Purpose: This study assessed the prevalence of maxillofacial lesions in children, i.e., 0-9 years, and adolescents, i.
View Article and Find Full Text PDFObjective: To assess the prevalence of oral mucosal disorders during pregnancy.
Methods: Observational studies were selected by two reviewers in a two-phase process. Search strategies were applied at CINAHL, LILACS, LIVIVO, PubMed, Scopus, Web of Science, Google Scholar, OpenGrey, and ProQuest.
Cells have developed an evolutionary obligation to survey and maintain proteome fidelity and avoid the possible toxic consequences of protein misfolding and aggregation. Disturbances to protein homoeostasis (proteostasis) can result in severe cellular phenotypes and are closely linked with the accumulation of microscopically visible deposits of aggregated proteins. These include inclusion bodies found in AD (Alzheimer's disease), HD (Huntington's disease) and ALS (amyotrophic lateral sclerosis) patient neurons.
View Article and Find Full Text PDFClearance of misfolded and aggregated proteins is central to cell survival. Here, we describe a new pathway for maintaining protein homeostasis mediated by the proteasome shuttle factor UBQLN2. The 26S proteasome degrades polyubiquitylated substrates by recognizing them through stoichiometrically bound ubiquitin receptors, but substrates are also delivered by reversibly bound shuttles.
View Article and Find Full Text PDFModification of proteins with ubiquitin (Ub) occurs through a variety of topologically distinct Ub linkages, including Ube2W-mediated monoubiquitylation of N-terminal alpha amines to generate peptide-linked linear mono-Ub fusions. Protein ubiquitylation can be reversed by the action of deubiquitylating enzymes (DUBs), many of which show striking preference for particular Ub linkage types. Here, we have screened for DUBs that preferentially cleave N-terminal Ub from protein substrates but do not act on Ub homopolymers.
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