Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone (Q28267634)

2

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Melda Onal

3

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Josh Campbell

4

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Joseph J Goellner

5

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Vladimir Dusevich

6

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Lynda Bonewald

7

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Stavros C Manolagas

8

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Charles A O'Brien

Creative Commons CC0 License

9

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language of work or name

English

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publication date

2015

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published in

PLOS One

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volume

10

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issue

9

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page(s)

e0138189

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copyright license

start time

22 September 2015

1 reference

April 2022 Public Data File from Crossref

copyright status

copyrighted, dedicated to the public domain by copyright holder

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cites work

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Evidence for osteocyte regulation of bone homeostasis through RANKL expression

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Matrix-embedded cells control osteoclast formation

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Central control of fever and female body temperature by RANKL/RANK

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Control of RANKL gene expression

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Sclerostin is an osteocyte-expressed negative regulator of bone formation, but not a classical BMP antagonist

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The osteoclast differentiation factor osteoprotegerin-ligand is essential for mammary gland development

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Birth and Death of Bone Cells: Basic Regulatory Mechanisms and Implications for the Pathogenesis and Treatment of Osteoporosis 1

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Generalized lacZ expression with the ROSA26 Cre reporter strain

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Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation

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

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RANKL Is Necessary and Sufficient to Initiate Development of Antigen-Sampling M Cells in the Intestinal Epithelium

20 March 2017

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A highly efficient Escherichia coli-based chromosome engineering system adapted for recombinogenic targeting and subcloning of BAC DNA

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Activated T cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand

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Transcriptional regulation of the human TNFSF11 gene in T cells via a cell type-selective set of distal enhancers

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Osteocyte-derived RANKL is a critical mediator of the increased bone resorption caused by dietary calcium deficiency

29 September 2017

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Progesterone receptor and Stat5 signaling cross talk through RANKL in mammary epithelial cells

29 September 2017

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Physiological functions of osteoblast lineage and T cell-derived RANKL in bone homeostasis

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Receptor activator of nuclear factor κB ligand (RANKL) protein expression by B lymphocytes contributes to ovariectomy-induced bone loss

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Osteocyte network; a negative regulatory system for bone mass augmented by the induction of Rankl in osteoblasts and Sost in osteocytes at unloading

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Cell autonomous requirement of connexin 43 for osteocyte survival: consequences for endocortical resorption and periosteal bone formation.

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Genome-scale techniques highlight the epigenome and redefine fundamental principles of gene regulation

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Mouse Rankl expression is regulated in T cells by c-Fos through a cluster of distal regulatory enhancers designated the T cell control region

29 September 2017

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A physical mechanism for coupling bone resorption and formation in adult human bone.

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Murine and chicken chondrocytes regulate osteoclastogenesis by producing RANKL in response to BMP2

29 September 2017

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Activation of receptor activator of NF-kappaB ligand gene expression by 1,25-dihydroxyvitamin D3 is mediated through multiple long-range enhancers

29 September 2017

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29 September 2017

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Crossref

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0138189

Kidney development and gene expression in the HIF2alpha knockout mouse.

21 January 2018

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Crossref

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0138189

Wnt5a-Ror2 signaling between osteoblast-lineage cells and osteoclast precursors enhances osteoclastogenesis.

21 January 2018

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Crossref

https://api.crossref.org/works/10.1371%2FJOURNAL.PONE.0138189

10.1371/JOURNAL.PONE.0138189

21 January 2018

Identifiers

DOI

1 reference

ADS bibcode

2015PLoSO..1038189X

0 references

1 reference

1 reference

PubMed publication ID

26393791

1 reference