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|Title:||Loss of Wip1 sensitizes cells to stress- and DNA damage-induced apoptosis||Authors:||Xia, Y.
|Issue Date:||26-Jun-2009||Citation:||Xia, Y., Ongusaha, P., Lee, S.W., Liou, Y.-C. (2009-06-26). Loss of Wip1 sensitizes cells to stress- and DNA damage-induced apoptosis. Journal of Biological Chemistry 284 (26) : 17428-17437. ScholarBank@NUS Repository. https://doi.org/10.1074/jbc.M109.007823||Abstract:||In response to various environmental stresses, the stress-responsive MAPKs p38 and JNK are activated and phosphorylate ATF2 and c-Jun transcription factors, thereby affecting cell-fate decision. Targeted gene disruption studies have established that JNK-c-Jun signaling plays a vital role in stress-induced apoptosis. The oncogenic phosphatase Wip1 acts as an important regulator in DNA damage pathway by dephosphorylating a spectrum of proteins including p53, p38, Chk1, Chk2, and ATM. In this study we show that Wip1 negatively regulates the activation of MKK4-JNK-c-Jun signaling during stress-induced apoptosis. The loss of Wip1 function sensitizes mouse embryonic fibroblasts to stress-induced apoptosis via the activation of both p38- ATF2 and JNK-c-Jun signaling. Here we reveal that Wip1 has dual roles in alternatively regulating stress- and DNA damageinduced apoptosis through p38/JNK MAPKs and p38/p53-dependent pathways, respectively. Our results point to Wip1 as a general regulator of apoptosis, which further supports its role in tumorigenesis. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.||Source Title:||Journal of Biological Chemistry||URI:||http://scholarbank.nus.edu.sg/handle/10635/101035||ISSN:||00219258||DOI:||10.1074/jbc.M109.007823|
|Appears in Collections:||Staff Publications|
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