Evidence map›Paper›PMID 23551095›Full record

ReviewAnnals of the New York Academy of Sciences2013

Role of SHIP1 in bone biology.

Sonia Iyer, Bryan S Margulies, William G Kerr

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
  2. Article
  3. SHIP1 is required for T cell surveillance of occult malignancies.Cellular and molecular life sciences : CMLS · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Pathological Roles of INPP5D in Alzheimer's Disease.Advances in experimental medicine and biology · 2023
    Article
  9. Hypoxia-Inducible Factors Signaling in Osteogenesis and Skeletal Repair.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
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

3 authors at 1 institution in 1 country.

Sonia IyerDepartment of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, New York 13210, USA.
Bryan S Margulies
William G Kerr
SUNY Upstate Medical 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 HL072523NHLBI NIH HHS R01 HL085580NHLBI NIH HHS R01- HL085580NHLBI NIH HHS R01 HL107127NHLBI NIH HHS R01-HL107127NHLBI NIH HHS R01-HL72523
6 · The paper itself

Abstract

The bone marrow milieu comprising both hematopoietic and nonhematopoietic lineages has a unique structural organization. Bone undergoes continuous remodeling throughout life. This dynamic process involves a balance between bone-forming osteoblasts (OBs) derived from multipotent mesenchymal stem cells (MSCs) and bone-resorbing osteoclasts (OCs) derived from hematopoietic stem cells (HSCs). Src homology 2-domain-containing inositol 5'-phosphatase 1 (SHIP1) regulates cellular processes such as proliferation, differentiation, and survival via the PI3K/Akt signaling pathway initiated at the plasma membrane. SHIP1-deficient mice also exhibit profound osteoporosis that has been proposed to result from hyperresorptive activity by OCs. We have previously observed that SHIP1 is expressed in primary OBs, which display defective development in SHIP1-deficient mice. These findings led us to question whether SHIP1 plays a functional role in osteolineage development from MSC in vivo, which contributes to the osteoporotic phenotype in germline SHIP1 knockout mice. In this short review, we discuss our current understanding of inositol phospholipid signaling downstream of SHIP1 in bone biology.

Indexed as

AnimalsBone and BonesCell DifferentiationCell ProliferationHumansInositol Polyphosphate 5-PhosphatasesMesenchymal Stem CellsMiceMice, KnockoutOsteoclastsPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesInositol Polyphosphate 5-PhosphatasesINPP5D protein, humanInpp5d protein, mousePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesPhosphoric Monoester Hydrolases

Identifiers

PMID23551095
PMCPMC3670113
OpenAlexW2132726972

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.