ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin.

By A. Goodarzi, Angela T. Noon, D. Deckbar, Y. Ziv, Yosef Shiloh, M. Löbrich, P. Jeggo. Molecules and Cells, 2008

902 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4944789aaaf163b021a7448d1864f1f2b9495997

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. S. Polo
3. J. Coates
4. G. Iliakis
5. Wenqi Wu
6. L. Zou
7. Alexandre Maréchal
8. A. Kinner

Citations in the corpus

• Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications. (2011, background): “Notably, the gH2AX foci that persist longest after damage in mammalian cells generally localize at the periphery of heterochromatin domains, suggesting that heterochromatic DSBs are refractory to repair; indeed, it has been shown that this gH2AX persistence can be alleviated by depletion of heteroch”
• γ-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin (2008, background): “Notably, a recent report postulates that ATM signaling temporarily perturbs heterochromatin via KAP-1 to facilitate DSB repair in these rather inaccessible regions of chromatin (132).”
• 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”
• 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].”
• Human HDAC1 and HDAC2 function in the DNA-damage response to promote DNA non-homologous end-joining (2010, positive): “We cannot rule out the possibility that, as well as deacetylating histones, HDAC1 and HDAC2 more directly influence DSB repair by targeting NHEJ factors themselves or other regulators, such as ATM, that might be important for NHEJ in particular chromatin context”
• DNA damage sensing by the ATM and ATR kinases. (2013, background): “…Chk2 by DNA ends leads to phosphorylation of KAP-1 and dissociation of heterochromatin protein HP1-b from H3K9me3 around DSBs, which may expose the histone mark to Tip60 and further stimulate the function of ATM in heterochromatin (Ayoub et al. 2008; Goodarzi et al. 2008; Bolderson et al. 2012).”
• Effects of Ionizing Radiation on Biological Molecules—Mechanisms of Damage and Emerging Methods of Detection (2014, background): “, Chk1/2 and p53), ATM mediates the phosphorylation of Kap1, promoting heterochromatin relaxation and increasing the efficiency of DNA repair (127, 250).”