Title : Arsenic trioxide augments Chk2/p53-mediated apoptosis by inhibiting oncogenic Wip1 phosphatase.

Pub. Date : 2008 Jul 4

PMID : 18482988






8 Functional Relationships(s)
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1 Arsenic trioxide augments Chk2/p53-mediated apoptosis by inhibiting oncogenic Wip1 phosphatase. Arsenic Trioxide tumor protein p53 Homo sapiens
2 It has been reported that arsenic trioxide (ATO), a potent cancer chemotherapeutic agent, in particular for acute promyelocytic leukemia, activates the Chk2/p53 pathway, leading to apoptosis. Arsenic Trioxide tumor protein p53 Homo sapiens
3 It has been reported that arsenic trioxide (ATO), a potent cancer chemotherapeutic agent, in particular for acute promyelocytic leukemia, activates the Chk2/p53 pathway, leading to apoptosis. Arsenic Trioxide tumor protein p53 Homo sapiens
4 ATO is also known to activate the p38 MAPK/p53 pathway. Arsenic Trioxide tumor protein p53 Homo sapiens
5 Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo. Arsenic Trioxide tumor protein p53 Homo sapiens
6 Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo. Arsenic Trioxide tumor protein p53 Homo sapiens
7 Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo. Arsenic Trioxide tumor protein p53 Homo sapiens
8 Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo. Arsenic Trioxide tumor protein p53 Homo sapiens