TRAF2 functions as an activator switch in the reactive oxygen species-induced stimulation of MST1

Kyung Hye Roh, Eui Ju Choi

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Reactive oxygen species (ROS) have many physiological and pathological effects on diverse cellular events. In particular, excessive ROS causes oxidative stress that leads to cell death. The mammalian STE20-like kinase-1 (MST1), a multifunctional serine-threonine kinase, plays a pivotal role in oxidative stress-induced cellular signaling events. Tumor necrosis factor receptor (TNFR)-associated factor 2 (TRAF2) is also known to be essential for oxidative stress-induced cell death. Here, we showed that H2O2 induced the physical interaction between TRAF2 and MST1, and that this interaction promoted the homodimerization as well as the activation of MST1. Furthermore, TRAF2 was required for MST1 to mediate the H2O2-induced stimulation of c-Jun N-terminal kinase and p38 kinase as well as apoptosis. Taken together, our results suggest that TRAF2 functions as a key activator of MST1 in oxidative stress-induced intracellular signaling processes.

Original languageEnglish
Pages (from-to)105-113
Number of pages9
JournalFree Radical Biology and Medicine
Volume91
DOIs
Publication statusPublished - 2016 Feb 1

Fingerprint

Activator Appliances
Reactive Oxygen Species
Oxidative stress
Phosphotransferases
Switches
Oxidative Stress
Cell death
Cell Death
Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
Cell signaling
JNK Mitogen-Activated Protein Kinases
Protein-Serine-Threonine Kinases
Chemical activation
Apoptosis

Keywords

  • Hydrogen peroxide
  • MST1
  • Oxidative stress
  • Reactive oxygen species
  • TRAF2

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)

Cite this

TRAF2 functions as an activator switch in the reactive oxygen species-induced stimulation of MST1. / Roh, Kyung Hye; Choi, Eui Ju.

In: Free Radical Biology and Medicine, Vol. 91, 01.02.2016, p. 105-113.

Research output: Contribution to journalArticle

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