : Concurrently, PAMM expression completely abolished RANKL induced p100 NF-kappaB and c-Jun activation, as well as osteoclast formation
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
Wei et al., Mol Cell Biol 2011 (Osteopetrosis) : Mechanistically, ß-catenin activation increases GATA2/Evi1 expression but abolishes RANKL induced c-Jun phosphorylation
He et al., Purinergic signalling 2012 : DPCPX also inhibited RANKL induced activation of NF-?B and JNK/c-Jun but had little effect on other mitogen activated protein kinases ( p38 and Erk )
Mun et al., J Bone Miner Res 2013 : MIF treatment of WT cultures suppressed RANKL induced activator protein 1 (AP-1) expression, which resulted in decreased osteoclast differentiation in vitro
Nepal et al., Eur J Pharmacol 2013 : Hispidulin was found to inhibit RANKL induced activation of Jun N-terminal kinase (JNK) and p38, in addition to NF-?B in vitro experiment
Wong et al., J Biol Chem 1997 : A recombinant soluble form of TRANCE composed of the entire ectodomain induced c-Jun N-terminal kinase (JNK) activation in T cells but not in splenic B cells or in bone marrow derived dendritic cells
Wong et al., J Exp Med 1997 : TRANCE ( tumor necrosis factor [TNF ] -related activation induced cytokine ) is a new member of the TNF family that is induced upon T cell receptor engagement and activates c-Jun N-terminal kinase (JNK) after interaction with its putative receptor ( TRANCE-R )