RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-β (Q57675150)

11

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author name string

Hiroshi Takayanagi

1

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Sunhwa Kim

2

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Hiroshi Suzuki

4

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Tomohiko Suzuki

5

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Kojiro Sato

6

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Taeko Yokochi

7

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Hiromi Oda

8

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Kozo Nakamura

9

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Nobutaka Ida

10

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Tadatsugu Taniguchi

Therapeutic approaches to bone diseases

12

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language of work or name

English

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publication date

April 2002

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published in

Nature

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volume

416

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issue

6882

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page(s)

744-749

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cites work

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Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL

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OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis

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Involvement of receptor activator of nuclear factor kappaB ligand/osteoclast differentiation factor in osteoclastogenesis from synoviocytes in rheumatoid arthritis

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T-cell-mediated regulation of osteoclastogenesis by signalling cross-talk between RANKL and IFN-γ

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Fosl1 is a transcriptional target of c-Fos during osteoclast differentiation

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Targeted disruption of the Stat1 gene in mice reveals unexpected physiologic specificity in the JAK-STAT signaling pathway

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CD8(+) T cell-mediated skin disease in mice lacking IRF-2, the transcriptional attenuator of interferon-alpha/beta signaling

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