Evidence map›Paper›PMID 25201198›Full record

ReviewSub-cellular biochemistry2014

p53-independent effects of Mdm2.

Stephen Bohlman, James J Manfredi

Open access · greenAbstract readReview
In one paragraph

Review in Sub-cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
10.3field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Discovery of Benzophenanthridine Alkaloids fromPharmaceuticals (Basel, Switzerland) · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. p53: The Multifaceted Roles of Covalent Modifications in Cancer.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Long noncoding RNA,Frontiers in cell and developmental biology · 2024
    Article
  15. Review
  16. Three-Dimensional Gene Regulation Network in Glioblastoma Ferroptosis.International journal of molecular sciences · 2023
    Article
  17. Advancements in MDM2 inhibition: Clinical and pre-clinical investigations of combination therapeutic regimens.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Review
  18. Article
  19. Article
  20. Article

4 more citing papers are in PubMed but not listed here.

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 1 country.

Stephen BohlmanDepartment of Oncological Sciences, The Graduate School of Biomedical Sciences Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
James J Manfredi
Icahn School of Medicine at Mount Sinai · USThe Graduate Center, CUNY · US

Funding

PW1--A mediator of cell survival by NFKB and cell death by p53P01CA080058 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI AARONSON, STUART A · 2000 to 2016
$20.2M
TRAINING PROGRAM IN CANCER THERAPYT32CA078207 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI James J Manfredi · 1999 to 2026
$11.6M
NCI NIH HHS P01 CA080058NCI NIH HHS T32 CA078207
6 · The paper itself

Abstract

Mdm2 is best known as the primary negative regulator of p53, but a growing body of evidence suggests that Mdm2 also has a number of functions independent of its role in regulating p53. Although these functions are not yet well-characterized, they have been implicated in regulating of a number of cellular processes, including cell-cycle control, apoptosis, differentiation, genome stability, and transcription, among others. It appears that Mdm2 exerts these functions through a surprisingly wide variety of mechanisms. For example, it has been shown that Mdm2 can ubiquitinate alternative targets, can stimulate the activity of transcription factors, and can directly bind to mRNA to regulate its stability. Dysregulation of p53-independent functions could be responsible for the oncogenic properties of Mdm2 seen even in the absence of p53, and may explain why approximately 10 % of human tumors overexpress Mdm2 instead of inactivating p53 through other mechanisms. As the p53-independent functions of Mdm2 present novel targets for potential therapeutic interventions, fully characterizing these cellular and pathogenic roles of Mdm2 will be important in the study of tumor biology and the treatment of cancer.

Indexed as

Genes, p53CarcinogenesisGenomic InstabilityHumansNeoplasmsProtein BiosynthesisProto-Oncogene Proteins c-mdm2Transcription, GeneticUbiquitinationMDM2 protein, humanProto-Oncogene Proteins c-mdm2

Identifiers

PMID25201198
PMCPMC5507576
OpenAlexW2105602271

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.