Checking on DNA damage in S phase

By J. Bartek, C. Lukas, J. Lukas. Nature reviews. Molecular cell biology, 2004

801 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e7078238b35d812514e9466f8d18936a820c0774

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. Stephen J. Elledge
4. Marcos Malumbres
5. M. Barbacid
6. C. Lukas
7. Ji Luo
8. M. Kastan

In Molecular Biology

1. J. Bartek
2. J. Lukas
3. C. Lukas
4. Marcos Malumbres
5. Stephen J. Elledge
6. M. Barbacid
7. Stephen P. Jackson
8. M. Kastan

Citations in the corpus

• A vertebrate gene, ticrr, is an essential checkpoint and replication regulator. (2010, background): “Two of these pathways function during DNA replication: The intraS-phase checkpoint stabilizes existing replication forks while inhibiting firing of late origins, and the S/M checkpoint prevents the cell from prematurely entering mitosis before it has fully replicated the genome (Bartek et al. 2004).”
• Identification of the FANCI protein, a monoubiquitinated FANCD2 paralog required for DNA repair. (2007, background): “…School, Boston, MA 02115, USA 2Department of Pathology, Massachusetts General Hospital, Boston, MA 02214, USA 3Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA 4Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA 5Miltenyi Biotec GmbH,…”
• Cell cycle, CDKs and cancer: a changing paradigm (2009, background): “These alterations are sensed by a signalling pathway that ultimately leads to CDK inhibition and cell cycle arres”
• Cell-cycle checkpoints and cancer (2004, background): “The ATR/CHK1 module (but not ATM/CHK2), through moderate constitutive phosphorylation of CDC25A on its several serine residues, then maintains an appropriate abundance of CDC25A through its ubiquitin-dependent, proteasome-mediated turnover during unperturbed proliferatio”
• DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis (2005, background): “When cells experience replicational stress, they activate their replication checkpoint to delay S phase progression and G2/M transitio”