Evidence map›Paper›PMID 18061646›Full record

ArticleMechanisms of ageing and development

Aging-associated truncated form of p53 interacts with wild-type p53 and alters p53 stability, localization, and activity.

Lynette Moore, Xiongbin Lu, Nader Ghebranious, Stuart Tyner, Lawrence A Donehower

Open access · greenAbstract read
In one paragraph

Article in Mechanisms of ageing and development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Relevance of the p53-MDM2 axis to aging.Cell death and differentiation · 2018
    Review
  7. Dysfunction of the MDM2/p53 axis is linked to premature aging.The Journal of clinical investigation · 2017
    Article
  8. No Evaluation of Serum P53 Levels in Iraqi Female Breast Cancer PatientsAsian Pacific journal of cancer prevention : APJCP · 2017
    Article
  9. Do p53 stress responses impact organismal aging?Translational cancer research · 2016
    Article
  10. p53 as an intervention target for cancer and aging.Pathobiology of aging & age related diseases · 2013
    Review
  11. Senescence regulation by the p53 protein family.Methods in molecular biology (Clifton, N.J.) · 2013
    Review
  12. mTORC1 and p53: clash of the gods?Cell cycle (Georgetown, Tex.) · 2013
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Using mice to examine p53 functions in cancer, aging, and longevity.Cold Spring Harbor perspectives in biology · 2009
    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

5 authors at 1 institution in 1 country.

Lynette MooreDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Xiongbin Lu
Nader Ghebranious
Stuart Tyner
Lawrence A Donehower
Baylor College of Medicine · US

Funding

P53 and Organismal AgingR01AG019693 · NIA · BAYLOR COLLEGE OF MEDICINE · PI DONEHOWER, LAWRENCE A. · 2002 to 2006
$2.7M
NIA NIH HHS R01 AG019693
6 · The paper itself

Abstract

Evidence has accumulated that p53, a prototypical tumor suppressor, may also influence aspects of organismal aging. We have previously described a p53 mutant mouse model, the p53+/m mouse, which is cancer resistant yet exhibits reduced longevity and premature aging phenotypes. p53+/m mice express one full length p53 allele and one truncated p53 allele that is translated into a C-terminal fragment of p53 termed the M protein. The augmented cancer resistance and premature aging phenotypes in the p53+/m mice are consistent with a hyperactive p53 state. To determine how the M protein could increase p53 activity, we examined the M protein in various cellular contexts. Here, we show that embryo fibroblasts from p53+/m mice exhibit reduced proliferation and cell cycle progression compared to embryo fibroblasts from p53+/- mice (with equivalent wild-type p53 dosage). The M protein interacts with wild-type p53, increases its stability, and facilitates its nuclear localization in the absence of stress. Despite increasing p53 stability, the M protein does not disrupt p53-Mdm2 interactions and does not prevent p53 ubiquitination. These results suggest molecular mechanisms by which the M protein could influence the aging and cancer resistance phenotypes in the p53+/m mouse.

Indexed as

Active Transport, Cell NucleusAgingAnimalsCell CycleCell LineCell ProliferationCellular SenescenceFibroblastsGenotypeHCT116 CellsHumansKineticsMiceMice, Mutant StrainsMutationPeptide FragmentsMDM2 protein, humanPeptide FragmentsProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID18061646
PMCPMC2680148
OpenAlexW2170493409

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.