Evidence map›Paper›PMID 20392259›Full record

ReviewAnnals of the New York Academy of Sciences2010

Regulation of bone turnover by calcium-regulated calcium channels.

Lisa J Robinson, Harry C Blair, John B Barnett, Mone Zaidi, Christopher L-H Huang

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Membrane Transport Proteins in Osteoclasts: The Ins and Outs.Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Review
  13. Calcium channels: the potential therapeutic targets for inflammatory bone destruction of rheumatoid arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Review
  14. Article
  15. Article
  16. Article
  17. Stimulation of Ca2+-channel Orai1/STIM1 by serum- and glucocorticoid-inducible kinase 1 (SGK1).FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011
    Article
  18. Article
  19. 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

5 authors at 4 institutions in 2 countries.

Lisa J RobinsonDepartment of Pathology, University of Pittsburgh, Pittsburgh, PA, USA. robinsonlj@upmc.edu
Harry C Blair
John B Barnett
Mone Zaidi
Christopher L-H Huang
VA Pittsburgh Healthcare System · USIcahn School of Medicine at Mount Sinai · USUniversity of Cambridge · GBWest Virginia University · US

Funding

Prevention of arthritis-induced bone erosion by inhibiting osteoclast differentiation by the haloanilide, N-Methyl DichloropropionanilineR42AR074812 · NIAMS · EXESALIBERO, INC. · PI BARNETT, JOHN B · 2019 to 2021
$1.7M
NIAMS NIH HHS R42 AR074812
6 · The paper itself

Abstract

Calcium plays multiple roles in osteoclast formation, survival, and activity. Intracellular calcium is determined both by the release of intracellular stores and the influx of extracellular calcium through a variety of calcium channels. Osteoclasts express several classes of calcium channels, including ryanodine receptors (RyRs), inositol-1,4,5-trisphosphate receptors (IP(3)Rs), and calcium release-activated calcium channels (CRACs), which respond to depletion of intracellular stores. IP(3)R2 is expressed in osteoclast precursors and activated by cytokines that stimulate osteoclast differentiation. In mature osteoclasts, the IP(3)R1 isoform is highly expressed and is implicated in nitric oxide-cGMP-stimulated processes. RyR calcium channels may contribute to the release of intracellular calcium stores, while RyR2 in the plasma membrane may act to limit osteoclast activity based on extracellular calcium concentration. Orai, through regulation by endoplasmic reticular store-sensing proteins, including Stim-1, may also mediate calcium influx and act as a signal amplifier for calcium release by other calcium channels. Together, these receptors allow intracellular Ca(2+) signals to modulate bone turnover and, through calcium-sensing functions, allow coupling of osteoclast activity to extracellular conditions and integrating additional cytokine and nitric oxide signals via transient intracellular calcium signals.

Indexed as

AnimalsBone RemodelingCalciumCalcium ChannelsCell MovementHumansInositol 1,4,5-Trisphosphate ReceptorsModels, BiologicalNitric OxideOsteoclastsRyanodine Receptor Calcium Release ChannelCalciumCalcium ChannelsInositol 1,4,5-Trisphosphate ReceptorsNitric OxideRyanodine Receptor Calcium Release Channel

Identifiers

PMID20392259
PMCPMC11610510
OpenAlexW1956061148

What OpenQuestion holds

Textmetadata
LicenceTDM
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.