Evidence map›Paper›PMID 23034281›Full record

ArticleBlood2012

Mouse natural killer cell development and maturation are differentially regulated by SHIP-1.

Cindy Banh, S M Shahjahan Miah, William G Kerr, Laurent Brossay

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Molecular Regulation of NK Cell Maturation.Frontiers in immunology · 2020
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Transcription factor KLF2 regulates homeostatic NK cell proliferation and survival.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  12. Role of SHIP1 in Invariant NKT Cell Development and Functions.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  13. Article
  14. PTEN regulates natural killer cell trafficking in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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

4 authors at 2 institutions in 1 country.

Cindy BanhDepartment of Molecular Microbiology and Immunology, Brown University, Providence, RI 02912, USA.
S M Shahjahan Miah
William G Kerr
Laurent Brossay
Brown University · USSUNY Upstate Medical University · US

Funding

Functions of the KLRG1 molecule on NK cells and T cellsR01AI058181 · NIAID · BROWN UNIVERSITY · PI BROSSAY, LAURENT · 2004 to 2008
$1.5M
Cadherins, Immune Receptors and their InteractionsR56AI058181 · NIAID · BROWN UNIVERSITY · PI BROSSAY, LAURENT · 2010 to 2010
$405k
KLRG1, Cadherins and their interactionsF31AI080230 · NIAID · BROWN UNIVERSITY · PI BANH, CINDY · 2009 to 2011
$80k
NIAID NIH HHS AI58181NIAID NIH HHS F31 0AI080230NIAID NIH HHS F31 AI080230NIAID NIH HHS R01 AI058181NIAID NIH HHS R56 AI058181
6 · The paper itself

Abstract

The SH2-containing inositol phosphatase-1 (SHIP-1) is a 5' inositol phosphatase known to negatively regulate the product of phosphoinositide-3 kinase (PI3K), phosphatidylinositol-3.4,5-trisphosphate. SHIP-1 can be recruited to a large number of inhibitory receptors expressed on natural killer (NK) cells. However, its role in NK cell development, maturation, and functions is not well defined. In this study, we found that the absence of SHIP-1 results in a loss of peripheral NK cells. However, using chimeric mice we demonstrated that SHIP-1 expression is not required intrinsically for NK cell lineage development. In contrast, SHIP-1 is required cell autonomously for NK cell terminal differentiation. These findings reveal both a direct and indirect role for SHIP-1 at different NK cell development checkpoints. Notably, SHIP-1-deficient NK cells display an impaired ability to secrete IFN-γ during cytokine receptor-mediated responses, whereas immunoreceptor tyrosine-based activation motif containing receptor-mediated responses is not affected. Taken together, our results provide novel insights on how SHIP-1 participates in the development, maturation, and effector functions of NK cells.

Indexed as

AnimalsCell DifferentiationFemaleFlow CytometryInositol Polyphosphate 5-PhosphatasesInterferon-gammaInterleukin Receptor Common gamma SubunitKiller Cells, NaturalLymphocyte CountMaleMiceMice, Inbred C57BLMice, KnockoutNK Cell Lectin-Like Receptor Subfamily ANK Cell Lectin-Like Receptor Subfamily DPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesIl2rg protein, mouseInositol Polyphosphate 5-PhosphatasesInpp5d protein, mouseInterferon-gammaInterleukin Receptor Common gamma SubunitNK Cell Lectin-Like Receptor Subfamily ANK Cell Lectin-Like Receptor Subfamily DPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphoric Monoester Hydrolases

Identifiers

PMID23034281
PMCPMC3512235
OpenAlexW2000386613

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.