PARP is activated at stalled forks to mediate Mre11‐dependent replication restart and recombination

By H. Bryant, E. Petermann, N. Schultz, A. Jemth, O. Loseva, N. Issaeva, F. Johansson, Serena Fernandez, P. McGlynn, Thomas Helleday. EMBO Journal, 2009

627 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/8b9f1f64cf35a255bf53885ca17cf086a1277804

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. Alberto Ciccia
2. L. Marácz
3. Stephen J. Elledge
4. Thomas Helleday
5. F. Grin
6. N. Pokorn
7. A. Bowie
8. S. Paludan

In Oncology

1. Alberto Ciccia
2. L. Marácz
3. Stephen J. Elledge
4. Thomas Helleday
5. F. Grin
6. N. Pokorn

Citations in the corpus

• PARP Inhibitors: Clinical Relevance, Mechanisms of Action and Tumor Resistance (2020, background): “Replication Fork Stalling and PARP Trapping It is well recognized that PARP activation is required at the site of stalled replication forks to facilitate MRE11-mediated restart of replication (Bryant et al., 2009; Koppensteiner et al., 2014).”
• Chapter 1. General introduction (2015, positive): “Parp1 regulates the activity of Pol β in long patch BER (89) and interacts with Mre11 for end processing in the restart of replication forks (90), suggesting that Pol β and MRN”
• The PARP Side of the Nucleus: Molecular Actions, Physiological Outcomes, and Clinical Targets (2010, neutral): “Based on studies in animal models, PARP-1 has been implicated in development, the function of the immune and nervous systems, aging, and cancer, all of which have been reviewed in detail previously (Beneke and Burkle, 2004; Burkle et al., 2004; Kim et al., 2005; Peralta-Leal et al., 2008).”
• The underlying mechanism for the PARP and BRCA synthetic lethality: Clearing up the misunderstandings (2011, background): “Although PARP-2 has been suggested to play a role in BER together with PARP1 (Schreiber et al., 2002), other reports suggest only a minor role for PARP-2 in SSBR (Fisher et al., 2007) and potentially amore important role in replication repair (Bryant et al., 2009).”
• The DNA Damage Response: Making it safe to play with knives (2010, background): “DNA end resection is regulated by ATM through CtIP, which interacts with BRCA1 and MRN in the BRCA1-C complex (Figure 2B) (Huen et al., 2010b).”