NF-κB p50 and p52 Regulate Receptor Activator of NF-κB Ligand (RANKL) and Tumor Necrosis Factor-induced Osteoclast Precursor Differentiation by Activating c-Fos and NFATc1 (Q57675122)

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scientific article published in Journal of Biological Chemistry

Language	Label	Description	Also known as
English	NF-κB p50 and p52 Regulate Receptor Activator of NF-κB Ligand (RANKL) and Tumor Necrosis Factor-induced Osteoclast Precursor Differentiation by Activating c-Fos and NFATc1	scientific article published in Journal of Biological Chemistry

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scholarly article

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NF-κB p50 and p52 Regulate Receptor Activator of NF-κB Ligand (RANKL) and Tumor Necrosis Factor-induced Osteoclast Precursor Differentiation by Activating c-Fos and NFATc1 (English)

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1 reference

based on heuristic

inferred from title

object named as

Koichi Matsuo

10

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Erwin F. Wagner

object named as

Erwin F. Wagner

8

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author name string

Teruhito Yamashita

1

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Zhenqiang Yao

2

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Fang Li

3

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Qian Zhang

4

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I. Raul Badell

5

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Edward M. Schwarz

6

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Sunao Takeshita

7

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Masaki Noda

9

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Lianping Xing

11

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Brendan F. Boyce

12

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language of work or name

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publication date

7 May 2007

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Journal of Biological Chemistry

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282

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25

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18245-18253

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Osteoclast differentiation and activation

1 reference

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Osteoclasts, integrins, and osteoporosis.

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Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation

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RANK is essential for osteoclast and lymph node development

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Osteoprotegerin: a novel secreted protein involved in the regulation of bone density

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TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal kinase in T cells

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Osteoprotegerin ligand: a common link between osteoclastogenesis, lymph node formation and lymphocyte development.

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Inflammatory Mediators as Essential Elements in Bone Remodeling

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The molecular mechanism of osteoclastogenesis in rheumatoid arthritis

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Transcriptional program of mouse osteoclast differentiation governed by the macrophage colony-stimulating factor and the ligand for the receptor activator of NFkappa B.

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Tumor necrosis factor alpha stimulates osteoclast differentiation by a mechanism independent of the ODF/RANKL-RANK interaction

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

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M-CSF mediates TNF-induced inflammatory osteolysis

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IL-1 alpha stimulates the formation of osteoclast-like cells by increasing M-CSF and PGE2 production and decreasing OPG production by osteoblasts

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Tumor necrosis factor-alpha increases circulating osteoclast precursor numbers by promoting their proliferation and differentiation in the bone marrow through up-regulation of c-Fms expression.

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Tumor necrosis factor-alpha (TNF) stimulates RANKL-induced osteoclastogenesis via coupling of TNF type 1 receptor and RANK signaling pathways

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Roles for NF-kappaB and c-Fos in osteoclasts

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

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Tumor necrosis factor-alpha activation of nuclear transcription factor-kappaB in marrow macrophages is mediated by c-Src tyrosine phosphorylation of Ikappa Balpha.

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Interleukin-1 alpha activates an NF-kappaB-like factor in osteoclast-like cells

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Induction and activation of the transcription factor NFATc1 (NFAT2) integrate RANKL signaling in terminal differentiation of osteoclasts

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Requirement for NF-kappaB in osteoclast and B-cell development

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Osteopetrosis in mice lacking NF-kappaB1 and NF-kappaB2.

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Reciprocal role of ERK and NF-kappaB pathways in survival and activation of osteoclasts

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Nuclear factor of activated T-cells (NFAT) rescues osteoclastogenesis in precursors lacking c-Fos

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NFAT signaling: choreographing the social lives of cells

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Transcription factors of the NFAT family: regulation and function

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NFAT proteins: key regulators of T-cell development and function

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Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis

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Large scale gene expression analysis of osteoclastogenesis in vitro and elucidation of NFAT2 as a key regulator

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The calcineurin/nuclear factor of activated T cells signaling pathway regulates osteoclastogenesis in RAW264.7 cells

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NF-kappaB p50 and p52 expression is not required for RANK-expressing osteoclast progenitor formation but is essential for RANK- and cytokine-mediated osteoclastogenesis

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A RANK/TRAF6-dependent signal transduction pathway is essential for osteoclast cytoskeletal organization and resorptive function

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Osteoclast differentiation independent of the TRANCE-RANK-TRAF6 axis

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RANK-L induces the expression of NFATc1, but not of NFkappaB subunits during osteoclast formation

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Autoamplification of NFATc1 expression determines its essential role in bone homeostasis

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Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems

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The molecular understanding of osteoclast differentiation

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Systemic tumor necrosis factor alpha mediates an increase in peripheral CD11bhigh osteoclast precursors in tumor necrosis factor alpha-transgenic mice

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NF-kappaB specifically activates BMP-2 gene expression in growth plate chondrocytes in vivo and in a chondrocyte cell line in vitro

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c-Fos suppresses systemic inflammatory response to endotoxin

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Receptor activator of NF-kappaB ligand (RANKL) activates TAK1 mitogen-activated protein kinase kinase kinase through a signaling complex containing RANK, TAB2, and TRAF6

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Identifiers

10.1074/JBC.M610701200

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