Virologie (Montrouge)
Inserm U944-CNRS UMR 7212, Université Paris-Diderot, Institut universitaire d'hématologie, 1, avenue Claude-Vellefaux, 75475 Paris Cedex 10, France, Conservatoire national des arts et métiers, Chaire de biologie, 2, rue Conté, 75003 Paris, France.
Published: October 2010
Post-translational modifications, such as SUMOylation, are exam- ples of cellular machineries hijacked by viruses to efficiently replicate. SUMOylation, which consists in the conjugation of small ubiquitin-like modi- fier (SUMO) peptides to a substrate, is exploited or hampered by numerous viruses during infection. Several viral proteins are SUMOylated, causing modulation of sub-cellular localization, stability or modifications of protein activities. In this review, recently described viral examples have been chosen to highlight the different strategies used by viruses to hijack SUMOylation in order to promote replication. The link between pathologies due to viral infec- tions and SUMOylation is discussed. Finally, the potential applications of SUMOylation inhibitors in the treatment of viral infections and associated cancer are evoked.
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http://dx.doi.org/10.1684/vir.2011.15885 | DOI Listing |
Am J Chin Med
January 2025
School of Pharmacy, Nantong University, 9 Seyuan Road, Nantong 226019, P. R. China.
Ginkgolic acids (GAs) are distinctive secondary metabolites of () primarily found in its leaves and seeds, with the highest concentration located in the exotesta. GAs are classified as long-chain phenolic compounds, and exhibit structural similarities to lignoceric acid. Their structural diversity arises from variations in the length of side chains and their number of double bonds, resulting in six distinct forms within extracts (GBE).
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Translational Research Centre of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Ferroptosis is one of the cell death programs occurring after spinal cord injury (SCI) and is driven by iron-dependent phospholipid peroxidation. However, little is known about its underlying regulation mechanism. The present study demonstrated that lipid peroxidation was promoted in patients with SCI.
View Article and Find Full Text PDFCell Death Differ
January 2025
Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Aging is a major risk factor for Alzheimer's disease (AD). With the prevalence of AD increased, a mechanistic linkage between aging and the pathogenesis of AD needs to be further addressed. Here, we report that a small ubiquitin-related modifier (SUMO) modification of p53 is implicated in the process which remarkably increased in AD patient's brain.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Cardiothoracic Surgery, The Affiliated Jiangyin Hospital of Nantong University, 214400 Jiangyin, Jiangsu, China.
Background: This study investigates the role of small ubiquitin-like modifier (SUMO)-specific peptidase 5 (SENP5), a key regulator of SUMOylation, in esophageal squamous cell carcinoma (ESCC), a lethal disease, and its underlying molecular mechanisms.
Methods: Differentially expressed genes between ESCC mouse oesophageal cancer tissues and normal tissues were analysed via RNA-seq; among them, SENP5 expression was upregulated, and this gene was selected for further analysis. Immunohistochemistry and western blotting were then used to validate the increased protein level of SENP5 in both mouse and human ESCC samples.
Biomolecules
January 2025
Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.
RAD18 is a conserved eukaryotic E3 ubiquitin ligase that promotes genome stability through multiple pathways. One of these is gap-filling DNA synthesis at active replication forks and in post-replicative DNA. RAD18 also regulates homologous recombination (HR) repair of DNA breaks; however, the current literature describing the contribution of RAD18 to HR in mammalian systems has not reached a consensus.
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