Evidence map›Paper›PMID 17881498›Full record

ArticleJournal of cell science2007

Specificity of RGS10A as a key component in the RANKL signaling mechanism for osteoclast differentiation.

Shuying Yang, Wei Chen, Philip Stashenko, Yi-Ping Li

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  5. Review
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  8. Article
  9. Review
  10. Article
  11. Role of Regulators of G Protein Signaling Proteins in Bone Physiology and Pathophysiology.Progress in molecular biology and translational science · 2015
    Review
  12. Article
  13. Review
  14. Article
  15. Role of regulator of G protein signaling proteins in bone.Frontiers in bioscience (Landmark edition) · 2014
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Shuying YangDepartment of Cytokine Biology, The Forsyth Institute, Boston, MA 02115, USA.
Wei Chen
Philip Stashenko
Yi-Ping Li

Funding

TRANSCRIPTION FACTORS CONTROL OSTEOCLAST DIFFERENTIATIONR01AR044741 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 1999 to 2016
$5.1M
Molecular Mechanisms of Bone FormationR01AR048133 · NIAMS · FORSYTH INSTITUTE · PI LI, YI-PING · 2002 to 2006
$2.2M
Role of RGS12, a Regulator of G protein Signaling, in Bone RemodelingR01AR066101 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI YANG, SHUYING · 2014 to 2018
$1.8M
Function of Regulator of G protein signaling in aging skeletonR01AG048388 · NIA · UNIVERSITY OF PENNSYLVANIA · PI YANG, SHUYING · 2014 to 2018
$1.7M
The Role and Mechanism of RGS12 in Bone ResorptionR03DE016857 · NIDCR · FORSYTH INSTITUTE · PI YANG, SHUYING · 2005 to 2006
$178k
NIAMS NIH HHS AR-44741NIAMS NIH HHS AR-48133-01NIAMS NIH HHS R01 AR044741NIAMS NIH HHS R01 AR048133NIAMS NIH HHS R01 AR066101NIA NIH HHS R01 AG048388NIDCR NIH HHS R03 DE016857
6 · The paper itself

Abstract

Significant progress has been made in studies of the mechanisms by which RANKL induces terminal osteoclast differentiation. However, many crucial details in the RANKL-evoked signaling pathway for osteoclast differentiation remain to be defined. We characterized genes specifically expressed in osteoclasts by differential screening of a human osteoclastoma cDNA library, and found that the regulator of G-protein signaling 10A (RGS10A), but not the RGS10B isoform, was specifically expressed in human osteoclasts. The expression of RGS10A is also induced by RANKL in osteoclast precursors and is prominently expressed in mouse osteoclast-like cells. RGS10A silencing by RNA interference blocked intracellular [Ca2+]i oscillations, the expression of NFAT2, and osteoclast terminal differentiation in both bone marrow cells and osteoclast precursor cell lines. Reintroduction of RGS10A rescued the impaired osteoclast differentiation. RGS10A silencing also resulted in premature osteoclast apoptosis. RGS10A silencing affected the RANKL-[Ca2+]i oscillation-NFAT2 signaling pathway but not other RANKL-induced responses. Our data demonstrate that target components of RGS10A are distinct from those of RGS12 in the RANKL signaling mechanism. Our results thus show the specificity of RGS10A as a key component in the RANKL-evoked signaling pathway for osteoclast differentiation, which may present a promising target for therapeutic intervention.

Indexed as

AnimalsBone Marrow CellsCell DifferentiationCells, CulturedGene LibraryHumansMacrophage Colony-Stimulating FactorMiceNFATC Transcription FactorsOsteoclastsProtein IsoformsRANK LigandRGS ProteinsRNA InterferenceSignal TransductionTissue DistributionMacrophage Colony-Stimulating FactorNFATC Transcription FactorsProtein IsoformsRANK LigandRGS10 protein, humanRgs10 protein, mouseRGS12 protein, humanRGS ProteinsTNFSF11 protein, humanTnfsf11 protein, mouse

Identifiers

PMID17881498
PMCPMC3587975
OpenAlexW2154914423

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.