About this Research Topic
Ubiquitination is an important post-translational modification (PTM) that plays a crucial role in the degradation of most intracellular proteins, pivotal to intracellular protein hemostasis. The process is mediated by a cascade of enzymatic reactions mediated by ubiquitin itself, the E1ubiquitin activating enzymes, the E2 ubiquitin-conjugating enzymes, and the E3 ubiquitin ligases, and the deubiquitinase (DUBs).
More recently, ubiquitination has been shown to have additional nonproteolytic roles in regulating diverse biological processes. Dysregulated ubiquitination, characterized by mutation or abnormal expression of E3 ligases or adaptors, has been implicated in various types of human diseases including cancer, neurodegenerative diseases, metabolic disorders, and cardiovascular diseases. Thus, from a clinical standpoint, there is an urgent need to further investigate the underlying mechanisms of dysregulated ubiquitination to understand the etiology of associated diseases as well as to develop innovative therapeutic approaches.
In this research topic, we welcome the submission of original research articles, review articles, and perspectives related to, but not limited to:
a) Genetic alteration of components(e.g., E3 ligases, DUBs, ubiquitin receptor proteins, etc.), leading to abnormal process of ubiquitination and deubiquitination
b) Role of known/novel factors (e.g., E3 ligases, DUBs, ubiquitin receptor proteins, etc.) regulating ubiquitination in a variety of human diseases
c) Molecular or computational methodologies to identify novel inhibitors or PROTAC degraders for ubiquitination machinery
d) Translational or therapeutic approaches to improve treatment of human diseases associated with ubiquitin-mediated signaling via targeting ubiquitination and subsequent degradation.
More recently, ubiquitination has been shown to have additional nonproteolytic roles in regulating diverse biological processes. Dysregulated ubiquitination, characterized by mutation or abnormal expression of E3 ligases or adaptors, has been implicated in various types of human diseases including cancer, neurodegenerative diseases, metabolic disorders, and cardiovascular diseases. Thus, from a clinical standpoint, there is an urgent need to further investigate the underlying mechanisms of dysregulated ubiquitination to understand the etiology of associated diseases as well as to develop innovative therapeutic approaches.
In this research topic, we welcome the submission of original research articles, review articles, and perspectives related to, but not limited to:
a) Genetic alteration of components(e.g., E3 ligases, DUBs, ubiquitin receptor proteins, etc.), leading to abnormal process of ubiquitination and deubiquitination
b) Role of known/novel factors (e.g., E3 ligases, DUBs, ubiquitin receptor proteins, etc.) regulating ubiquitination in a variety of human diseases
c) Molecular or computational methodologies to identify novel inhibitors or PROTAC degraders for ubiquitination machinery
d) Translational or therapeutic approaches to improve treatment of human diseases associated with ubiquitin-mediated signaling via targeting ubiquitination and subsequent degradation.
Keywords: Ubiquitination, Human disease, Mutation, Aberrant expression
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