Interfaces Between the Detection, Signaling, and Repair of DNA Damage

By J. Rouse, Stephen P. Jackson. Science, 2002

735 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/0e3407b709a3028635c7f55485057c5021bce3a6

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. M. Lieber
5. Yosef Shiloh
6. C. Lukas
7. J. R. Chapman
8. J. Falck

In Oncology

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

Citations in the corpus

• Regulation and mechanisms of mammalian double-strand break repair (2003, background): “…signaling in mammalian cells (Petrini et al., 1997; Kanaar et al., 1998; Dasika et al., 1999; Schmidt-Ullrich et al., 2000; Durocher and Jackson, 2001; Jackson, 2001; Johnson and Jasin, 2001; Khanna and Jackson, 2001; Thompson and Schild, 2001; Daboussi et al., 2002; Rouse and Jackson, 2002).”
• Mechanism and regulation of human non-homologous DNA end-joining (2003, background): “For more abundant DSBs or for lesions that require more time to repair, it will be interesting to understand how this is integrated with other cellular processes, such as DNA replication or transcriptio”
• Identification and Characterization of a Novel and Specific Inhibitor of the Ataxia-Telangiectasia Mutated Kinase ATM (2004, background): “The cellular response to DNA damage is one of coordinated repair and moderation of proliferation (1).”
• Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage (2005, methodology): “b, Complemented NBS-ILB1 cells were pre-incubated with DMSO (2) or specific inhibitors of ATM (ATMi) or DNA-PKcs (DNA-PKi), irradiated with 2 Gy of ionizing radiation, and 1 h later, extracts were prepared and immunoblotted as indicated.”
• Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaks (2003, background): “The cellular response to DNA damage includes the accumulation of signalling–repair complexes into IRIF, which contain hundreds to thousands of proteins sequestered in the vicinity of a DS”
• ATM and related protein kinases: safeguarding genome integrity (2003, background): “Researchers are becoming aware, however, that the DNA-damage response is considerably broader than DNA repair, and actually encompasses additional processe”
• Checking on DNA damage in S phase (2004, background): “Once recruited, MDC1 serves as a molecular bridge between the DSB-flanking chromatin and NBS1 — the core component of the MRN complex that is critical for the detection, processing, signalling and repair of DSB”
• DNA damage response and cellular senescence in tissues of aging mice (2009, background): “This response is characterized by the activation of Ataxia Telangiectasia Mutated (ATM) and RAD-3 related kinase (ATR) (Rouse & Jackson, 2002) being recruited to the site of damage and leading to phosphorylation of Ser-139 of histone H2A.”
• The genetics and genomics of cancer (2003, background): “Somatic genetic changes in cancer cells A cardinal feature of almost all cancer cells is genomic instability (reviewed in refs”
• DNA helicases Sgs1 and BLM promote DNA double-strand break resection. (2008, background): “To survive DSB exposure and maximize genome stability, cells possess a complex machinery to detect DSBs, signal their presence, and mediate their repair (Zhou and Elledge 2000; Rouse and Jackson 2002; Lisby and Rothstein 2004; Wyman and Kanaar 2006).”