Evidence map›Paper›PMID 20700465›Full record

ArticlePloS one2010

Involvement of Caveolin-1 in repair of DNA damage through both homologous recombination and non-homologous end joining.

Hua Zhu, Jingyin Yue, Zui Pan, Hao Wu, Yan Cheng, Huimei Lu, Xingcong Ren, Ming Yao, Zhiyuan Shen, Jin-Ming Yang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 20% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  6. Effect of radiotherapy on the DNA cargo and cellular uptake mechanisms of extracellular vesicles.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023
    Review
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  17. Thymosin β4 impeded murine stem cell proliferation with an intact cardiovascular differentiation.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016
    Article
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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

10 authors at 2 institutions in 1 country.

Hua ZhuDepartment of Pharmacology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, New Jersey, United States of America. zhuhu2@umdnj.edu
Jingyin Yue
Zui Pan
Hao Wu
Yan Cheng
Huimei Lu
Xingcong Ren
Ming Yao
Zhiyuan Shen
Jin-Ming Yang
Johnson University · USPenn State Milton S. Hershey Medical Center · US

Funding

REGULATION OF MULTIDRUG RESISTANCE PHENOTYPER01CA066077 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI YANG, JIN-MING · 1996 to 2007
$1.7M
role of ubiquitinin in cancer progressionR21CA109371 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI YANG, JIN-MING · 2004 to 2005
$385k
NCI NIH HHS CA066077NCI NIH HHS CA109371NCI NIH HHS CA137738NCI NIH HHS R01 CA066077NCI NIH HHS R21 CA109371
6 · The paper itself

Abstract

backgroundCaveolin-1 (Cav-1), the major component of caveolae, is a 21-24 kDa integral membrane protein that interacts with a number of signaling molecules. By acting as a scaffolding protein, Cav-1 plays crucial roles in the regulation of various physiologic and patho-physiologic processes including oncogenic transformation and tumorigenesis, and tumor invasion and metastasis. METHODOLOGY/PRINCIPAL

findingsIn the present study we sought to explore the role of Cav-1 in response to DNA damage and the mechanism involved. We found that the level of Cav-1 was up-regulated rapidly in cells treated with ionizing radiation. The up-regulation of Cav-1 following DNA damage occurred only in cells expressing endogenous Cav-1, and was associated with the activation of DNA damage response pathways. Furthermore, we demonstrated that the expression of Cav-1 protected cells against DNA damage through modulating the activities of both the homologous recombination (HR) and non-homologous end joining (NHEJ) repair systems, as evidenced by the inhibitory effects of the Cav-1-targeted siRNA on cell survival, HR frequency, phosphorylation of DNA-dependent protein kinase (DNA-PK), and nuclear translocation of epidermal growth factor receptor (EGFR) following DNA damage, and by the stimulatory effect of the forced expression of Cav-1 on NHEJ frequency. CONCLUSION/SIGNIFICANCE: Our results indicate that Cav-1 may play a critical role in sensing genotoxic stress and in orchestrating the response of cells to DNA damage through regulating the important molecules involved in maintaining genomic integrity.

Indexed as

DNA DamageDNA RepairRecombination, GeneticAnimalsCaveolin 1Cell Line, TumorDNADNA Breaks, Double-StrandedGene SilencingHumansSignal TransductionUp-RegulationCaveolin 1DNA

Identifiers

PMID20700465
PMCPMC2917373
OpenAlexW2091939702

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.