Gene interactions and pathways from curated databases and text-mining

◀ Back to TNF

TNF — TNFSF11

Text-mined interactions from Literome

Zou et al., J Cell Biochem 2001 : RANKL increased the level of TNF-alpha mRNA and induced TNF-alpha release from osteoclast progenitors
Romas et al., Bone 2002 (Arthritis, Rheumatoid) : In the presence of permissive levels of RANKL , TNF-alpha acts directly to stimulate osteoclast differentiation of macrophages and myeloid progenitor cells
Zou et al., J Biol Chem 2003 : In the co-cultures CpG ODN induces RANKL expression in osteoblasts as a result of the more efficient TNF-alpha induction
O' Gradaigh et al., Ann Rheum Dis 2004 (Arthritis, Rheumatoid...) : In animal studies, TNF potently increases osteoclast formation in the presence of RANKL ... TNFalpha potently increased osteoclast proliferation/differentiation in the presence of RANKL
Takada et al., Blood 2004 : We also found that tumor necrosis factor (TNF) receptor associated factor 6 ( TRAF6 ), which mediates RANKL signaling, was constitutively bound to RANK in TNF receptor deleted cells but not in wild-type cells, and this binding was enhanced by RANKL
Abu-Amer et al., J Cell Biochem 2004 : Thus, we reasoned that TNF/TNFr1 may regulate RANKL and possibly RANK expression by stromal cells and osteoclast precursors ( OCPs ), respectively
Dai et al., Ann Rheum Dis 2004 (Arthritis, Rheumatoid...) : In PHA prestimulated T cells or RA synovial T cells, IL18, IL1 beta, or TNFalpha increased soluble RANKL production and membrane bound RANKL expression in a dose dependent manner
Wei et al., J Clin Invest 2005 (MAP Kinase Signaling System...) : These data suggest that TNF regulates RANKL expression via IL-1, and, therefore, IL-1 plays a role in TNF induced periarticular osteolysis
Shaarawy et al., J Soc Gynecol Investig 2005 (Bone Resorption...) : The increased osteoclastic activity in preeclampsia may be attributed to increased RANKL induced by increased interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) , and transforming growth factor beta2 ( TGF-beta2 ) production
Wu et al., Arthritis Rheum 2005 (Arthritis, Rheumatoid...) : TNFalpha , produced by both BXD2 MSFs and BXD2 mouse macrophages, had a strong stimulatory effect on RANKL expression
Liu et al., Eur J Oral Sci 2005 : Tumor necrosis factor-alpha enhances RANKL gene expression in vitro and it may be responsible for up-regulating RANKL in vivo
Park et al., Exp Mol Med 2005 : In addition, RANKL increased the expression of TNFalpha , MCP-1, and IL-6 but not of IL-10, IL-12, IFN-gamma, and iNOS
Amcheslavsky et al., J Cell Physiol 2006 : Since both RANKL-RANK and CpG-ODN-TLR9 interactions result in NF-kappaB activation, p38 and ERK phosphorylation, and TNF-alpha synthesis ( all implicated in osteoclastogenesis ), we hypothesized that CpG-ODN ( but not RANKL ) in addition induces the synthesis of an anti-osteoclastogenic factor
Rahman et al., J Lipid Res 2006 (Bone Resorption) : RANKL induced osteoclastogenesis in these monocytic cells, and CLA inhibited RANKL induced tumor necrosis factor-alpha production and osteoclast differentiation, including osteoclast-specific genes such as tartrate-resistant acid phosphatase, cathepsin K, calcitonin receptor, and matrix metalloproteinase-9 expression and osteoclast-specific transcription factors such as c-Fos, nuclear factor of activated T-cells expression, and bone resorption pit formation
Yongchaitrakul et al., J Periodontol 2006 : HPDL cells are capable of secreting M-CSF and expressing RANKL in response to TNF-alpha
Koreny et al., Arthritis Rheum 2006 (Bone Resorption...) : In addition, interface membrane fibroblasts expressed RANKL and osteoprotegerin in response to stimulation with conditioned media, TNFalpha , or IL-1beta
