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• W2058514252 abstract "It is easy to conceive that in a toxic environment most cells would abandon the division process. In the past decades, it has indeed become clear that cells have developed complex cell cycle checkpoint mechanisms, which slow-down or stop cells from proliferating under challenging conditions. More recently, however, is the discovery and molecular characterization of signaling cascades capable of integrating classical stress-activated responses and cell cycle checkpoints. A report published in a recent issue of Cell Cycle1 sheds light on the increasing complexity of such pathways. The authors found that the stress-activated protein kinases p38 and JNK cooperate with Chk1 to block progression into mitosis under conditions that alter DNA replication (i.e., treatments of cells with antiproliferative drugs such as hydroxyurea, aphidicolin, camptothecin or etoposide). By using a combination of pharmacological and genetic tools, together with precise protocols of cell cycle synchronization, the study shows compelling evidence that in murine NIH3T3 and embryonic fibroblasts, hydroxyurea (used at concentrations capable of abrogating DNA synthesis) added during progression through S-phase first induces an early acute activation of Chk1 that is immediately followed by a phasic activation of both p38 and JNK. Remarkably, p38 and JNK activities are triggered completely independent of ATM-ATR and Chk1 activation, since their activities were similarly induced in the presence of caffeine and UCN-01, respectively." @default.
• W2058514252 created "2016-06-24" @default.
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• W2058514252 date "2012-11-01" @default.
• W2058514252 modified "2023-09-28" @default.
• W2058514252 title "UnCHKed DNA replication" @default.
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• W2058514252 doi "https://doi.org/10.4161/cc.22394" @default.
• W2058514252 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3507485" @default.
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