Please use this identifier to cite or link to this item:
|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|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Feb 8, 2023
WEB OF SCIENCETM
checked on Jan 31, 2023
checked on Feb 2, 2023
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.