The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
KAT5 tyrosine phosphorylation couples chromatin sensing to ATM signalling
Open accessAbstract
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“H3K9me3 is required for activation of the Tip60 acetyltransferase (4, 17).”
From DNA double-strand breaks promote methylation of histone H3 on lysine 9 and transient formation of repressive chromatin (2014) · cites this paper as [17]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Consequently, loss of H3K9me2/3 leads to failure to activate the ATM signaling pathway, loss of H4 acetylation during DSB repair, disruption of heterochromatin, genomic instability, and defective DSB repair (4,(17)(18)(19).”
From DNA double-strand breaks promote methylation of histone H3 on lysine 9 and transient formation of repressive chromatin (2014) · cites this paper as [17]
Experimental — accuracy not yet measuredIn the citing paper
“phosphorylation enhances the acetyltransferase activity of TIP60, and this modification can be induced by chromatin alterations, leading to ATM signaling independently of DNA breaks”
From Activation of DNA Damage Response Signaling by Condensed Chromatin (2014) · cites this paper as Kaidi and Jackson, 2013
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
The DNA-damage response in human biology and disease
Jackson, S. P., & Bartek, J. (2009) · Nature · doi:10.1038/nature08467 · Cited by 6,092
Self-citationGenome-wide maps of chromatin state in pluripotent and lineage-committed cells
Mikkelsen, T. S., Ku, M., Jaffe, D. B., Issac, B., Lieberman, E., Giannoukos, G., Alvarez, P., Brockman, W., Kim, T.-K., Koche, R. P., et al. (2007) · Nature · doi:10.1038/nature06008 · Cited by 4,129
DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation
Bakkenist, C. J., & Kastan, M. B. (2003) · Nature · doi:10.1038/nature01368 · Cited by 3,466
The DNA Damage Response: Ten Years After
Harper, J. W., & Elledge, S. J. (2007) · Molecular Cell · doi:10.1016/j.molcel.2007.11.015 · Cited by 1,705
ATM Activation by DNA Double-Strand Breaks Through the Mre11-Rad50-Nbs1 Complex
Lee, J.-H., & Paull, T. T. (2005) · Science · doi:10.1126/science.1108297 · Cited by 1,424
Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage
Falck, J., Coates, J., & Jackson, S. P. (2005) · Nature · doi:10.1038/nature03442 · Cited by 1,304
Self-citationHickson, I., Zhao, Y., Richardson, C. J., Green, S. J., Martin, N. M. B., Orr, A. I., Reaper, P. M., Jackson, S. P., Curtin, N. J., & Smith, G. C. M. (2004) · Cancer Research · doi:10.1158/0008-5472.can-04-2727 · Cited by 1,220
Self-citationLamin A-dependent nuclear defects in human aging
Scaffidi, P., & Misteli, T. (2006) · Science · doi:10.1126/science.1127168 · Cited by 1,125
Requirement of the MRN complex for ATM activation by DNA damage
Uziel, T., Lerenthal, Y., Moyal, L., Andegeko, Y., Mittelman, L., & Shiloh, Y. (2003) · The EMBO Journal · doi:10.1093/emboj/cdg541 · Cited by 1,075
Buchdunger, E., Zimmermann, J., Mett, H., Meyer, T., Müller, M., Druker, B. J., & Lydon, N. (1996) · PubMed · Cited by 1,057
Cited by
Sorted by citations
ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response
Blackford, A. N., & Jackson, S. P. (2017) · Molecular Cell · doi:10.1016/j.molcel.2017.05.015 · Cited by 2,050
Self-citationPaull, T. T. (2015) · Annual Review of Biochemistry · doi:10.1146/annurev-biochem-060614-034335 · Cited by 492
Ayrapetov, M. K., Gursoy-Yuzugullu, O., Xu, C., Xu, Y., & Price, B. D. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1403565111 · Cited by 391
The epigenetics of aging and neurodegeneration
Lardenoije, R., Iatrou, A., Kenis, G., Kompotis, K., Steinbusch, H. W. M., Mastroeni, D., Coleman, P., Lemere, C. A., Hof, P. R., van den Hove, D. L. A., et al. (2015) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2015.05.002 · Cited by 381
Quantitative Proteomic Atlas of Ubiquitination and Acetylation in the DNA Damage Response
Elia, A. E. H., Boardman, A. P., Wang, D. C., Huttlin, E. L., Everley, R. A., Dephoure, N., Zhou, C., Koren, I., Gygi, S. P., & Elledge, S. J. (2015) · Molecular Cell · doi:10.1016/j.molcel.2015.05.006 · Cited by 341
Metadata
- Authors
- Kaidi, A., & Jackson, S. P.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Jackson, Stephen P.
- Venue
- Nature
- Published
- 2013-05-26
- Volume
- 498
- Issue
- 7452
- Pages
- 70-74
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3859897
- OpenAlex
- W2045041347
- Cited by
- 167
- References
- 35
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 15 · 2018: 27 · 2017: 21 · 2016: 26 · 2015: 32 · 2014: 20 · 2013: 12
- FWCI
- 13.43
- Type
- journal article
- Language
- en
- Status
- Retracted
- Update notices
- retraction (2019-04-11)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Bristol Research (University of Bristol) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Wellcome Trust (WT092096, 092096)
- Cancer Research UK (C6/A11224, 11224, A11224)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- KAT5, Tip60, tyrosine phosphorylation, c-Abl, ATM kinase, H3K9me3, histone acetylation, DNA damage checkpoint, DNA double-strand breaks, histone acetyltransferase
- MeSH terms
- Lysine Acetyltransferase 5, Proto-Oncogene Mas, Amino Acid Sequence, Animals, Cell Line, Cell Survival, Chromatin, DNA Damage, DNA-Binding Proteins, Enzyme Activation, HeLa Cells, Histones, Humans, Lysine, Methylation, Molecular Sequence Data, Phosphorylation, Signal Transduction, Proto-Oncogene Proteins c-abl, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Phosphotyrosine, Tumor Suppressor Proteins, Histone Acetyltransferases, Cell Cycle Checkpoints, Ataxia Telangiectasia Mutated Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
