Evidence map›Paper›PMID 26951863›Full record

ReviewBiochimica et biophysica acta2016

Long story short: p53 mediates innate immunity.

Jessica Miciak, Fred Bunz

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. International journal of molecular sciences · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Viruses · 2022
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.International journal of molecular sciences · 2020
    Review
  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

2 authors at 1 institution in 1 country.

Jessica MiciakGraduate Program in Cellular and Molecular Medicine, Department of Radiation Oncology and Molecular Radiation Sciences, The Kimmel Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA. Electronic address: jmiciak@gmail.com.
Fred BunzGraduate Program in Cellular and Molecular Medicine, Department of Radiation Oncology and Molecular Radiation Sciences, The Kimmel Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA. Electronic address: fredbunz@jhmi.edu.
Johns Hopkins University · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Training Program in Cellular and Molecular MedicineT32GM008752 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2000 to 2019
$11.7M
Targeting the ATR pathway in p53-deficient cancersR01CA157535 · NCI · JOHNS HOPKINS UNIVERSITY · PI BUNZ, FRED · 2011 to 2015
$1.7M
A Genetic Model for Early-Onset Breast and Colon Cancer in African AmericansU01CA158428 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI BUCKHAULTS, PHILLIP JOE, BUNZ, FRED · 2012 to 2016
$1.5M
NCI NIH HHS CA157535NCI NIH HHS CA158428NCI NIH HHS P30 CA006973NCI NIH HHS R01 CA157535NCI NIH HHS U01 CA158428NIGMS NIH HHS T32 GM008752
6 · The paper itself

Abstract

The story of p53 and how we came to understand it is punctuated by fundamental insights into the essence of cancer. In the decades since its discovery, p53 has been shown to be centrally involved in most, if not all, of the cellular processes that maintain tissue homeostasis. Extensive functional analyses of p53 and its tumor-associated mutants have illuminated many of the common defects shared by most cancer cells. As the central character in a tale that continues to unfold, p53 has become increasingly familiar and yet remains surprisingly inscrutable. New relationships periodically come to light, and surprising, novel activities continue to emerge, thereby revealing new dimensions and aspects of its function. What lies at the very core of this complex protagonist? What is its prime motivation? As every avid reader knows, the elements of character are profoundly shaped by adversity--originating from within and without. And so it is with p53. This review will briefly recap the coordinated responses of p53 to viral infection, and outline a hypothetical model that would explain how an abundance of seemingly unrelated phenotypic attributes may in the end reflect a singular function. All stories eventually draw to a conclusion. This epic tale may eventually leave us with the realization that p53, most simply described, is a protein that evolved to mediate immune surveillance.

Indexed as

Immunity, InnateAnimalsCell CommunicationDNA DamageGlucoseHumansNeoplasmsTumor Suppressor Protein p53GlucoseTumor Suppressor Protein p53AdenovirusDNA damageInterferonP53

Identifiers

PMID26951863
PMCPMC4860023
OpenAlexW2289485382

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.