Evidence map›Paper›PMID 17626792›Full record

ArticleGenes & development2007

RGS10-null mutation impairs osteoclast differentiation resulting from the loss of [Ca2+]i oscillation regulation.

Shuying Yang, Yi-Ping Li

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
–field-weighted citation impact
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

81 citing papers in PubMed, 139 citations in OpenAlex.

  1. Review
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  8. Metabolic acidosis regulates RGS16 and G protein signaling in osteoblasts.American journal of physiology. Renal physiology · 2021
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21 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Shuying YangDepartment of Cytokine Biology, The Forsyth Institute, Boston, Massachusetts 02115, USA.
Yi-Ping Li
Harvard University · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI CHEN, CHINFEI · 1985 to 2015
$26.2M
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 of IFT80 in bone formationR03AR061052 · NIAMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI YANG, SHUYING · 2012 to 2014
$232k
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-48133NIAMS NIH HHS R01 AR044741NIAMS NIH HHS R01 AR048133NIAMS NIH HHS R01 AR066101NIAMS NIH HHS R03 AR061052NIA NIH HHS R01 AG048388NICHD NIH HHS P30 HD018655NICHD NIH HHS P30 HD 18655NIDCR NIH HHS DE016857NIDCR NIH HHS R03 DE016857
6 · The paper itself

Abstract

Increased osteoclastic resorption leads to many bone diseases, including osteoporosis and rheumatoid arthritis. While rapid progress has been made in characterizing osteoclast differentiation signaling pathways, how receptor activator of nuclear factor kappaB (NF-kappaB) ligand (RANKL) evokes essential [Ca2+]i oscillation signaling remains unknown. Here, we characterized RANKL-induced signaling proteins and found regulator of G-protein signaling 10 (RGS10) is predominantly expressed in osteoclasts. We generated RGS10-deficient (RGS10-/-) mice that exhibited severe osteopetrosis and impaired osteoclast differentiation. Our data demonstrated that ectopic expression of RGS10 dramatically increased the sensitivity of osteoclast differentiation to RANKL signaling; the deficiency of RGS10 resulted in the absence of [Ca2+]i oscillations and loss of NFATc1; ectopic NFATc1 expression rescues impaired osteoclast differentiation from deletion of RGS10; phosphatidylinositol 3,4,5-trisphosphate (PIP3) is essential to PLCgamma activation; and RGS10 competitively interacts with Ca2+/calmodulin and PIP3 in a [Ca2+]i-dependent manner to mediate PLCgamma activation and [Ca2+]i oscillations. Our results revealed a mechanism through which RGS10 specifically regulates the RANKL-evoked RGS10/calmodulin-[Ca2+]i oscillation-calcineurin-NFATc1 signaling pathway in osteoclast differentiation using an in vivo model. RGS10 provides a potential therapeutic target for the treatment of bone diseases.

Indexed as

Calcium SignalingAnimalsCalmodulinCell DifferentiationCell LineEmbryonic DevelopmentFemaleGrowth DisordersHumansIn Vitro TechniquesMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutModels, BiologicalCalmodulinNfatc1 protein, mouseNFATC Transcription FactorsPhospholipase C gammaRANK LigandRgs10 protein, mouseRGS ProteinsTnfsf11 protein, mouse

Identifiers

PMID17626792
PMCPMC1920174
OpenAlexW2116603858

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.