Evidence map›Paper›PMID 28794999›Full record

ArticleTranslational cancer research2016

Modulation of the p53 family network by RNA-binding proteins.

Chris Lucchesi, Jin Zhang, Xinbin Chen

Open access · hybridAbstract read
In one paragraph

Article in Translational cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Reciprocal modulation of long noncoding RNA EMS and p53 regulates tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. NOVA1 acts as an oncogene in melanoma via regulating FOXO3a expression.Journal of cellular and molecular medicine · 2018
    Article
  12. 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

3 authors at 1 institution in 1 country.

Chris LucchesiComparative Oncology Laboratory, School of Veterinary Medicine, School of Medicine, University of California at Davis, Davis, California 95616, USA.
Jin ZhangComparative Oncology Laboratory, School of Veterinary Medicine, School of Medicine, University of California at Davis, Davis, California 95616, USA.
Xinbin ChenComparative Oncology Laboratory, School of Veterinary Medicine, School of Medicine, University of California at Davis, Davis, California 95616, USA.
University of California, Davis · US

Funding

MECHANISM OF P73 DEPENDENT TUMOR SUPPRESSIONR01CA081237 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 1999 to 2022
$6.8M
Mechanism of p53-Mediated Tumor SuppressionR01CA076069 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2002 to 2017
$4.5M
Training Program in Oncogenic Signals and Chromosome BiologyT32CA108459 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HEYER, WOLF-DIETRICH · 2006 to 2020
$3.6M
Regulation of Mutant P53 Expression and Oncogenic ActivityR01CA121137 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2007 to 2016
$2.8M
The role of the p63-RBM38 loop in tumor suppressionR01CA195828 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2016 to 2020
$1.8M
MECHANISM OF P53 DEPENDENT APOPTOSISR29CA076069 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHEN, XINBIN · 1998 to 2002
$276k
NCI NIH HHS R01 CA076069NCI NIH HHS R01 CA081237NCI NIH HHS R01 CA121137NCI NIH HHS R01 CA195828NCI NIH HHS R29 CA076069NCI NIH HHS T32 CA108459
6 · The paper itself

Abstract

Since its discovery more than three decades ago, tumor suppressor p53 has been shown to play pivotal roles in both maintaining genomic integrity and tumor suppression. p53 functions as a transcription factor responding to a multitude of cellular stressors, regulating the transcription of many genes involved in cell-cycle arrest, senescence, autophagy, and apoptosis. Extensive work has revealed that p53 is one of the most commonly mutated tumor suppressor genes. The last three decades have demonstrated that p53 activity is controlled through transcriptional regulation and posttranslational modifications. However, evolving work is now uncovering that p53, and other p53 family members, are post-transcriptionally regulated by multiple RNA-binding proteins (RBPs). Understanding the regulation of p53 by RBPs may potentially open up the possibility for cancer therapeutic intervention. This review focuses on the posttranscriptional regulation of p53, and p53 family members, by RNA binding proteins and the reciprocal feedback pathways between several RNA-biding proteins modulating p53, and p53 family members.

Indexed as

p53post-transcriptional regulationRbm38RNA-binding proteins (RBPs)

Identifiers

PMID28794999
PMCPMC5546219
OpenAlexW2524267545

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.