Rapid destruction of human Cdc25A in response to DNA damage.

By Niels Mailand, J. Falck, C. Lukas, R. Syljuåsen, M. Welcker, J. Bartek, J. Lukas. Science, 2000

879 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/1f08139bde6778c5cd790c93c99581ab421f622b

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. C. Lukas
4. B. Kaina
5. R. Abraham
6. W. Roos
7. Yosef Shiloh

In Molecular Biology

1. J. Bartek
2. J. Lukas
3. C. Lukas
4. R. Abraham
5. B. Kaina
6. W. Roos
7. J. Lees
8. Michael B. Yaffe

In Oncology

1. J. Bartek
2. J. Lukas
3. C. Lukas
4. B. Kaina
5. W. Roos
6. Michael B. Yaffe
7. J. Lees
8. Aaron Aslanian

Citations in the corpus

• DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis (2005, background): “Analogous to cyclin E, overexpression of tetracycline-regulatable Cdc25”
• Cell cycle checkpoint signaling through the ATM and ATR kinases. (2001, background): “…to the p53 phosphorylation mechanism discussed earlier, it will be interesting to determine whether the down-regulation of Cdc25A by UV light (Mailand et al. 2000) or HU (if this occurs) is mediated predominantly through an ATR-dependent pathway, perhaps via an alternative avenue involving…”
• ATR-Mediated Checkpoint Pathways Regulate Phosphorylation and Activation of Human Chk1 (2001, background): “A recent study reported that the G1 cell cycle arrest induced by UV-damaged DNA requires ubiquitin-mediated proteolysis of Cdc25A, and this in turn requires Chk1 (46).”
• Toward maintaining the genome: DNA damage and replication checkpoints. (2002, background): “ATM-dependent activation of Chk2 leads to phosphorylation of Cdc25A, thereby priming it for ubiquitination and proteasome destruction (123).”
• Mechanisms of human DNA repair: an update. (2003, background): “ATR-activated Chk1 can also phosphorylate Cdc25a at Ser123.”
• p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. (2007, background): “…of Cdc25A in vivo has been shown to facilitate its ubiquitin-mediated proteolysis in a complex and incompletely understood manner (Jin et al., 2003; Mailand et al., 2000), and MK2 and Chk1 phosphorylate the identical optimal sequence motifs when analyzed by oriented peptide library screening…”