Evidence map›Paper›PMID 22573816›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Control of bone resorption in mice by Schnurri-3.

Marc N Wein, Dallas C Jones, Jae-Hyuck Shim, Antonios O Aliprantis, Rosalyn Sulyanto, Vanja Lazarevic, Sandra L Poliachik, Ted S Gross, Laurie H Glimcher

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Schnurri-3 inhibition suppresses bone and joint damage in models of rheumatoid arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. WNT-modulating gene silencers as a gene therapy for osteoporosis, bone fracture, and critical-sized bone defects.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  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

9 authors.

Marc N WeinDepartment of Immunology and Infectious Disease, Harvard School of Public Health, Boston, MA 02115, USA.
Dallas C Jones
Jae-Hyuck Shim
Antonios O Aliprantis
Rosalyn Sulyanto
Vanja Lazarevic
Sandra L Poliachik
Ted S Gross
Laurie H Glimcher

Funding

Regulation of osteoclast biology by anion exchanger SLC4A2 in mouse and human sysR01AR060363 · NIAMS · HARVARD SCHOOL OF PUBLIC HEALTH · PI CHARLES, JULIA F · 2011 to 2015
$1.9M
Novel Regulators of Bone FormationR01HD055601 · NICHD · WEILL MEDICAL COLL OF CORNELL UNIV · PI GLIMCHER, LAURIE HOLLIS · 2008 to 2012
$1.4M
Novel regulatory mechanisms of the osteoclast transcriptional programK08AR054859 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI ALIPRANTIS, ANTONIOS O · 2008 to 2012
$655k
Novel Regulators of Osteoblast DifferentiationK99AR055668 · NIAMS · HARVARD SCHOOL OF PUBLIC HEALTH · PI JONES, DALLAS C. · 2008 to 2009
$179k
NIAMS NIH HHS K08 AR054859NIAMS NIH HHS K08AR054859NIAMS NIH HHS K99 AR055668NIAMS NIH HHS K99AR055668NIAMS NIH HHS R01 AR060363NIAMS NIH HHS R01AR060363NICHD NIH HHS HD055601NICHD NIH HHS R01 HD055601
6 · The paper itself

Abstract

Mice lacking the large zinc finger protein Schnurri-3 (Shn3) display increased bone mass, in part, attributable to augmented osteoblastic bone formation. Here, we show that in addition to regulating bone formation, Shn3 indirectly controls bone resorption by osteoclasts in vivo. Although Shn3 plays no cell-intrinsic role in osteoclasts, Shn3-deficient animals show decreased serum markers of bone turnover. Mesenchymal cells lacking Shn3 are defective in promoting osteoclastogenesis in response to selective stimuli, likely attributable to reduced expression of the key osteoclastogenic factor receptor activator of nuclear factor-κB ligand. The bone phenotype of Shn3-deficient mice becomes more pronounced with age, and mice lacking Shn3 are completely resistant to disuse osteopenia, a process that requires functional osteoclasts. Finally, selective deletion of Shn3 in the mesenchymal lineage recapitulates the high bone mass phenotype of global Shn3 KO mice, including reduced osteoclastic bone catabolism in vivo, indicating that Shn3 expression in mesenchymal cells directly controls osteoblastic bone formation and indirectly regulates osteoclastic bone resorption.

Indexed as

AgingAnimalsBone ResorptionCells, CulturedCoculture TechniquesCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsHyperparathyroidism, SecondaryMesenchymal Stem CellsMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutOsteoblastsOsteoclastsPhenotypeCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsRANK LigandSchnurri-3 protein, mouse

Identifiers

PMID22573816
PMCPMC3361406

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.