A ribonucleotide reductase gene involved in a p53-dependent cell-cycle checkpoint for DNA damage

By Hiroshi Tanaka, H. Arakawa, Tatsuya Yamaguchi, Kenji Shiraishi, S. Fukuda, K. Matsui, Y. Takei, Yusuke Nakamura. Nature, 2000

974 citations recorded by the source corpus.

Subfields: Biotechnology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/02f52188b154454f7685ad5cea5815eafd8b7112

How researchers see this paper

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

In Biotechnology

1. Stephen J. Elledge
2. D. G. Gibson

In Molecular Biology

1. Stephen P. Jackson
2. Stephen J. Elledge
3. Kum Khanna
4. C. Sherr
5. D. Richardson
6. D. Kalinowski
7. J. Bartek
8. J. Lukas

In Oncology

1. Stephen P. Jackson
2. Stephen J. Elledge
3. C. Sherr
4. J. Bartek
5. P. Jeggo
6. J. Lukas
7. R. Weinberg
8. Yosef Shiloh

Citations in the corpus

• The DNA damage response: putting checkpoints in perspective (2000, background): “Blocking p53R2 expression increases cell killing by a variety of DNA-damaging agent”
• Nucleotide Deficiency Promotes Genomic Instability in Early Stages of Cancer Development (2011, neutral): “RRM2B is required for deoxynucleotide biosynthesis during DNA repair (Kimura et al., 2003; Tanaka et al., 2000).”
• The Evolution of Iron Chelators for the Treatment of Iron Overload Disease and Cancer (2005, background): “The p53R2 enzyme is a p53 target gene that has only recently been discovered to be transactivated upon DNA damage (Nakano et al., 2000; Tanaka et al., 2000).”
• Toward maintaining the genome: DNA damage and replication checkpoints. (2002, background): “Checkpoint proteins also regulate dNTP pools, perhaps a common feature involved in DNA repair, since limiting dNTP pools enhances damage sensitivity (183, 210, 231).”
• DNA double-strand breaks: signaling, repair and the cancer connection (2001, background): “Recent evidence for a linkage between these two types of event is provided by the induction of p53R2—a nuclear subunit of ribonucleotide reductase implicated in DNA repair by p53—in response to DNA damag”
• Role of p53 in Cell Death and Human Cancers (2011, neutral): “reductase small subunit (R2) [78].”
• The Pezcoller lecture: cancer cell cycles revisited. (2000, background): “The recent realization that cells lacking a p53-inducible nuclear subunit of ribonucleotide reductase may rely on a cytoplasmic form of this enzyme to resist drug-induced genotoxic damage (115) may provide another opportunity for targeted therapy.”