Title : Rigosertib-Activated JNK1/2 Eliminate Tumor Cells through p66Shc Activation.

Pub. Date : 2020 May 15

PMID : 32429320






7 Functional Relationships(s)
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1 Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. Reactive Oxygen Species mitogen-activated protein kinase 8 Homo sapiens
2 Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. Reactive Oxygen Species mitogen-activated protein kinase 8 Homo sapiens
3 Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. Reactive Oxygen Species mitogen-activated protein kinase 8 Homo sapiens
4 Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. Reactive Oxygen Species mitogen-activated protein kinase 8 Homo sapiens
5 JNK1/2 are not only regulated by ROS-they in turn can also control ROS production. Reactive Oxygen Species mitogen-activated protein kinase 8 Homo sapiens
6 JNK1/2 are not only regulated by ROS-they in turn can also control ROS production. Reactive Oxygen Species mitogen-activated protein kinase 8 Homo sapiens
7 Here, we provide evidence that establishes p66Shc, an oxidoreductase, as a JNK1/2 effector downstream of Rigosertib-induced ROS production, DNA damage, and cell death. Reactive Oxygen Species mitogen-activated protein kinase 8 Homo sapiens