Abstract
Small ubiquitin-like modifier (SUMO)ylation is a crucial post-translational modification that controls functions of a wide collection of proteins and biological processes. Hence, given its pleiotropic role, viruses have developed many approaches to usurp SUMO conjugation to exploit the cellular host environment for their own benefit. Consistently, cancer cells also frequently impact on SUMO to force cellular transformation, underlining the importance of SUMO in health and diseases. Therefore, after a brief introduction to the multistep SUMOylation pathway, in this review we will focus our attention on several examples of strategies adopted by oncogenic viruses to hijack SUMOylation in order to promote infection, persistence and malignant transformation of host cells.
MeSH terms
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Chromatin / genetics
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Chromatin / metabolism
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Hepacivirus / genetics
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Hepacivirus / metabolism
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Hepacivirus / pathogenicity
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Hepatitis B virus / genetics
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Hepatitis B virus / metabolism
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Hepatitis B virus / pathogenicity
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Herpesvirus 4, Human / genetics
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Herpesvirus 4, Human / metabolism
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Herpesvirus 4, Human / pathogenicity
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Herpesvirus 8, Human / genetics
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Herpesvirus 8, Human / metabolism
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Herpesvirus 8, Human / pathogenicity
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Human T-lymphotropic virus 1 / genetics
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Human T-lymphotropic virus 1 / metabolism
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Human T-lymphotropic virus 1 / pathogenicity
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Humans
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Merkel cell polyomavirus / genetics
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Merkel cell polyomavirus / metabolism
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Merkel cell polyomavirus / pathogenicity
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Neoplasms / genetics
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Neoplasms / metabolism*
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Neoplasms / virology*
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Papillomaviridae / genetics
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Papillomaviridae / metabolism
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Papillomaviridae / pathogenicity
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Retroviridae / genetics
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Retroviridae / growth & development
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Retroviridae / metabolism*
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Retroviridae / pathogenicity
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Small Ubiquitin-Related Modifier Proteins / genetics
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Small Ubiquitin-Related Modifier Proteins / metabolism*
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Sumoylation*
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Ubiquitin-Protein Ligases / metabolism
Substances
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Chromatin
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Small Ubiquitin-Related Modifier Proteins
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Ubiquitin-Protein Ligases