Protein Homeostasis in Physiology

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 5787

Special Issue Editors


E-Mail Website
Guest Editor
College of Medicine, University of Ulsan, Seoul, Republic of Korea
Interests: ER stress; unfolded protein response; integrated stress response; apoptosis; aging; neurodegeneration

E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Ulsan College of Medicine, ASAN Medical Center, Seoul, Korea
Interests: cell cycle; lung cancer; dendritic cell; immunotherapy

Special Issue Information

Dear Colleagues, 

Protein homeostasis (proteostasis) is an essential cellular mechanism that controls the biogenesis, trafficking, folding and degradation of proteins in cells. Perturbations in protein homeostasis may lead to the aberrant accumulation/aggregation of misfolded proteins, trigger stress responses, or excessive protein degradation. Dysregulation of proteostasis has been implicated in many human diseases and aging as well as organismal health.

For this Special issue, we welcome original research and mini-review articles covering the mechanistic aspects of  protein homoestasis including proteostasis in organelles, proteostasis in disease and aging. Articles discussing methodological approaches with test tubes, living cells or organisms are also encouraged. 

Dr. Min-ji Kang
Dr. Peter Chang-Whan Lee
Guest Editors

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Keywords

  • Stress response in organelle
  • Protein Quality Control
  • Protein trafficking
  • Protein degradation
  • Neurodegeneration
  • Aging

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Published Papers (1 paper)

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Review

13 pages, 1582 KiB  
Review
Modulating the Ubiquitin–Proteasome System: A Therapeutic Strategy for Autoimmune Diseases
by Dhananjay Yadav, Ji Yeon Lee, Nidhi Puranik, Pallavi S. Chauhan, Vishal Chavda, Jun-O. Jin and Peter C. W. Lee
Cells 2022, 11(7), 1093; https://doi.org/10.3390/cells11071093 - 24 Mar 2022
Cited by 22 | Viewed by 5052
Abstract
Multiple sclerosis (MS) is an autoimmune, neurodegenerative disease associated with the central nervous system (CNS). Autoimmunity is caused by an abnormal immune response to self-antigens, which results in chronic inflammation and tissue death. Ubiquitination is a post-translational modification in which ubiquitin molecules are [...] Read more.
Multiple sclerosis (MS) is an autoimmune, neurodegenerative disease associated with the central nervous system (CNS). Autoimmunity is caused by an abnormal immune response to self-antigens, which results in chronic inflammation and tissue death. Ubiquitination is a post-translational modification in which ubiquitin molecules are attached to proteins by ubiquitinating enzymes, and then the modified proteins are degraded by the proteasome system. In addition to regulating proteasomal degradation of proteins, ubiquitination also regulates other cellular functions that are independent of proteasomal degradation. It plays a vital role in intracellular protein turnover and immune signaling and responses. The ubiquitin–proteasome system (UPS) is primarily responsible for the nonlysosomal proteolysis of intracellular proteins. The 26S proteasome is a multicatalytic adenosine-triphosphate-dependent protease that recognizes ubiquitin covalently attached to particular proteins and targets them for degradation. Damaged, oxidized, or misfolded proteins, as well as regulatory proteins that govern many essential cellular functions, are removed by this degradation pathway. When this system is affected, cellular homeostasis is altered, resulting in the induction of a range of diseases. This review discusses the biochemistry and molecular biology of the UPS, including its role in the development of MS and proteinopathies. Potential therapies and targets involving the UPS are also addressed. Full article
(This article belongs to the Special Issue Protein Homeostasis in Physiology)
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