Molecular functions of ASK family in diseases caused by stress-induced inflammation and apoptosis

Kazuki Kojima1, Hidenori Ichijo1, Isao Naguro1

  • 1Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.

Journal of Biochemistry
|December 30, 2020
PubMed

Insights

Cellular stress triggers critical responses like inflammation and apoptosis. This review highlights how Apoptosis Signal-Regulating Kinase (ASK) family members regulate these processes and their role in inflammatory diseases.

Area of Science:

  • Cellular biology
  • Molecular mechanisms of disease
  • Stress response pathways

Background:

  • Cellular stress disrupts essential processes, leading to diseases.
  • Inflammation and apoptosis are critical cellular responses that require tight regulation.
  • Dysregulation of these responses contributes to various pathological conditions.

Purpose of the Study:

  • To review the role of the Apoptosis Signal-Regulating Kinase (ASK) family in inflammatory diseases.
  • To focus on the upstream stimuli that modulate ASK family member activity.
  • To provide insights into the molecular regulation of stress responses.

Main Methods:

  • Literature review of recent reports on ASK family kinases.
  • Analysis of studies investigating stress stimuli (e.g., oxidative stress, ER stress).
  • Examination of the link between ASK family members and inflammatory disease pathogenesis.

Main Results:

  • ASK family members are key regulators of inflammation and apoptosis.
  • Various stress stimuli, including oxidative and endoplasmic reticulum stress, activate ASK pathways.
  • Aberrant regulation of ASK signaling is implicated in the development of inflammatory diseases.

Conclusions:

  • The ASK family plays a crucial role in mediating cellular responses to stress.
  • Understanding ASK regulation is vital for developing therapeutic strategies for inflammatory diseases.
  • Further research into upstream stimuli controlling ASK activity is warranted.

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