Evidence map›Paper›PMID 11359916›Full record

ArticleMolecular biology of the cell2001

UV-induced hyperphosphorylation of replication protein a depends on DNA replication and expression of ATM protein.

G G Oakley, L I Loberg, J Yao, M A Risinger, R L Yunker, M Zernik-Kobak, K K Khanna, M F Lavin, M P Carty, K Dixon

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 90 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

10 authors at 2 institutions in 2 countries.

G G OakleyDepartment of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
L I Loberg
J Yao
M A Risinger
R L Yunker
M Zernik-Kobak
K K Khanna
M F Lavin
M P Carty
K Dixon
University of Cincinnati Medical Center · USQIMR Berghofer Medical Research Institute · AU

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI YADAV, JAGJIT S · 1992 to 2022
$35.4M
CELLULAR RESPONSES TO UV-LIGHT IN ATAXIA TELANGIECTASIAR01NS034782 · NINDS · UNIVERSITY OF CINCINNATI · PI DIXON, KATHLEEN · 1997 to 2007
$2.1M
NIEHS NIH HHS P30 ES006096NIEHS NIH HHS P30-ES06096NINDS NIH HHS R01 NS034782NINDS NIH HHS R01-NS34782
6 · The paper itself

Abstract

Exposure to DNA-damaging agents triggers signal transduction pathways that are thought to play a role in maintenance of genomic stability. A key protein in the cellular processes of nucleotide excision repair, DNA recombination, and DNA double-strand break repair is the single-stranded DNA binding protein, RPA. We showed previously that the p34 subunit of RPA becomes hyperphosphorylated as a delayed response (4-8 h) to UV radiation (10-30 J/m(2)). Here we show that UV-induced RPA-p34 hyperphosphorylation depends on expression of ATM, the product of the gene mutated in the human genetic disorder ataxia telangiectasia (A-T). UV-induced RPA-p34 hyperphosphorylation was not observed in A-T cells, but this response was restored by ATM expression. Furthermore, purified ATM kinase phosphorylates the p34 subunit of RPA complex in vitro at many of the same sites that are phosphorylated in vivo after UV radiation. Induction of this DNA damage response was also dependent on DNA replication; inhibition of DNA replication by aphidicolin prevented induction of RPA-p34 hyperphosphorylation by UV radiation. We postulate that this pathway is triggered by the accumulation of aberrant DNA replication intermediates, resulting from DNA replication fork blockage by UV photoproducts. Further, we suggest that RPA-p34 is hyperphosphorylated as a participant in the recombinational postreplication repair of these replication products. Successful resolution of these replication intermediates reduces the accumulation of chromosomal aberrations that would otherwise occur as a consequence of UV radiation.

Indexed as

Ultraviolet RaysAmino Acid SequenceAphidicolinAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell FractionationCell LineCulture Media, Serum-FreeDNA-Binding ProteinsDNA DamageDNA RepairDNA ReplicationEnzyme InhibitorsHumansImmunoblottingMolecular Sequence DataAphidicolinAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsCulture Media, Serum-FreeDNA-Binding ProteinsEnzyme InhibitorsProtein Serine-Threonine KinasesRecombinant ProteinsReplication Protein ARPA1 protein, humanTumor Suppressor Proteins

Identifiers

PMID11359916
PMCPMC34578
OpenAlexW2166989062

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.