Merkel cell polyomavirus small T antigen induces genome instability by E3 ubiquitin ligase targeting

H. J. Kwun, J. A. Wendzicki, Y. Shuda, P. S. Moore, Y. Chang

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The formation of a bipolar mitotic spindle is an essential process for the equal segregation of duplicated DNA into two daughter cells during mitosis. As a result of deregulated cellular signaling pathways, cancer cells often suffer a loss of genome integrity that might etiologically contribute to carcinogenesis. Merkel cell polyomavirus (MCV) small T (sT) oncoprotein induces centrosome overduplication, aneuploidy, chromosome breakage and the formation of micronuclei by targeting cellular ligases through a sT domain that also inhibits MCV large T oncoprotein turnover. These results provide important insight as to how centrosome number and chromosomal stability can be affected by the E3 ligase targeting capacity of viral oncoproteins such as MCV sT, which may contribute to Merkel cell carcinogenesis.

Original languageEnglish (US)
Pages (from-to)6784-6792
Number of pages9
JournalOncogene
Volume36
Issue number49
DOIs
StatePublished - Jan 1 2017

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Merkel cell polyomavirus
Polyomavirus Transforming Antigens
Ubiquitin-Protein Ligases
Genomic Instability
Oncogene Proteins
Centrosome
Carcinogenesis
Merkel Cells
Chromosome Breakage
Chromosomal Instability
Spindle Apparatus
Aneuploidy
Ligases
Mitosis
Genome
DNA
Neoplasms

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics
  • Cancer Research

Cite this

Kwun, H. J. ; Wendzicki, J. A. ; Shuda, Y. ; Moore, P. S. ; Chang, Y. / Merkel cell polyomavirus small T antigen induces genome instability by E3 ubiquitin ligase targeting. In: Oncogene. 2017 ; Vol. 36, No. 49. pp. 6784-6792.
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Merkel cell polyomavirus small T antigen induces genome instability by E3 ubiquitin ligase targeting. / Kwun, H. J.; Wendzicki, J. A.; Shuda, Y.; Moore, P. S.; Chang, Y.

In: Oncogene, Vol. 36, No. 49, 01.01.2017, p. 6784-6792.

Research output: Contribution to journalArticle

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