Evidence map›Paper›PMID 28096294›Full record

ReviewJournal of molecular cell biology2017

Mouse modelling of the MDM2/MDMX-p53 signalling axis.

Nicole R Tackmann, Yanping Zhang

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-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

19 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. NEnvironmental pollution (Barking, Essex : 1987) · 2020
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

2 authors at 2 institutions in 2 countries.

Nicole R TackmannDepartment of Radiation Oncology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
Yanping ZhangDepartment of Radiation Oncology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27514, USA.
University of North Carolina at Chapel Hill · USXuzhou Medical College · CN

Funding

NRSA IN GENETICST32GM007092 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SEKELSKY, JEFF J. · 1985 to 2019
$5.9M
Regulation of MDM2 by the ribosomal protein L11R01CA100302 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZHANG, YANPING · 2003 to 2013
$3.2M
In vivo regulation of p53 by MDM2 and MDMXR01CA212407 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZHANG, YANPING · 2017 to 2021
$1.9M
Mitochondrial p32 regulation of the Mdm2-p53 tumor suppression signaling and apopR01CA155235 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZHANG, YANPING · 2012 to 2016
$1.5M
The in vivo role of the Mdm2-MdmX interaction in p53 regulationR01CA167637 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZHANG, YANPING · 2012 to 2016
$1.5M
In vivo function of Mdm2 E3 ubiquitin ligaseR01CA127770 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZHANG, YANPING · 2008 to 2013
$1.5M
NCI NIH HHS R01 CA100302NCI NIH HHS R01 CA127770NCI NIH HHS R01 CA155235NCI NIH HHS R01 CA167637NCI NIH HHS R01 CA212407NIGMS NIH HHS T32 GM007092
6 · The paper itself

Abstract

It is evident that p53 activity is critical for tumour prevention and stress response through its transcriptional activation of genes affecting cellular senescence, apoptosis, cellular metabolism, and DNA repair. The regulation of p53 is highly complex, and MDM2 and MDMX are thought to be critical for deciding the fate of p53, both through inhibitory binding and post-translational modification. Many mouse models have been generated to study the regulation of p53 in vivo, and they have altered our interpretations of how p53 is regulated by MDM2 and MDMX. Although MDM2 is absolutely required for p53 regulation, certain functions are dispensable under unstressed conditions, including the ability of MDM2 to degrade p53. MDMX, on the other hand, may only be required in select situations, like embryogenesis. These models have also clarified how cellular stress signals modify the p53-inhibiting activities of MDM2 and MDMX in vivo. It is clear that more work will need to be performed to further understand the contexts for each of these signals and the requirements of various MDM2 and MDMX functions. Here, we will discuss what we have learned from mouse modelling of MDM2 and MDMX and underscore the ways in which these models could inform future therapies.

Indexed as

Models, BiologicalSignal TransductionAnimalsMiceOrgan SpecificityProtein StabilityProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Proto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53cancerE3 ubiquitin ligaseMDM2MDMXp53

Identifiers

PMID28096294
PMCPMC5907827
OpenAlexW2577077700

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.