RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-β

By Hiroshi Takayanagi, Sunhwa Kim, K. Matsuo, H. Suzuki, Tomohiko Suzuki, Kojiro Sato, T. Yokochi, H. Oda, Kozo Nakamura, N. Ida and 2 more. Nature, 2002

761 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/54302413798b6b73cdd733c8483b5239734bc79a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. H. Yanai
2. A. Takaoka
3. Hiroshi Takayanagi
4. L. Ivashkiv
5. Tadatsugu Taniguchi
6. Xu Feng
7. J. McDonald
8. Xiaoyu Hu

In Molecular Biology

1. Hiroshi Takayanagi
2. T. Suda
3. Xu Feng
4. J. McDonald
5. K. Matsuo
6. D. Lacey
7. N. Irie
8. W. J. Boyle

In Oncology

1. Hiroshi Takayanagi
2. A. Takaoka
3. H. Yanai
4. L. Ivashkiv
5. T. Suda
6. Tadatsugu Taniguchi
7. Xu Feng
8. J. McDonald

Citations in the corpus

• Bidirectional ephrinB2-EphB4 signaling controls bone homeostasis. (2006, background): “In addition, c-Fos activates transcription of Ifnb (encoding IFN-b), which mediates a negative feedback loop that suppresses osteoclast differentiation (Takayanagi et al., 2002b).”
• Cross-regulation of Signaling and Immune Responses by IFN-γ and STAT1 (2009, background): “However, instead of targeting TRAF6, IFN-b inhibits translation of c-Fos, an AP-1 family transcription factor essential for the induction of NFATc1, the master regulator of osteoclastogenesis (Takayanagi et al., 2002).”
• Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems (2007, background): “Similar to TLRs, RANKL induces the IFNB gene in osteoclast precursor cells, and IFNβ functions as a negative-feedback regulator that inhibits the differentiation of osteoclasts by interfering with the RANKL-induced expression of cFO”
• Genetic regulation of osteoclast development and function (2003, neutral): “The IFNβ signalling pathway also affects osteoclastogenesi”
• The molecular triad OPG/RANK/RANKL: involvement in the orchestration of pathophysiological bone remodeling. (2004, background): “RANKL also induced the expression of suppressors of cytokine signaling SOCS1 and SOCS3 that inhibits IFN signaling [126].”
• Osteoclast differentiation and activation (2003, background): “Induction of osteoclastogenesis by RANKL leads to the induction of interferon-β, which is secreted and acts in an autocrine fashion to downregulate the expression of c-Fos, a critical factor involved in osteoclast developmen”
• Disorders of bone remodeling. (2011, background): “RANK contains three functional TRAF-binding motifs (PFQEP369−373, PVQEET560−565, and PVQEQG604−609) that collectively activate six major signaling pathways [NF-κB; c-jun N-terminal kinase ( JNK); extracellular signal– related kinase (ERK); p38; nuclear factor of activated T cells, cytoplasmic 1 (NFA”
• Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis (2004, methodology): “Histological, histomorphometric and microradiographic examinations were performed using essentially the same method as described previousl”
• Interferons, interferon‐like cytokines, and their receptors (2004, background): “involved in the modulation of bone metabolism (88).”
• Interferon signalling network in innate defence (2006, background): “We also reported that the IFN-β gene is induced in bone marrow macrophages upon stimulation by the RANK ligand (receptor activator of NF-κB ligand), a negative regulator of osteoclast differentiation, and that this induction is not dependent on IRF-3 or IRF-7, but on RANKLinduced c-Fos, one of the e”