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Deletion of TRADD Sensitizes Oxidative Stress-induced Necrotic-Cell Death

Authors
Koo, Ki-Bang; Oh, Ji-Youn; Lee, Yun-Sun; Lee, Da-Gyum; Kim, You-Sun
Department
Institute for Medical Sciences
Abstract
TNF Receptor-Associated Death Domain (TRADD) is an essential mediator of TNF receptor-1-mediated TNF signaling and is responsible for recruitment of other effector proteins. Recruitment of these adaptor proteins leads to the activation of MAP kinases and NF-kB, as well as cell death. It is well known that aspect of ROS biological effects is their regulatory roles on cell death to function as direct activator of cell death or as second messengers in the cell death processes. ROS may initiate cell death processes through affecting various signaling cascades. Several studies on the oxidative stress-induced cell death has shown that some of the key TNF signaling molecules serve as the molecular targets of ROS in cell death. However, there is no report concerning whether TRADD has a function in oxidative stress-induced cell death. The availability of TRADD deficiency mice let us investigate the physiological functions of TRADD on oxidative stress-induce cell death. In this study, we found that TRADD deficiency renders cells more susceptible to oxidative stress-induced cell death through the persistent activation of JNK.
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