Evidence map›Paper›PMID 20160506›Full record

ReviewCell cycle (Georgetown, Tex.)2010

Tip60: connecting chromatin to DNA damage signaling.

Yingli Sun, Xiaofeng Jiang, Brendan D Price

Open access · greenAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

122 citing papers in PubMed, 223 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

62 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 1 institution in 1 country.

Yingli SunDivision of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Xiaofeng Jiang
Brendan D Price
Center for Economic and Policy Research · US

Funding

RADIATION BIOLOGY TRAINING PROGRAMT32CA009078 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI D'ANDREA, ALAN D. · 1985 to 2009
$4.6M
RADIATION MODULATION OF THE P53 GENER01CA064585 · NCI · DANA-FARBER CANCER INSTITUTE · PI PRICE, BRENDAN D · 1995 to 2016
$4.6M
Functional Analysis of the Tip60 ComplexR01CA093602 · NCI · DANA-FARBER CANCER INSTITUTE · PI PRICE, BRENDAN D · 2002 to 2018
$4.3M
NCI NIH HHS CA64585NCI NIH HHS CA93602NCI NIH HHS R01 CA064585NCI NIH HHS R01 CA093602NCI NIH HHS T32 CA009078NCI NIH HHS T32 CA09078
6 · The paper itself

Abstract

Cells are constantly exposed to genotoxic events that can damage DNA. To counter this, cells have evolved a series of highly conserved DNA repair pathways to maintain genomic integrity. The ATM protein kinase is a master regulator of the DNA double-strand break (DSB) repair pathway. DSBs activate ATM's kinase activity, promoting the phosphorylation of proteins involved in both checkpoint activation and DNA repair. Recent work has revealed that two DNA damage response proteins, the Tip60 acetyltransferase and the mre11- rad50-nbs1 (MRN) complex, co-operate in the activation of ATM in response to DSBs. MRN functions to target ATM and the Tip60 acetyltransferase to DSBs. Tip60's chromodomain then interacts with histone H3 trimethylated on lysine 9, activating Tip60's acetyltransferase activity and stimulating the subsequent acetylation and activation of ATM's kinase activity. These results underscore the importance of chromatin structure in regulating DNA damage signaling and emphasize how histone modifications co-ordinate DNA repair. In addition, human tumors frequently exhibit altered patterns of histone methylation. This rewriting of the histone methylation code in tumor cells may impact the efficiency of DSB repair, increasing genomic instability and contributing to the initiation and progression of cancer.

Indexed as

DNA Breaks, Double-StrandedDNA RepairAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsChromatinDNA-Binding ProteinsHistone AcetyltransferasesHistonesHumansLysine Acetyltransferase 5MRE11 Homologue ProteinProtein Serine-Threonine KinasesSignal TransductionTumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsChromatinDNA-Binding ProteinsHistone AcetyltransferasesHistonesKAT5 protein, humanLysine Acetyltransferase 5MRE11 Homologue ProteinMRE11 protein, humanProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID20160506
PMCPMC2901859
OpenAlexW2072607093

What OpenQuestion holds

Textmetadata
LicenceTDM
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.