Evidence map›Paper›PMID 30032309›Full record

ArticleNucleic acids research2018

Mechanistic insights into the regulation of transcription and transcription-coupled DNA repair by Cockayne syndrome protein B.

Erica L Boetefuer, Robert J Lake, Hua-Ying Fan

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Topology Resetting During Transcription-Coupled Nucleotide Excision Repair.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Nucleotide excision repair: a versatile and smart toolkit.Acta biochimica et biophysica Sinica · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Heterochromatin: an epigenetic point of view in aging.Experimental & molecular medicine · 2020
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
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 1 country.

Erica L BoetefuerDepartment of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Robert J LakeDepartment of Internal Medicine, Division of Molecular Medicine, Program in Cancer Genetics, Epigenetics and Genomics, University of New Mexico Comprehensive Cancer Center, Albuquerque, NM 87131, USA.
Hua-Ying FanDepartment of Internal Medicine, Division of Molecular Medicine, Program in Cancer Genetics, Epigenetics and Genomics, University of New Mexico Comprehensive Cancer Center, Albuquerque, NM 87131, USA.
University of New Mexico · USUniversity of Pennsylvania · US

Funding

WOMEN'S CANCERS RESEARCH PROGRAMP30CA118100 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Yolanda Sanchez · 2005 to 2026
$57.1M
TRAINING PROGRAM IN CELL AND MOLECULAR BIOLOGYT32GM007229 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BARTOLOMEI, MARISA S. · 1985 to 2023
$14.0M
Basis for Distinct Functions of ATP-Dependent Chromatin Remodeling ComplexesR01GM084983 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI FAN, HUA-YING · 2008 to 2012
$1.6M
Basis for genotoxic stress relief by ATP-dependent chromatin remodelersR01GM115888 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI FAN, HUA-YING · 2015 to 2018
$1.2M
NCI NIH HHS P30 CA118100NIGMS NIH HHS R01 GM084983NIGMS NIH HHS R01 GM115888NIGMS NIH HHS T32 GM007229
6 · The paper itself

Abstract

Cockayne syndrome protein B (CSB) is a member of the SNF2/SWI2 ATPase family and is essential for transcription-coupled nucleotide excision DNA repair (TC-NER). CSB also plays critical roles in transcription regulation. CSB can hydrolyze ATP in a DNA-dependent manner, alter protein-DNA contacts and anneal DNA strands. How the different biochemical activities of CSB are utilized in these cellular processes have only begun to become clear in recent years. Mutations in the gene encoding CSB account for majority of the Cockayne syndrome cases, which result in extreme sun sensitivity, premature aging features and/or abnormalities in neurology and development. Here, we summarize and integrate recent biochemical, structural, single-molecule and somatic cell genetic studies that have advanced our understanding of CSB. First, we review studies on the mechanisms that regulate the different biochemical activities of CSB. Next, we summarize how CSB is targeted to regulate transcription under different growth conditions. We then discuss recent advances in our understanding of how CSB regulates transcription mechanistically. Lastly, we summarize the various roles that CSB plays in the different steps of TC-NER, integrating the results of different studies and proposing a model as to how CSB facilitates TC-NER.

Indexed as

Adenosine TriphosphateCockayne SyndromeDNADNA HelicasesDNA RepairDNA Repair EnzymesGene Expression RegulationHumansMutationPoly-ADP-Ribose Binding ProteinsSchizosaccharomycesTranscription, GeneticAdenosine TriphosphateDNADNA HelicasesDNA Repair EnzymesERCC6 protein, humanPoly-ADP-Ribose Binding Proteins

Identifiers

PMID30032309
PMCPMC6125617
OpenAlexW2884110922

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.