The DNA damage response: ten years after.
By J. Harper, Stephen J. Elledge. Molecules and Cells, 2007
1,755 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/505f0f7be9bb3b8ebf3a2139f5a8d94a2286997c
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
- Ryuji Hamamoto
- Yusuke Nakamura
- Stephen P. Jackson
- D. Hanahan
- J. Coates
- S. Polo
- R. Weinberg
- Alberto Ciccia
In Oncology
- D. Hanahan
- Stephen P. Jackson
- Stephen J. Elledge
- R. Weinberg
- J. Coates
- S. Polo
- Alberto Ciccia
- J. O’Sullivan
Citations in the corpus
- Hallmarks of cancer: the next generation. (2011, positive): “The telomeres, composed of multiple tandem hexanucleotide repeats, shorten progressively in nonimmortalized cells propagated in culture, eventually losing the ability to protect the ends of chromosomal DNAs from end-to-end fusions; such fusions generate unstable dicentric chromosomes whose resolutio”
- Targeting Suppressor of Variegation 3-9 Homologue 2 (SUV39H2) in Acute Lymphoblastic Leukemia (ALL) (2015, background): “Phosphorylated histone H2AX (γ-H2AX) is associated with activation of DNA-damage repair pathways and enhanced radio and chemoresistance of cancer cells [21–25].”
- Radiation-induced bystander signalling in cancer therapy (2009, positive): “This has included exhaustive study of the DNA damage sensing and signalling pathways underpinning the DNA damage response that is present in cellular system”
- Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, positive): “Mutations in genes of this pathway result in increased sensitivity to DNA damage (Harper and Elledge, 2007).”
- Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “Once DSBs are generated, ataxia telangiectasia mutated (ATM) is recruited by the MRE-11-Rad50-NBS1 (MRN) complex to sites of broken DNA and phosphorylates downstream substrates such as checkpoint kinase 2 (Chk2) and p53 [175, 178] (Figure 3).”
- Effects of Ionizing Radiation on Biological Molecules—Mechanisms of Damage and Emerging Methods of Detection (2014, background): “The principal proteins implicated as sensors and transducers of DNA damage include the Mre11–Rad50–Nbs1 complex, BRCA1/2 proteins, ATM/ATR, DNA-dependent protein kinase (DNAPK), checkpoint kinases 1/2 (Chk1/2), and poly(ADP-ribose) polymerase (143, 265, 297, 342, 364, 365).”
- Human HDAC1 and HDAC2 function in the DNA-damage response to promote DNA non-homologous end-joining (2010, positive): “1899" language="eng" relation="no"> Because DNA damage represents a formidable challenge to the integrity of genetic material, cells have evolved multifaceted systems, collectively termed the DNA-damage response (DDR), to detect, signal and repair various types of DNA damag”
- A vertebrate gene, ticrr, is an essential checkpoint and replication regulator. (2010, background): “In addition to the core replication machinery, multiple checkpoint pathways exist to protect cells from DNA damage arising from replication errors and/or genotoxins (Bartek et al. 2004; Harper and Elledge 2007).”
- Transcription-coupled DNA repair: two decades of progress and surprises (2008, background): “The cellular 'toolbox' of responses to genomic stress includes checkpoints that result in arrested cell cycle progression, stabilization of DNA at blocked replication forks and recruitment of DNA repair enzymes, to facilitate progression of DNA and RNA synthesi”
- Sequential Application of Anti-Cancer Drugs Enhances Cell Death by Re-wiring Apoptotic Signaling Networks (2012, background): “…understanding of this process suggests that the DNA damage response (DDR) functions as part of a complex network controlling many cellular functions, including cell cycle, DNA repair, and various forms of 780 Cell 149, 780–794, May 11, 2012 ª2012 Elsevier Inc. cell death (Harper and Elledge, 2007).”