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Regulation of NFATc1 in Osteoclast Differentiation
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PubMed
review article
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Europe PubMed Central
title
Regulation of NFATc1 in Osteoclast Differentiation
(English)
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author name string
Jung Ha Kim
series ordinal
1
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Crossref
Nacksung Kim
series ordinal
2
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language of work or name
English
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PubMed
publication date
November 2014
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PubMed
published in
Journal of bone metabolism : JBM
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PubMed
volume
21
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PubMed
issue
4
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PubMed
page(s)
233-41
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PubMed
copyright license
Creative Commons Attribution-NonCommercial 3.0 Unported
start time
1 January 2014
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April 2022 Public Data File from Crossref
copyright status
copyrighted
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RANK is essential for osteoclast and lymph node development
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Nuclear factor of activated T cells c1 induces osteoclast-associated receptor gene expression during tumor necrosis factor-related activation-induced cytokine-mediated osteoclastogenesis
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OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis
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Signaling to NF-kappaB
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Osteoclast differentiation and activation
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Transcriptional regulation by calcium, calcineurin, and NFAT
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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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Lhx2 regulates bone remodeling in mice by modulating RANKL signaling in osteoclasts
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Inactivation of glycogen synthase kinase-3β is required for osteoclast differentiation
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RANKL induces NFATc1 acetylation and stability via histone acetyltransferases during osteoclast differentiation
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The Blimp1-Bcl6 axis is critical to regulate osteoclast differentiation and bone homeostasis.
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Negative feedback control of osteoclast formation through ubiquitin-mediated down-regulation of NFATc1.
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Interferon regulatory factor-8 regulates bone metabolism by suppressing osteoclastogenesis
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NFATc1 in mice represses osteoprotegerin during osteoclastogenesis and dissociates systemic osteopenia from inflammation in cherubism
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The role of NFAT in osteoclast formation
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28 September 2017
PLCgamma2 regulates osteoclastogenesis via its interaction with ITAM proteins and GAB2.
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Id helix-loop-helix proteins negatively regulate TRANCE-mediated osteoclast differentiation
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NFAT and Osterix cooperatively regulate bone formation
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I{kappa}B kinase (IKK){beta}, but not IKK{alpha}, is a critical mediator of osteoclast survival and is required for inflammation-induced bone loss
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A conserved docking motif for CK1 binding controls the nuclear localization of NFAT1.
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The immunomodulatory adapter proteins DAP12 and Fc receptor gamma-chain (FcRgamma) regulate development of functional osteoclasts through the Syk tyrosine kinase
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28 September 2017
Nuclear factor of activated T-cells (NFAT) rescues osteoclastogenesis in precursors lacking c-Fos
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28 September 2017
The IkappaB function of NF-kappaB2 p100 controls stimulated osteoclastogenesis
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The transcription factor NF-ATc1 regulates lymphocyte proliferation and Th2 cytokine production
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Requirement for NF-kappaB in osteoclast and B-cell development
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28 November 2018
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28 November 2018
Protein inhibitor of activated STAT 3 modulates osteoclastogenesis by down-regulation of NFATc1 and osteoclast-associated receptor
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Inhibition of RANKL-induced osteoclastogenesis by (-)-DHMEQ, a novel NF-kappaB inhibitor, through downregulation of NFATc1.
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Identifiers
DOI
10.11005/JBM.2014.21.4.233
1 reference
stated in
Consolidated OpenCitations Corpus – April 2017
OpenCitations bibliographic resource ID
3060709
OpenCitations bibliographic resource ID
3060709
1 reference
stated in
Consolidated OpenCitations Corpus – April 2017
OpenCitations bibliographic resource ID
3060709
PMC publication ID
4255043
1 reference
stated in
Consolidated OpenCitations Corpus – April 2017
OpenCitations bibliographic resource ID
3060709
PubMed publication ID
25489571
1 reference
stated in
Consolidated OpenCitations Corpus – April 2017
OpenCitations bibliographic resource ID
3060709
ResearchGate publication ID
269721624
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