A pathway of double-strand break rejoining dependent upon ATM, Artemis, and proteins locating to gamma-H2AX foci.

By E. Riballo, M. Kühne, N. Rief, A. Doherty, G. Smith, M. Recio, C. Reis, Kirsten Dahm, A. Fricke, A. Krempler and 5 more. Molecules and Cells, 2004

921 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/44035f7bfe7a17460e9514b14acfe113e02ca186

How researchers see this paper

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

In Cancer Research

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

In Molecular Biology

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

In Oncology

1. J. Bartek
2. J. Lukas
3. P. Jeggo
4. C. Lukas
5. Yosef Shiloh
6. M. Löbrich
7. M. Lieber
8. M. O’Driscoll

Citations in the corpus

• The Mechanism of Double-Strand DNA Break Repair by the Nonhomologous DNA End Joining Pathway (2010, background): “Follicular lymphomas’ BCL-2/IgH junctions contain templated nucleotide insertions: novel insights into the mechanism of t(14;18) translocation.”
• The role of double-strand break repair — insights from human genetics (2006, background): “There is mounting evidence for an interplay between the damage-response signalling machinery and DNA-repair pathways; recent studies indicate that at least some aspects of HR and NHEJ are regulated in an ATR-dependent or ATM-dependent manne”
• γ-H2AX in recognition and signaling of DNA double-strand breaks in the context of chromatin (2008, background): “Particularly intriguing is also the observation that H2AX is involved in the repair of a subset of DSBs, the repair of which requires, due to some as of yet unidentified reasons, the ATM kinase and the Artemis nuclease (110).”
• Non-homologous DNA end joining and alternative pathways to double-strand break repair (2017, positive): “Follicular lymphomas BCL-2/IgH junctions contain templated nucleotide insertions: novel insights into the mechanism of t(14;18) translocation.”
• Biological consequences of radiation-induced DNA damage: relevance to radiotherapy. (2013, background): “The protein kinase ataxia-telangiectasia mutated (ATM) plays a facilitating step in the repair of a subset (about 10%) of radiation-induced complex DSB [14].”
• ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin. (2008, methodology): “Previously, we used a particles to induce multiply damaged DSBs (Riballo et al., 2004).”
• Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM- and KAP-1 dependent pathway (2006, background): “It has been suggested that the radiosensitivity of A-T cells reflects a subtle defect in DSB repair that leaves a minute fraction of DSBs unseale”
• DNA double-strand break repair: from mechanistic understanding to cancer treatment. (2007, background): “However, it is clear that difficult DSBs require more time for repair [28], which is consistent with the possibility that they are somehow shunted toward homologous recombination.”