Evidence map›Paper›PMID 18548087›Full record

ArticleGenes and immunity2008

Deletion of PI3K-p85alpha gene impairs lineage commitment, terminal maturation, cytokine generation and cytotoxicity of NK cells.

A Awasthi, A Samarakoon, X Dai, R Wen, D Wang, S Malarkannan

Abstract read
In one paragraph

Article in Genes and immunity, 2008. 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
1.0field-weighted citation impact, top 24% 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, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Transcriptional Regulation of NK Cell Development by mTOR Complexes.Frontiers in cell and developmental biology · 2020
    Review
  5. Cancer immunology research · 2019
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Downregulation of PI3Kcb utilizing adenovirus-mediated transfer of siRNA attenuates bone cancer pain.International journal of clinical and experimental pathology · 2014
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  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

6 authors at 2 institutions in 1 country.

A AwasthiLaboratory of Molecular Immunology, Blood Research Institute, Milwaukee, WI, USA.
A Samarakoon
X Dai
R Wen
D Wang
S Malarkannan
Versiti Blood Center of Wisconsin · USMedical College of Wisconsin · US

Funding

Viral Vector CoreU19AI062627 · NIAID · VERSITI WISCONSIN, INC. · PI ECKELS, DAVID D · 2004 to 2008
$11.6M
Identification of Novel Immune Cell- the NKDCR01AI064826 · NIAID · JOHNS HOPKINS UNIVERSITY · PI PARDOLL, DREW M. · 2006 to 2010
$2.0M
Stat5 dephosphorylation by Shp-2R01HL073284 · NHLBI · VERSITI WISCONSIN, INC. · PI WANG, DEMIN · 2003 to 2007
$1.3M
Individual and Collaborative Roles in T Cell ActivationR01AI052327 · NIAID · BLOODCENTER OF WISCONSIN, INC. · PI WEN, RENREN · 2002 to 2005
$1.1M
NHLBI NIH HHS R01 HL073284NIAID NIH HHS R01 AI052327NIAID NIH HHS R01 AI064826NIAID NIH HHS R01 AI52327NIAID NIH HHS U19 AI062627NIAID NIH HHS U19 AI062627-01PHS HHS N01-HHSN26600500032CPHS HHS R01 A1064826-01
6 · The paper itself

Abstract

Class IA phosphotidylinositol-3-kinases (PI3Ks) are a family of p85/p110 heterodimeric lipid kinases that are important in regulating signaling events in B and T cells. However, their role in natural killer (NK) cells is not understood. Here, using mice that lack the regulatory p85alpha subunit and its alternatively spliced variants p55alpha/p50alpha (collectively termed as p85alpha(-/-)), we defined the role of PI3K in NK cell development and function. p85alpha(-/-) mice had impaired lineage commitment leading to reduced NK cellularity in the bone marrow and liver. p85alpha(-/-) NK cells showed a defective Ly49 subset specification and a decreased expression of CD43. Lack of p85alpha severely reduced the NK-mediated cytotoxicity against tumor cells representing 'induced-self' and 'missing-self'. More importantly, NKG2D and NK1.1 receptor-mediated cytokine and chemokine generation was significantly compromised in p85alpha(-/-) NK cells. These results reveal a previously unrecognized role of p85alpha in the development, terminal maturation, cytokine/chemokine generation and tumor clearance of NK cells.

Indexed as

AnimalsBone MarrowCell DifferentiationChemokinesCytokinesIntegrin alphaVKiller Cells, NaturalLeukosialinLiverMiceNK Cell Lectin-Like Receptor Subfamily KPhosphatidylinositol 3-KinasesReceptors, ImmunologicReceptors, Natural Killer CellChemokinesCytokinesIntegrin alphaVKlrk1 protein, mouseLeukosialinNK Cell Lectin-Like Receptor Subfamily KPhosphatidylinositol 3-KinasesReceptors, ImmunologicReceptors, Natural Killer Cell

Identifiers

PMID18548087
PMCPMC4623703
OpenAlexW2085477403

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.