Chk1 and Chk2 kinases in checkpoint control and cancer.

By J. Bartek, J. Lukas. Cancer Cell, 2003

1,615 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/82c178d46ed78eb2ea95506497937426ac1571e8

How researchers see this paper

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

In Cell Biology

1. J. Bartek
2. J. Lukas
3. Stephen P. Jackson
4. C. Lukas
5. Antonio Giordano
6. S. Lapenna

In Molecular Biology

1. Stephen P. Jackson
2. J. Bartek
3. J. Lukas
4. C. Lukas
5. J. Falck
6. David A. Gillespie
7. J. Smith
8. Naihan Xu

In Oncology

1. Stephen P. Jackson
2. J. Bartek
3. J. Lukas
4. C. Lukas
5. J. Falck
6. David A. Gillespie
7. J. Smith
8. Naihan Xu

Citations in the corpus

• The cell-cycle checkpoint kinase Chk1 is required for mammalian homologous recombination repair (2005, neutral): “dtd" [ ]> The essential checkpoint kinase Chk1 is required for cell-cycle delays after DNA damage or blocked DNA replicatio”
• p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. (2007, background): “Disruption of normal checkpoint function from inherited and acquired genetic mutations is increasingly recognized as a pathophysiological mechanism responsible for tumor-prone human disease syndromes (Bartek and Lukas, 2003; Kastan and Bartek, 2004; O'Driscoll et al., 2004; Shiloh, 2003).”
• Cell cycle kinases as therapeutic targets for cancer (2009, background): “The intriguing phenotype of CHK2-null mice fuelled the idea that chemical inhibition of CHK2 could be exploited to protect sensitive tissues, such as lymphoid tissue and epithelial tissue, from the side effects of radiotherapy or DNA-damaging drug”
• ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks (2006, background): “After their recruitment to sites of damage, ATM and ATR then phosphorylate a number of substrates, including the protein kinases Chk1 and Chk2 , which in turn target other proteins to induce cell-cycle arrest and facilitate DNA repai”
• Checking on DNA damage in S phase (2004, background): “The regulation of the intra-S-phase checkpoint by the DNA-damage-induced, ubiquitin–proteasome-dependent degradation of CDC25A has been reviewed elsewher”
• The ATM-Chk2 and ATR-Chk1 pathways in DNA damage signaling and cancer. (2010, background): “, 1998), subsequent genetic and biochemical data have increasingly emphasized ATR–Chk1 as the principal, direct effector of the DNA damage and replication checkpoints, with ATM–Chk2 playing an auxiliary role specifically in the response to DSBs (Bartek and Lukas, 2003; Kastan and Bartek, 2004).”