Evidence map›Paper›PMID 22902626›Full record

ArticleThe Journal of biological chemistry2012

KIAA1530 protein is recruited by Cockayne syndrome complementation group protein A (CSA) to participate in transcription-coupled repair (TCR).

Jia Fei, Junjie Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

37 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
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  9. The ARK2N-CK2 complex initiates transcription-coupled repair through enhancing the interaction of CSB with lesion-stalled RNAPII.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
  11. Nucleotide excision repair: a versatile and smart toolkit.Acta biochimica et biophysica Sinica · 2022
    Review
  12. Article
  13. Article
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  16. Review
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  19. Article
  20. The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019
    Review
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

2 authors at 2 institutions in 1 country.

Jia FeiDepartment of Experimental Radiation Oncology, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030.
Junjie ChenDepartment of Experimental Radiation Oncology, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030. Electronic address: jchen8@mdanderson.org.
Radiation Oncology Associates · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS CA016672NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

Transcription-coupled repair (TCR) is the major pathway involved in the removal of UV-induced photolesions from the transcribed strand of active genes. Two Cockayne syndrome (CS) complementation group proteins, CSA and CSB, are important for TCR repair. The molecular mechanisms by which CS proteins regulate TCR remain elusive. Here, we report the characterization of KIAA1530, an evolutionarily conserved protein that participates in this pathway through its interaction with CSA and the TFIIH complex. We found that UV irradiation led to the recruitment of KIAA1530 onto chromatin in a CSA-dependent manner. Cells lacking KIAA1530 were highly sensitive to UV irradiation and displayed deficiency in TCR. In addition, KIAA1530 depletion abrogated stability of the CSB protein following UV irradiation. More excitingly, we found that a unique CSA mutant (W361C), which was previously identified in a patient with UV(s)S syndrome, showed defective KIAA1530 binding and resulted in a failure of recruiting KIAA1530 and stabilizing CSB after UV treatment. Together, our data not only reveal that KIAA1530 is an important player in TCR but also lead to a better understanding of the molecular mechanism underlying UV(s)S syndrome.

Indexed as

DNA RepairTranscription, GeneticAmino Acid SubstitutionCarrier ProteinsDNA Repair EnzymesHEK293 CellsHumansMutation, MissensePhotosensitivity DisordersProtein StabilitySyndromeTranscription FactorsUltraviolet RaysCarrier ProteinsDNA Repair EnzymesERCC8 protein, humanTranscription FactorsUVSSA protein, human

Identifiers

PMID22902626
PMCPMC3471710
OpenAlexW2013671885

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.