Evidence map›Paper›PMID 24857423›Full record

ArticleStem cells and development2014

SHIP1 regulates MSC numbers and their osteolineage commitment by limiting induction of the PI3K/Akt/β-catenin/Id2 axis.

Sonia Iyer, Dennis R Viernes, John D Chisholm, Bryan S Margulies, William G Kerr

Open access · hybridAbstract read
In one paragraph

Article in Stem cells and development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. SHIP1 is required for T cell surveillance of occult malignancies.Cellular and molecular life sciences : CMLS · 2026
    Article
  4. Article
  5. Article
  6. Hypoxia-Inducible Factors Signaling in Osteogenesis and Skeletal Repair.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. DOK3 Modulates Bone Remodeling by Negatively Regulating Osteoclastogenesis and Positively Regulating Osteoblastogenesis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017
    Article
  14. Article
  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

5 authors at 2 institutions in 1 country.

Sonia Iyer1 Department of Microbiology and Immunology, SUNY Upstate Medical University , Syracuse, New York.
Dennis R Viernes
John D Chisholm
Bryan S Margulies
William G Kerr
SUNY Upstate Medical University · USSyracuse University · US

Funding

Role of SHIP in NK Cell BiologyR01HL072523 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI KERR, WILLIAM GARROW · 2002 to 2014
$4.3M
Chemical Inhibition of SHIP1 To Facilitate Allogeneic Bone Marrow TransplantationR01HL107127 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI KERR, WILLIAM GARROW · 2011 to 2014
$1.6M
SHIP and Immunoregulatory Cell FunctionR01HL085580 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI KERR, WILLIAM GARROW · 2008 to 2011
$1.5M
NHLBI NIH HHS R01 HL085580NHLBI NIH HHS R01 HL107127NHLBI NIH HHS R01 HL72523
6 · The paper itself

Abstract

Here, we show that Src homology 2-domain-containing inositol 5'-phosphatase 1 (SHIP1) is required for the efficient development of osteoblasts from mesenchymal stem cells (MSCs) such that bone growth and density are reduced in mice that lack SHIP1 expression in MSCs. We find that SHIP1 promotes the osteogenic output of MSCs by limiting activation of the PI3K/Akt/β-catenin pathway required for induction of the MSC stemness factor Id2. In parallel, we demonstrate that mice with myeloid-restricted ablation of SHIP1, including osteoclasts (OCs), show no reduction in bone mass or density. Hence, diminished bone mass and density in the SHIP1-deficient mice results from SHIP deficiency in MSC and osteolineage progenitors. Intriguingly, mice with a SHIP-deficient MSC compartment also exhibit decreased OC numbers. In agreement with our genetic findings we also show that treatment of mice with an SHIP1 inhibitor (SHIPi) significantly reduces bone mass. These findings demonstrate a novel role for SHIP1 in MSC fate determination and bone growth. Further, SHIPi may represent a novel therapeutic approach to limit bone development in osteopetrotic and sclerotic bone diseases.

Indexed as

Signal TransductionAnimalsbeta CateninCell LineageInositol Polyphosphate 5-PhosphatasesMesenchymal Stem CellsMice, Inbred C57BLMice, TransgenicOsteoclastsPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesPhosphorylationProto-Oncogene Proteins c-aktbeta CateninCTNNB1 protein, mouseInositol Polyphosphate 5-PhosphatasesInpp5d protein, mousePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-akt

Identifiers

PMID24857423
PMCPMC4172390
OpenAlexW2001143683

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.