Evidence map›Paper›PMID 21057544›Full record

ArticleOncogene2011

p85α mediates p53 K370 acetylation by p300 and regulates its promoter-specific transactivity in the cellular UVB response.

L Song, M Gao, W Dong, M Hu, J Li, X Shi, Y Hao, Y Li, C Huang

Open access · greenAbstract readComparative Study
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

L SongNelson Institute of Environmental Medicine, Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY, USA. lunsong@yahoo.com
M Gao
W Dong
M Hu
J Li
X Shi
Y Hao
Y Li
C Huang
Institute of Basic Medical Sciences of the Chinese Academy of Medical SciencesNew York University · US

Funding

Water/sediment &model &criteria for arsenic &chromeP42ES010344 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX · 2000 to 2010
$15.0M
Molecular Mechanisms of Nickel-Induced TumorigenicityR01CA112557 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, CHUANSHU · 2004 to 2016
$2.9M
Mechanisms of As-Induced CarcinogenesisR01CA119028 · NCI · UNIVERSITY OF KENTUCKY · PI SHI, XIANGLIN · 2006 to 2010
$1.8M
Mechanisms of Tumor Promotion Effects of B[a]PDER01ES012451 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, CHUANSHU · 2004 to 2008
$1.7M
NCI NIH HHS CA112557NCI NIH HHS CA119028-05S110NCI NIH HHS R01 CA112557NCI NIH HHS R01 CA119028NIEHS NIH HHS ES010344NIEHS NIH HHS ES012451NIEHS NIH HHS P42 ES010344NIEHS NIH HHS R01 ES012451
6 · The paper itself

Abstract

Inducible acetylation of p53 at lysine residues has a great impact on regulating the transactivation of this protein, which is associated with cell growth arrest and/or apoptosis under various stress conditions. However, the factor(s) for regulating p53 acetylation remains largely unknown. In the current study, we have shown that p85α, the regulatory subunit of phosphatidylinositol-3-kinase, has a critical role in mediating p53 acetylation and promoter-specific transactivation in the ultraviolet B (UVB) response. Depletion of p85α in mouse embryonic fibroblasts significantly impairs UVB-induced apoptosis, as well as p53 transactivation and acetylation at Lys370 (Lys373 of human p53); however, the accumulation, nuclear translocation and phosphorylation of p53 are not affected. Interestingly, p85α binds to p300, promotes the p300-p53 interaction and the subsequent recruitment of the p53/p300 complex to the promoter region of the specific p53 target gene in response to UVB irradiation. Moreover, ablation of p53 acetylation at Lys370 by site-directed mutagenesis dramatically suppresses UVB-induced expression of the specific p53-responsive gene as well as cell apoptosis. Therefore, we conclude that p85α is a novel regulator of p53-mediated response under certain stress conditions, and targeting the p85α-dependent p53 pathway may be promising for cancer therapy.

Indexed as

Genes, p53Ultraviolet RaysAcetylationAnimalsApoptosisCell CycleCell LineCell ProliferationClass Ia Phosphatidylinositol 3-KinaseE1A-Associated p300 ProteinHumansMiceMutagenesis, Site-DirectedPhosphorylationProtein Processing, Post-TranslationalTranscriptional ActivationClass Ia Phosphatidylinositol 3-KinaseE1A-Associated p300 ProteinEP300 protein, human

Identifiers

PMID21057544
PMCPMC3761396
OpenAlexW2020736452

What OpenQuestion holds

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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.