Evidence map›Paper›PMID 8233823›Full record

ArticleNucleic acids research1993

In vivo analysis of Pim-1 deficiency.

P W Laird, N M van der Lugt, A Clarke, J Domen, K Linders, J McWhir, A Berns, M Hooper

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Nucleic acids research, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

56 citing papers in PubMed, 122 citations in OpenAlex.

  1. Review
  2. Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Pim Kinases: Important Regulators of Cardiovascular Disease.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Super-enhancers conserved within placental mammals maintain stem cell pluripotency.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. PIM1: a promising target in patients with triple-negative breast cancer.Medical oncology (Northwood, London, England) · 2017
    Review
  15. Research in pharmaceutical sciences · 2017
    Article
  16. Article
  17. Article
  18. Identification of quinones as novel PIM1 kinase inhibitors.Bioorganic & medicinal chemistry letters · 2016
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

P W LairdDivision of Molecular Genetics, The Netherlands Cancer Institute, Amsterdam.
N M van der Lugt
A Clarke
J Domen
K Linders
J McWhir
A Berns
M Hooper
Cancer Research UK · GBThe Netherlands Cancer Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Pim-1 proto-oncogene encodes a highly conserved serine/threonine phosphokinase which is predominantly expressed in hematopoietic organs and gonads in mammals. Overexpression of Pim-1 predisposes to lymphomagenesis in mice. To develop a further understanding of Pim-1 in molecular terms, as well as in terms of its potential role in hematopoietic development, we have generated mice deficient in Pim-1 function. Pim-1-deficient mice are ostensibly normal, healthy and fertile. Detailed comparative analyses of the hematopoietic systems of the mutant mice and their wild-type littermates showed that they are indistinguishable for most of the parameters studied. Our analyses revealed one unexpected phenotype that correlated with the level of Pim-1 expression: Pim-1 deficiency correlated with a erythrocyte microcytosis, whereas overexpression of Pim-1 in E mu-Pim-1-transgenic mice resulted in erythrocyte macrocytosis. In order to confirm that the observed decrease in erythrocyte Mean Cell Volume (MCV) was attributable to the Pim-1 deficiency, we developed mice transgenic for a Pim-1 gene construct with its own promoter and showed that this transgene could restore the low erythrocyte Mean Cell Volume observed in the Pim-1-deficient mice to near wild-type levels. These results might be relevant to the observed involvement of the Pim-1 gene in mouse erythroleukemogenesis. The surprising lack of a readily observed phenotype in the lymphoid compartment of the Pim-1-deficient mice, suggests a heretofore unrecognized degree of in vivo functional redundancy of this highly conserved proto-oncogene.

Indexed as

Protein Serine-Threonine KinasesAnimalsFemaleFlow CytometryMaleMiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicOncogenesPrecipitin TestsProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-pim-1Restriction MappingPim1 protein, mouseProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-pim-1

Identifiers

PMID8233823
PMCPMC331501
OpenAlexW1966370450

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.