Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM- and KAP-1 dependent pathway

By Y. Ziv, D. Bielopolski, Y. Galanty, C. Lukas, Y. Taya, D. C. Schultz, J. Lukas, Simon Bekker-Jensen, J. Bartek, Yosef Shiloh. Nature Cell Biology, 2006

774 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/67ca0ff7321df0647d0c406ed27a0bc864465bb2

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Stephen P. Jackson
2. J. Bartek
3. J. Lukas
4. Yosef Shiloh
5. P. Jeggo
6. C. Lukas
7. M. Löbrich
8. Dana Branzei

In Oncology

1. Stephen P. Jackson
2. J. Bartek
3. J. Lukas
4. Yosef Shiloh
5. P. Jeggo
6. M. Löbrich
7. C. Lukas
8. M. Foiani

Citations in the corpus

• Repair of strand breaks by homologous recombination. (2013, background): “It is interesting to note that increased mobility is not associated with a higher coefficient of diffusion, suggesting that global changes in the properties of chromatin after damage (Kruhlak et al. 2006; Ziv et al. 2006) may affect the movement of chromosomal loci.”
• ATM Activation by Oxidative Stress (2010, background): “At the same time we also failed to detect the phosphorylation of heterochromatin protein Kap1, which was shown to be an ATM substrate upon IR or NCS treatment [36, 109].”
• ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin. (2008, methodology): “Based upon these data and previous work (Lavin et al., 2005; Ziv et al., 2006), we propose the following model.”
• DNA damage checkpoints: from initiation to recovery or adaptation. (2007, background): “The increased local concentration of ATM is important to boost phosphorylation of ATM targets, including pan-nuclear signal messengers such as the Chk2 kinase and the Kap1 protein, the latter of which is implicated in the regulation of global chromatin compaction [4,23].”
• The DNA-damage response in human biology and disease (2009, background): “Notably, ATM activation leads to chromatin relaxation at sites of DSBs 32 , and H2AX tyrosine 142 phosphorylation was recently shown tofunctionintheDDR 33,34 .”
• 53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress (2011, methodology): “To exclude unwanted effects of prolonged siRNA treatment, we exploited an observation that an induction of DSBs by clastogens such as neocarzinostati”
• Regulation of DNA repair throughout the cell cycle (2008, background): “As a more general response to DSBs, ATM phosphorylation of KAP1 promotes chromatin relaxatio”
• An ATM-Dependent Transcriptional Silencing Program is Transmitted Through Chromatin in Cis to DNA Double Strand Breaks (2010, background): “ATM Is Required for Transcriptional Silencing and Accumulation of Hypophosphorylated RNA Polymerase II at DSBs ATM has been implicated in multiple DNA damage responses, including global alterations to both chromatin structure and transcriptional programs (Bredemeyer et al., 2008; Goodarzi et al., 20”