Evidence map›Paper›PMID 29065514›Full record

ReviewInternational journal of molecular sciences2017

The Role of MDM2 in Promoting Genome Stability versus Instability.

M Reza Saadatzadeh, Adily N Elmi, Pankita H Pandya, Khadijeh Bijangi-Vishehsaraei, Jixin Ding, Christopher W Stamatkin, Aaron A Cohen-Gadol, Karen E Pollok

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. 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
1.5field-weighted citation impact, top 15% 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, 35 citations in OpenAlex.

  1. Trial
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  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. New insights into cancer: MDM2 binds to the citrullinating enzyme PADI4.Protein science : a publication of the Protein Society · 2023
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Exon 3 of theG3 (Bethesda, Md.) · 2019
    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

8 authors at 3 institutions in 1 country.

M Reza SaadatzadehDepartment of Pediatrics (Division of Hematology/Oncology), Indianapolis, IN 46202, USA. msaadatz@iu.edu.ORCID 0000-0002-7976-7970
Adily N ElmiHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA. aelmi@indiana.edu.
Pankita H PandyaDepartment of Pediatrics (Division of Hematology/Oncology), Indianapolis, IN 46202, USA. phpandya@iu.edu.
Khadijeh Bijangi-VishehsaraeiDepartment of Pediatrics (Division of Hematology/Oncology), Indianapolis, IN 46202, USA. khbijang@iupui.edu.
Jixin DingDepartment of Pediatrics (Division of Hematology/Oncology), Indianapolis, IN 46202, USA. jixiding@iu.edu.
Christopher W StamatkinHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA. cstamatk@iu.edu.
Aaron A Cohen-GadolGoodman Campbell Brain and Spine, Indianapolis, IN 46032, USA. acohenmd@gmail.com.ORCID 0000-0002-4946-1524
Karen E PollokDepartment of Pediatrics (Division of Hematology/Oncology), Indianapolis, IN 46202, USA. kpollok@iu.edu.
Indiana University Health · USIndiana Spine Group · USIndiana University School of Medicine

Funding

Dual Targeting of DNA Repair and p53 pathways for treatment of brain cancerR01CA138798 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI POLLOK, KAREN ELIZABETH · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA138798
6 · The paper itself

Abstract

In cancer, the mouse double minute 2 (MDM2) is an oncoprotein that contributes to the promotion of cell growth, survival, invasion, and therapeutic resistance. The impact of MDM2 on cell survival versus cell death is complex and dependent on levels of MDM2 isoforms, p53 status, and cellular context. Extensive investigations have demonstrated that MDM2 protein-protein interactions with p53 and other p53 family members (p63 and p73) block their ability to function as transcription factors that regulate cell growth and survival. Upon genotoxic insults, a dynamic and intricately regulated DNA damage response circuitry is activated leading to release of p53 from MDM2 and activation of cell cycle arrest. What ensues following DNA damage, depends on the extent of DNA damage and if the cell has sufficient DNA repair capacity. The well-known auto-regulatory loop between p53-MDM2 provides an additional layer of control as the cell either repairs DNA damage and survives (i.e., MDM2 re-engages with p53), or undergoes cell death (i.e., MDM2 does not re-engage p53). Furthermore, the decision to live or die is also influenced by chromatin-localized MDM2 which directly interacts with the Mre11-Rad50-Nbs1 complex and inhibits DNA damage-sensing giving rise to the potential for increased genome instability and cellular transformation.

Indexed as

DNA DamageDNA RepairGenomic InstabilityAnimalsDNAHumansMiceProto-Oncogene Proteins c-mdm2DNAProto-Oncogene Proteins c-mdm2DNA damagegenome instabilityMDM2p53

Identifiers

PMID29065514
PMCPMC5666895
OpenAlexW2767197248

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.