Evidence map›Paper›PMID 20122405›Full record

ArticleMolecular cell2010

UV-induced association of the CSB remodeling protein with chromatin requires ATP-dependent relief of N-terminal autorepression.

Robert J Lake, Anastasia Geyko, Girish Hemashettar, Yu Zhao, Hua-Ying Fan

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

73 citing papers in PubMed, 100 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. 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
  6. Article
  7. High UV damage and low repair, but not cytosine deamination, stimulate mutation hotspots at ETS binding sites in melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Impacts of arsenic on Rad18 and translesion synthesis.Toxicology and applied pharmacology · 2022
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

13 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

5 authors at 1 institution in 1 country.

Robert J LakeEpigenetics and Progenitor Cells Keystone Program, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
Anastasia Geyko
Girish Hemashettar
Yu Zhao
Hua-Ying Fan
Fox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
Basis for Distinct Functions of ATP-Dependent Chromatin Remodeling ComplexesR01GM084983 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI FAN, HUA-YING · 2008 to 2012
$1.6M
NCI NIH HHS CA 006927NCI NIH HHS P30 CA006927NIGMS NIH HHS GM 084983NIGMS NIH HHS R01 GM084983
6 · The paper itself

Abstract

The ATP-dependent chromatin remodeler CSB is essential for transcription-coupled DNA repair, and mutations in CSB lead to Cockayne syndrome. Here, we examined the recruitment of CSB to chromatin after ultraviolet (UV) irradiation and uncovered a regulatory mechanism that ensures the specific association of this remodeler with chromatin. We demonstrate that ATP hydrolysis by CSB is essential for stable CSB-chromatin association after UV irradiation and that defects in this association underlie some forms of Cockayne syndrome. We also show that the N-terminal region of CSB negatively regulates chromatin association during normal cell growth. Of interest, in the absence of the negative regulatory region, ATP hydrolysis becomes dispensable for chromatin association, indicating that CSB uses energy from ATP hydrolysis to overcome the inhibitory effect imposed by its N-terminal region. Together, our results suggest that the recruitment of CSB to lesion-stalled transcription is an ATP-dependent process and involves a gross conformational change of CSB.

Indexed as

Ultraviolet RaysAdenosine TriphosphatasesAdenosine TriphosphateChromatinChromatin Assembly and DisassemblyCockayne SyndromeDNA HelicasesDNA Repair EnzymesHumansModels, GeneticPoly-ADP-Ribose Binding ProteinsAdenosine TriphosphatasesAdenosine TriphosphateChromatinDNA HelicasesDNA Repair EnzymesERCC6 protein, humanPoly-ADP-Ribose Binding Proteins

Identifiers

PMID20122405
PMCPMC2818792
OpenAlexW2052978365

What OpenQuestion holds

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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.