Evidence map›Paper›PMID 27041565›Full record

ReviewOncogene2016

MDM2 oligomers: antagonizers of the guardian of the genome.

P L Leslie, Y Zhang

Abstract readReview
In one paragraph

Review in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. GPCR targeting of E3 ubiquitin ligase MDM2 by inactive β-arrestin.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. Article
  5. MDM2, MDMX, and p73 regulate cell-cycle progression in the absence of wild-type p53.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. WIP1 phosphatase as pharmacological target in cancer therapy.Journal of molecular medicine (Berlin, Germany) · 2017
    Review
  12. Article
  13. 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.

P L LeslieDepartment of Radiation Oncology and Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Y ZhangDepartment of Radiation Oncology and Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.

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
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 CA167637NIGMS NIH HHS T32 GM007092
6 · The paper itself

Abstract

Over two decades of MDM2 research has resulted in the accumulation of a wealth of knowledge of many aspects of MDM2 regulation and function, particularly with respect to its most prominent target, p53. For example, recent knock-in mouse studies have shown that MDM2 heterooligomer formation with its homolog, MDMX, is necessary and sufficient in utero to suppress p53 but is dispensable during adulthood. However, despite crucial advances such as these, several aspects regarding basic in vivo functions of MDM2 remain unknown. In one such example, although abundant evidence suggests that MDM2 forms homooligomers and heterooligomers with MDMX, the function and regulation of these homo- and heterooligomers in vivo remain incompletely understood. In this review, we discuss the current state of our knowledge of MDM2 oligomerization as well as current efforts to target the MDM2 oligomer as a broad therapeutic option for cancer treatment.

Indexed as

GenomeProtein MultimerizationAnimalsAntineoplastic AgentsCarrier ProteinsHumansMolecular Targeted TherapyNeoplasmsProtein BindingProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Antineoplastic AgentsCarrier ProteinsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53

Identifiers

PMID27041565
PMCPMC5520534

What OpenQuestion holds

Textmetadata
LicenceTDM
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.