Abstract 2950: Deletion of TRADD sensitizes oxidative stress-induced necrotic cell death.

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 cell death or as second messengers in the cell death processes. ROS may initiate cell death processes through affecting various signaling cascade. 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. Citation Format: Ki-Bang Koo, Da-gyum Lee, Ji-Yoon Oh, Yun-Sun Lee, You-Sun Kim. Deletion of TRADD sensitizes oxidative stress-induced necrotic cell death. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2950. doi:10.1158/1538-7445.AM2013-2950