Evidence map›Paper›PMID 20947453›Full record

ArticleDNA repair2011

UV-induced histone H2AX phosphorylation and DNA damage related proteins accumulate and persist in nucleotide excision repair-deficient XP-B cells.

Kyu-Seon Oh, Michael Bustin, Sharlyn J Mazur, Ettore Appella, Kenneth H Kraemer

Abstract read
In one paragraph

Article in DNA repair, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

31 citing papers in PubMed, 59 citations in OpenAlex.

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  15. Oncotarget · 2017
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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.

Kyu-Seon OhDNA Repair Section, Dermatology Branch, CCR, National Cancer Institute, Bethesda, MD 20892, USA.
Michael Bustin
Sharlyn J Mazur
Ettore Appella
Kenneth H Kraemer
National Cancer Institute · US

Funding

DNA Repair in Human Cancer-Prone Genetic DiseasesZIABC004517 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KRAEMER, KENNETH H · 2009 to 2024
$26.5M
Chromosomal Proteins and Chromosomal FunctionsZIABC004496 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BUSTIN, MICHAEL · 2009 to 2023
$12.9M
Regulation and Function of WIP1 Phosphatase and its Role in Tumor CellsZIABC011197 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI APPELLA, ETTORE · 2009 to 2025
$11.5M
Biological Functions of Chromosomal ProteinsZIABC011154 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BUSTIN, MICHAEL · 2009 to 2023
$11.0M
Intramural NIH HHS ZIA BC004517
6 · The paper itself

Abstract

DNA double strand breaks (DSB) may be caused by ionizing radiation. In contrast, UV exposure forms dipyrimidine photoproducts and is not considered an inducer of DSB. We found that uniform or localized UV treatment induced phosphorylation of the DNA damage related (DDR) proteins H2AX, ATM and NBS1 and co-localization of γ-H2AX with the DDR proteins p-ATM, p-NBS1, Rad51 and FANCD2 that persisted for about 6h in normal human fibroblasts. This post-UV phosphorylation was observed in the absence of nucleotide excision repair (NER), since NER deficient XP-B cells (lacking functional XPB DNA repair helicase) and global genome repair-deficient rodent cells also showed phosphorylation and localization of these DDR proteins. Resolution of the DDR proteins was dependent on NER, since they persisted for 24h in the XP-B cells. In the normal and XP-B cells p53 and p21 was detected at 6h and 24h but Mdm2 was not induced in the XP-B cells. Post-UV induction of Wip1 phosphatase was detected in the normal cells but not in the XP-B cells. DNA DSB were detected with a neutral comet assay at 6h and 24h post-UV in the normal and XP-B cells. These results indicate that UV damage can activate the DDR pathway in the absence of NER. However, a later step in DNA damage processing involving induction of Wip1 and resolution of DDR proteins was not observed in the absence of NER.

Indexed as

DNA RepairAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell LineComet AssayDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA DamageFibroblastsFluorescent Antibody Technique, IndirectHistonesHumansMiceMutationAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsH2AX protein, humanHistonesNBN protein, humanNuclear ProteinsPhosphoprotein PhosphatasesPPM1D protein, humanPpm1d protein, mouseProtein Phosphatase 2CProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID20947453
PMCPMC3010519
OpenAlexW2025993893

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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.