Redox control of cell fate by MAP kinase: physiological roles of ASK1-MAP kinase pathway in stress signaling

Atsushi Matsuzawa, Hidenori Ichijo

Research output: Contribution to journalReview article

347 Citations (Scopus)

Abstract

The intracellular redox state is a key determinant of cell fate, such as cell survival, proliferation, differentiation, and apoptosis. Redox imbalance is closely linked to a variety of human diseases, so that the intracellular redox condition should be tightly regulated. The redox state of the cell is a consequence of the precise balance between the levels of oxidizing and reducing equivalents, such as reactive oxygen species (ROS) and endogenous antioxidants. ROS are not only toxicants to the cell, but also second messengers in intracellular signal transduction, and control the action of several signaling pathways, including mitogen-activated protein (MAP) kinases. Apoptosis signal-regulating kinase 1 (ASK1) is a MAP kinase kinase kinase of the c-Jun N-terminal kinase (JNK) and p38 MAP kinase pathways, which is preferentially activated in response to various types of stress such as oxidative stress and plays pivotal roles in a wide variety of cellular responses. Recent studies have revealed that ASK1 is also required for innate immune response through ROS production. In this review, we focus on redox control of cell function by MAP kinase signaling, and provide the advanced mechanism of redox-regulated ASK1 activation and physiological roles of the ASK1-MAP kinase pathway in stress signaling.

Original languageEnglish
Pages (from-to)1325-1336
Number of pages12
JournalBiochimica et Biophysica Acta - General Subjects
Volume1780
Issue number11
DOIs
Publication statusPublished - 2008 Nov 1
Externally publishedYes

Keywords

  • ASK1
  • Apoptosis
  • Innate immunity
  • JNK
  • MAP kinase
  • ROS
  • Signalosome
  • TLR4
  • p38

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology

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