Evidence map›Paper›PMID 21193487›Full record

ArticleNucleic acids research2011

Regulation of nucleotide excision repair activity by transcriptional and post-transcriptional control of the XPA protein.

Tae-Hong Kang, Joyce T Reardon, Aziz Sancar

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

74 citing papers in PubMed, 122 citations in OpenAlex.

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  13. Epigenetic Regulation of Nucleotide Excision Repair.Frontiers in cell and developmental biology · 2022
    Review
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14 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Tae-Hong KangDepartment of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
Joyce T Reardon
Aziz Sancar
Dong-A University · KRUniversity of North Carolina at Chapel Hill · US

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa A. Troester · 2001 to 2026
$36.3M
STRUCTURE AND FUNCTION OF UVRABC EXCISION NUCLEASER01GM032833 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SANCAR, AZIZ · 1985 to 2015
$8.9M
STRUCTURE/FUNCTION OF DNA PHOTOLYASER01GM031082 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SANCAR, AZIZ · 1985 to 2015
$4.9M
STRUCTURE/FUNCTION OF DNA PHOTOLYASER37GM031082 · NIGMS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI SANCAR, AZIZ · 1995 to 2004
$2.6M
NIEHS NIH HHS P30 ES010126NIGMS NIH HHS GM31082NIGMS NIH HHS GM32833NIGMS NIH HHS R01 GM031082NIGMS NIH HHS R01 GM032833NIGMS NIH HHS R37 GM031082
6 · The paper itself

Abstract

The XPA (Xeroderma pigmentosum A) protein is one of the six core factors of the human nucleotide excision repair system. In this study we show that XPA is a rate-limiting factor in all human cell lines tested, including a normal human fibroblast cell line. The level of XPA is controlled at the transcriptional level by the molecular circadian clock and at the post-translational level by a HECT domain family E3 ubiquitin ligase called HERC2. Stabilization of XPA by downregulation of HERC2 moderately enhances excision repair activity. Conversely, downregulation of XPA by siRNA reduces excision repair activity in proportion to the level of XPA. Ubiquitination and proteolysis of XPA are inhibited by DNA damage that promotes tight association of the protein with chromatin and its dissociation from the HERC2 E3 ligase. Finally, in agreement with a recent report, we find that XPA is post-translationally modified by acetylation. However, contrary to the previous claim, we find that in mouse liver only a small fraction of XPA is acetylated and that downregulation of SIRT1 deacetylase in two human cell lines does not affect the overall repair rate. Collectively, the data reveal that XPA is a limiting factor in excision repair and that its level is coordinately regulated by the circadian clock, the ubiquitin-proteasome system and DNA damage.

Indexed as

DNA RepairAcetylationAnimalsCell LineCircadian ClocksDNA DamageFibroblastsHumansMiceTranscription, GeneticUbiquitinationUbiquitin-Protein LigasesXeroderma Pigmentosum Group A ProteinUbiquitin-Protein LigasesXeroderma Pigmentosum Group A ProteinXPA protein, human

Identifiers

PMID21193487
PMCPMC3082913
OpenAlexW2116594363

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.