Regulation of Noxin cell signaling

  • Hit 409
  • Writer 최고관리자
  • 2019-11-01


[2019 Fall Life Sciences & IBB Seminar]


▶Subject: Regulation of Noxin cell signaling

▶Speaker: Prof. Yun Soo Bae (EwhaWomansUniversity)

▶Date: 4:30PM/Nov. 8(Fri.)/2019


▶Place: Auditorium(1F), Postech Biotech Center


Substantial evidence has indicated that transient reactive oxygen species (ROS) can be produced by receptor-mediated biochemical processes, although ROS including superoxide anion and hydrogen peroxide (H2O2) are thought to be by-products of aerobic respiration damaging effects on DNA, protein, and lipid. ROS generation in cell signaling has been extensively studied in terms of NADPH oxidase (gp91phox) in phagocytic cells. However, after identification of the homologs of gp91phox (Nox1, Nox3-5, Duox1-2) from non-phagocytic cells, the function of the generated ROS has been extended into an understanding of various cellular events, including cell growth, differentiation, apoptosis, and inflammation responses. Toll-like receptors (TLRs) recognize pathogen-associated molecular patterns (PAMPs) of microorganisms, including bacteria, viruses and fungi. Innate immunity not only kills invading microorganisms but also triggers acute cellular responses leading to sepsis and its associated organ failure. It is a widely held view that oxidative stress is associated with sepsis-induced acute kidney injury (AKI). Although Noxisozyme activity is tightly regulated, the overexpression of Noxisozymes and their regulatory proteins in pathologic lesions induces uncontrolled and high levels of reactive oxygen species (ROS) generation, leading to cytotoxic damage to cells. In this seminar I will present the activation mechanism of NADPH oxidase in response to Toll-like receptor agonists in AKI.

▶Inquiry: Prof. Cheol-Sang Hwang (279-2352)