Evidence map›Paper›PMID 25525673›Full record

ArticleStem cells and development2015

SHIP1-expressing mesenchymal stem cells regulate hematopoietic stem cell homeostasis and lineage commitment during aging.

Sonia Iyer, Robert Brooks, Matthew Gumbleton, William G Kerr

Abstract read
In one paragraph

Article in Stem cells and development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. SHIP1 is required for T cell surveillance of occult malignancies.Cellular and molecular life sciences : CMLS · 2026
    Article
  3. Article
  4. SHIPi improves hematologic recovery after chemotherapy.Molecular medicine (Cambridge, Mass.) · 2025
    Article
  5. Loss of Inpp5d has disease-relevant and sex-specific effects on glial transcriptomes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Role of SHIP1 in Invariant NKT Cell Development and Functions.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  14. Review
  15. 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

4 authors at 1 institution in 1 country.

Sonia Iyer1 Department of Microbiology & Immunology, SUNY Upstate Medical University , Syracuse, New York.
Robert Brooks
Matthew Gumbleton
William G Kerr
Syracuse 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

Hematopoietic stem cell (HSC) self-renewal and lineage choice are subject to intrinsic control. However, this intrinsic regulation is also impacted by external cues provided by niche cells. There are multiple cellular components that participate in HSC support with the mesenchymal stem cell (MSC) playing a pivotal role. We had previously identified a role for SH2 domain-containing inositol 5'-phosphatase-1 (SHIP1) in HSC niche function through analysis of mice with germline or induced SHIP1 deficiency. In this study, we show that the HSC compartment expands significantly when aged in a niche that contains SHIP1-deficient MSC; however, this expanded HSC compartment exhibits a strong bias toward myeloid differentiation. In addition, we show that SHIP1 prevents chronic G-CSF production by the aging MSC compartment. These findings demonstrate that intracellular signaling by SHIP1 in MSC is critical for the control of HSC output and lineage commitment during aging. These studies increase our understanding of how myeloid bias occurs in aging and thus could have implications for the development of myeloproliferative disease in aging.

Indexed as

Cell LineageHomeostasisAgingAnimalsHematopoietic Stem CellsInositol Polyphosphate 5-PhosphatasesMesenchymal Stem CellsMicePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphoric Monoester HydrolasesStem Cell NicheInositol Polyphosphate 5-PhosphatasesInpp5d protein, mousePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphoric Monoester Hydrolases

Identifiers

PMID25525673
PMCPMC4403265
OpenAlexW1913377297

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.