Description
Title: A Therapeutic Approach for Autoimmune Diseases: Modulating the Ubiquitin-Proteasome System
Abstract:The central nervous system is affected by the autoimmune, neurodegenerative disease known as multiple sclerosis (MS) (CNS). An abnormal immune response to self-antigens leads to autoimmune disease and causes tissue death and chronic inflammation. A post-translational modification known as ubiquitination involves the attachment of ubiquitin molecules to proteins by ubiquitinating enzymes, followed by the proteasome system’s degradation of the modified proteins. In addition to controlling how proteins are broken down by proteasomes, ubiquitination also controls various other cellular processes. It is essential for the cellular turnover of proteins inside of cells as well as immune signaling and reactions. The primary mechanism for the nonlysosomal proteolysis of intracellular proteins is the ubiquitin-proteasome system (UPS). The 26S proteasome is a multi-catalytic, ATP-dependent protease that selects specific proteins for degradation by recognizing ubiquitin covalently attached to those proteins. This degradation pathway eliminates proteins that are harmed, oxidized, or misfolded as well as regulatory proteins that control numerous crucial cellular functions. When this system is harmed, cellular homeostasis is changed, which causes a variety of diseases to be induced. The biochemistry and molecular biology of the UPS are covered in this review, along with how it affects diseases like MS and proteinopathies. The UPS-related potential therapies and targets are also discussed.
Keywords: autoimmune disease; central nervous system; multiple sclerosis; UPS; therapeutic target; 26S proteasome; E3 ligase
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biology
Writer Experience: 20+ Years
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