Evidence map›Paper›PMID 23708966›Full record

ArticleNature2013

KAT5 tyrosine phosphorylation couples chromatin sensing to ATM signalling.

Abderrahmane Kaidi, Stephen P Jackson

RetractedAbstract readRetracted Publication
In one paragraph

Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
13.0field-weighted citation impact, top 1% 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

106 citing papers in PubMed, 161 citations in OpenAlex.

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46 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Abderrahmane KaidiThe Gurdon Institute and Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.
Stephen P Jackson
University of Cambridge · GBWellcome Sanger Institute · GB

Funding

Cancer Research UK 11224Cancer Research UK A11224Cancer Research UK C6/A11224European Research Council 268536Wellcome Trust 092096
6 · The paper itself

Abstract

The detection of DNA lesions within chromatin represents a critical step in cellular responses to DNA damage. However, the regulatory mechanisms that couple chromatin sensing to DNA-damage signalling in mammalian cells are not well understood. Here we show that tyrosine phosphorylation of the protein acetyltransferase KAT5 (also known as TIP60) increases after DNA damage in a manner that promotes KAT5 binding to the histone mark H3K9me3. This triggers KAT5-mediated acetylation of the ATM kinase, promoting DNA-damage-checkpoint activation and cell survival. We also establish that chromatin alterations can themselves enhance KAT5 tyrosine phosphorylation and ATM-dependent signalling, and identify the proto-oncogene c-Abl as a mediator of this modification. These findings define KAT5 tyrosine phosphorylation as a key event in the sensing of genomic and chromatin perturbations, and highlight a key role for c-Abl in such processes.

Indexed as

Signal TransductionAmino Acid SequenceAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle CheckpointsCell Cycle ProteinsCell LineCell SurvivalChromatinDNA-Binding ProteinsDNA DamageEnzyme ActivationHeLa CellsHistone AcetyltransferasesHistonesHumansAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsChromatinDNA-Binding ProteinsHistone AcetyltransferasesHistonesKAT5 protein, humanLysineLysine Acetyltransferase 5MAS1 protein, humanPhosphotyrosineProtein Serine-Threonine KinasesProto-Oncogene MasProto-Oncogene Proteins c-ablTumor Suppressor Proteins

Identifiers

PMID23708966
PMCPMC3859897
OpenAlexW2045041347

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.