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 ... Here, we report that IL-1beta and TNF-alpha induced RANKL requires p38 mitogen activating protein kinase ( MAPK ) pathway activation for maximal expression ... Real-time PCR was used to assess the p38 contribution toward IL-1beta and TNF-alpha induced RANKL mRNA expression ... Results from these studies indicate that p38 MAPK is a major signaling pathway involved in IL-1beta and TNF-alpha induced RANKL expression in bone marrow stromal cells
Nakao et al., Biochem Biophys Res Commun 2007 : RANKL stimulated TNFalpha production in osteoclast precursor cells promotes osteoclastogenesis by modulating RANK signaling pathways ... Furthermore, TNFalpha production in pOCs was stimulated by RANKL ... These results indicate that TNFalpha is induced by RANKL in pOCs and serves as an autocrine factor promoting osteoclastogenesis through c-Fos and NFATc1 activation
An et al., Yonsei Med J 2007 : In contrast, tumor necrosis factor-alpha (TNF-alpha) increased the expression of both OPG and RANKL in a time dependent manner
Bu et al., Calcif Tissue Int 2008 : NO and tumor necrosis factor (TNF)-alpha were also suppressed in the presence of RANKL during osteoclastogenesis by the polyphenols
Hashizume et al., Rheumatology (Oxford) 2008 (Arthritis, Rheumatoid) : IL-6 trans signalling directly induces RANKL on fibroblast-like synovial cells and is involved in RANKL induction by TNF-alpha and IL-17 ... On the other hand, TNF-alpha and IL-17 did not induce RANKL expression, although TNF-alpha, IL-17 or IL-1beta stimulated cell growth and IL-6 production ... However, in the presence of sIL-6R, TNF-alpha or IL-17 induced RANKL expression ... IL-6/sIL-6R directly induced RANKL expression in RA-FLS and it is essential for RANKL induction by TNF-alpha and IL-17
Frodge et al., J Periodontol 2008 (Alveolar Bone Loss...) : Salivary levels of TNF-alpha were detected in all subjects, whereas levels of ICTP and RANKL were detected in only a minority of subjects
Yun et al., Rheumatol Int 2009 (Arthritis, Rheumatoid) : AM affected IL-1-, TNF-alpha induced RANKL and OPG expression in RASFs
Wu et al., Int Immunopharmacol 2009 : The results showed that EM inhibited TNF-alpha induced expressions of RANKL and NF-kappaB at both mRNA and protein levels in a concentration dependent manner
Kwan Tat et al., Rheumatology (Oxford) 2009 (Osteoarthritis, Knee) : OPG and membranous RANKL levels were significantly enhanced by IL-1beta, TNF-alpha and PGE ( 2 ), whereas membranous RANK was significantly increased only with IL-1beta
Ishizuka et al., J Bone Miner Res 2011 (Bone Resorption) : In contrast, ADAM8 KO mice did not display a bone phenotype in vivo, but unlike WT littermates, they did not increase RANKL production, OCL formation, or calvarial fibrosis in response to tumor necrosis factor a (TNF-a) in vivo
Goto et al., Cytokine 2011 : The purpose of this study was to evaluate the effect of Tumor necrosis factor-alpha ( TNF-a ) on RANKL expression in bone marrow adipocytes, and osteoclast differentiation supported by human bone marrow adipocytes ... TNF-a increased RANKL expression in primary human bone marrow adipocytes
Fujii et al., Bone 2012 : IL-4 also inhibited TNF-a induced RANKL expression in the presence of TNF-a-responsive stromal cells in vivo
Zheng et al., Biochem Pharmacol 2013 (Bone Resorption) : Coumermycin A1 also abrogated RANKL induced expression of interleukin-1ß, tumor necrosis factor-a , and inducible nitric oxide synthase in mouse BMMs. Consistent with the in vitro anti-osteoclastogenic effect, the aminocoumarin suppressed lipopolysaccharide induced osteoclast formation and bone loss in in vivo mouse experiments