The Function of ASK1 in Sepsis and Stress-Induced Disorders

Authors

John Kostyak, Thomas Jefferson UniversityFollow
Steven McKenzie, Thomas Jefferson UniversityFollow
Ulhas Naik, Thomas Jefferson UniversityFollow

Document Type

Article

Publication Date

12-22-2023

Comments

This article is the author's final published version in International Journal of Molecular Sciences, Volume 25, Issue 1, 2023, Article number 213.

The published version is available at https://doi.org/10.3390/ijms25010213.

Copyright © 2023 by the authors

Abstract

Apoptosis signal-regulating kinase 1 (ASK1) is a serine-threonine kinase that is ubiquitously expressed in nucleated cells and is responsible for the activation of multiple mitogen-activated protein kinases (MAPK) to regulate cell stress. Activation of ASK1 via cellular stress leads to activation of downstream signaling components, activation of transcription factors, and proinflammatory cytokine production. ASK1 is also expressed in anucleate platelets and is a key player in platelet activation as it is important for signaling. Interestingly, the mechanism of ASK1 activation is cell type-dependent. In this review we will explore how ASK1 regulates a variety of cellular processes from innate immune function to thrombosis and hemostasis. We will discuss how ASK1 influences FcγRIIA-mediated platelet reactivity and how that reactivity drives platelet clearance. Furthermore, we will explore the role of ASK1 in thromboxane (TxA₂) generation, which highlights differences in the way ASK1 functions in mouse and human platelets.

Recommended Citation

Kostyak, John; McKenzie, Steven; and Naik, Ulhas, "The Function of ASK1 in Sepsis and Stress-Induced Disorders" (2023). Cardeza Foundation for Hematologic Research. Paper 79.
https://jdc.jefferson.edu/cardeza_foundation/79

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 License.

Language

English