Evidence map›Paper›PMID 16170338›Full record

ArticleOncogene2006

Targeted disruption of the mouse ing1 locus results in reduced body size, hypersensitivity to radiation and elevated incidence of lymphomas.

J V Kichina, M Zeremski, L Aris, K V Gurova, E Walker, R Franks, A Y Nikitin, H Kiyokawa, A V Gudkov

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Altered endocytosis in cellular senescence.Ageing research reviews · 2021
    Review
  5. Review
  6. Article
  7. Senescence and Apoptosis: Architects of Mammalian Development.Frontiers in cell and developmental biology · 2020
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. INGs are potential drug targets for cancer.Journal of cancer research and clinical oncology · 2017
    Review
  18. Article
  19. ING1 and ING2: multifaceted tumor suppressor genes.Cellular and molecular life sciences : CMLS · 2013
    Review
  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

9 authors at 5 institutions in 1 country.

J V KichinaDepartment of Molecular Genetics, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
M Zeremski
L Aris
K V Gurova
E Walker
R Franks
A Y Nikitin
H Kiyokawa
A V Gudkov
University of Illinois Chicago · USCleveland Clinic Lerner College of Medicine · USCleveland BioLabs (United States) · USCleveland Clinic · USCornell University · US

Funding

GENETIC ELEMENTS TRANSFORMING MOUSE FIBROBLASTSR01CA060730 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GUDKOV, ANDREI V · 1994 to 2009
$2.6M
NCI NIH HHS CA 17579NCI NIH HHS CA 60730
6 · The paper itself

Abstract

Ing1 belongs to the family of evolutionary conserved genes encoding nuclear PHD finger-containing proteins implicated in a variety of processes, including tumorigenesis, replicative senescence, excision repair and response to genotoxic stress. We have generated mice deficient in all the isoforms of Ing1 by targeted disruption of the exon that is common for all ing1 transcripts. Embryonic fibroblasts from ing1-knockout mice were similar to the wild-type cells in their growth characteristics, replicative lifespan in culture, p53 induction and sensitivity to various cytotoxic treatments with minor alterations in cell cycle distribution in response to genotoxic stress. ing1-deficient animals are characterized by reduced size with no obvious morphological, physiological or behavioral abnormalities, indicating that ing1 function is dispensable for the viability of mice under normal physiological conditions. Loss of ing1 was associated with earlier onset and higher incidence of lymphomas. Consistent with the possible involvement of Ing1 in DNA repair, ing1-deficient mice were more sensitive to total body gamma radiation. Our observations are well in line with the suggested role of ing1 as a candidate tumor suppressor gene involved in control of DNA damage response.

Indexed as

Abnormalities, MultipleAge of OnsetAgingAnimalsBody SizeCells, CulturedDNA RepairFibroblastsInhibitor of Growth Protein 1Intracellular Signaling Peptides and ProteinsLymphomaMiceMice, Mutant StrainsNuclear ProteinsRadiation ToleranceTumor Suppressor Protein p53Ing1 protein, mouseInhibitor of Growth Protein 1Intracellular Signaling Peptides and ProteinsNuclear ProteinsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID16170338
OpenAlexW1981290840

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.