Evidence map›Paper›PMID 26907686›Full record

ArticleThe Journal of biological chemistry2016

RNA-binding Protein PCBP2 Regulates p73 Expression and p73-dependent Antioxidant Defense.

Cong Ren, Jin Zhang, Wensheng Yan, Yanhong Zhang, Xinbin Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. PCBP2 Regulates p16Aging cell · 2025
    Article
  4. PCBP2 in gastrointestinal cancers: fundamental mechanism and clinical potential.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
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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

5 authors at 1 institution in 1 country.

Cong RenFrom the Comparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 95616.
Jin ZhangFrom the Comparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 95616 jinzhang@ucdavis.edu.
Wensheng YanFrom the Comparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 95616.
Yanhong ZhangFrom the Comparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 95616.
Xinbin ChenFrom the Comparative Oncology Laboratory, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 95616 xbchen@ucdavis.edu.
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
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 DNA polymerase eta in DNA damage response and p53 activationR01CA123227 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2010 to 2014
$1.4M
NCI NIH HHS R01 CA081237NCI NIH HHS R01 CA121137NCI NIH HHS R01 CA123227
6 · The paper itself

Abstract

TAp73, a member of the p53 family tumor suppressors, plays a critical rule in tumor suppression and neuronal development. However, how p73 activity is controlled at the posttranscriptional level is not well understood. Here, we showed that TAp73 activity is regulated by RNA-binding protein PCBP2. Specifically, we found that knockdown or knock-out of PCBP2 reduces, whereas ectopic expression of PCBP2 increases, TAp73 expression. We also showed that PCBP2 is necessary for p73 mRNA stability via the CU-rich elements in p73 3'-UTR. To uncover the biological relevance of PCBP2-regulated TAp73 expression, we showed that ectopic expression of PCBP2 inhibits, whereas knockdown or knock-out of PCBP2 increases, the production of reactive oxygen species (ROS) in a TAp73-dependent manner. Additionally, we found that glutaminase 2 (GLS2), a modulator of p73-dependent antioxidant defense, is also involved in PCBP2-regulated ROS production. Moreover, we generated PCBP2-deficient mice and primary mouse embryonic fibroblasts (MEFs) and showed that loss of PCBP2 leads to decreased p73 expression and, subsequently, increased ROS production and accelerated cellular senescence. Together, our data suggest that PCBP2 regulates p73 expression via mRNA stability and p73-dependent biological function in ROS production and cellular senescence.

Indexed as

3' Untranslated RegionsAnimalsAntioxidantsCellular SenescenceDNA-Binding ProteinsEmbryo, MammalianFibroblastsGene Expression RegulationMiceMice, KnockoutNuclear ProteinsReactive Oxygen SpeciesRNA-Binding ProteinsRNA StabilityTransaminasesTumor Protein p733' Untranslated RegionsAntioxidantsDNA-Binding Proteinsglutamine-pyruvate aminotransferaseNuclear ProteinsPcbp2 protein, mouseReactive Oxygen SpeciesRNA-Binding ProteinsTransaminasesTumor Protein p73Tumor Suppressor Proteinscellular senescencemRNA decayp53p73PCBP2reactive oxygen species (ROS)

Identifiers

PMID26907686
PMCPMC4850300
OpenAlexW2279444834

What OpenQuestion holds

Textmetadata
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.