Evidence map›Paper›PMID 15199164›Full record

ArticleMolecular and cellular biology2004

Mice deficient for all PIM kinases display reduced body size and impaired responses to hematopoietic growth factors.

Harald Mikkers, Martijn Nawijn, John Allen, Conny Brouwers, Els Verhoeven, Jos Jonkers, Anton Berns

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% 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

155 citing papers in PubMed, 1 synthesis or guideline pooled it, 318 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
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  8. Article
  9. The role of Pim-1 kinases in inflammatory signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
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  17. Targeting BET Proteins Downregulates miR-33a To Promote Synergy with PIM Inhibitors in CMML.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  18. Pim Kinases: Important Regulators of Cardiovascular Disease.International journal of molecular sciences · 2023
    Review
  19. Article
  20. Article

95 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Harald MikkersDivision of Molecular Genetics and Centre of Biomedical Genetics, Netherlands Cancer Institute, Amsterdam, The Netherlands.
Martijn Nawijn
John Allen
Conny Brouwers
Els Verhoeven
Jos Jonkers
Anton Berns
The Netherlands Cancer Institute · NLOncode Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Pim family of proto-oncogenes encodes a distinct class of serine/threonine kinases consisting of PIM1, PIM2, and PIM3. Although the Pim genes are evolutionarily highly conserved, the contribution of PIM proteins to mammalian development is unclear. PIM1-deficient mice were previously described but showed only minor phenotypic aberrations. To assess the role of PIM proteins in mammalian physiology, compound Pim knockout mice were generated. Mice lacking expression of Pim1, Pim2, and Pim3 are viable and fertile. However, PIM-deficient mice show a profound reduction in body size at birth and throughout postnatal life. In addition, the in vitro response of distinct hematopoietic cell populations to growth factors is severely impaired. In particular, PIM proteins are required for the efficient proliferation of peripheral T lymphocytes mediated by synergistic T-cell receptor and interleukin-2 signaling. These results indicate that members of the PIM family of proteins are important but dispensable factors for growth factor signaling.

Indexed as

Body ConstitutionAnimalsCell DifferentiationCell DivisionColony-Stimulating FactorsHematopoiesisHematopoietic Stem CellsInterleukin-2MiceMice, KnockoutProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-pim-1Receptors, Antigen, T-CellSignal TransductionT-LymphocytesColony-Stimulating FactorsInterleukin-2Pim1 protein, mousePim2 protein, mousePim3 protein, mouseProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-pim-1proto-oncogene proteins pimReceptors, Antigen, T-Cell

Identifiers

PMID15199164
PMCPMC480904
OpenAlexW2100136475

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.