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The role of adenovirus E1B-55k in targeting host-cell proteins that possess antiviral activity for proteasomal degradation is now well established. To expand our understanding of E1B-55k in regulating the levels of host-cell proteins, we performed comparative proteome analysis of wild-type, and E1B-55k-deletion, adenovirus-infected cancer cells. As such we performed quantitative MS\/MS analysis to monitor protein expression changes affected by viral E1B-55k. We identified 5937 proteins, and of these, 69 and 58 proteins were down-regulated during wild-type and E1B-55k (<jats:italic>dl<\/jats:italic>1520) adenovirus infection, respectively. This analysis revealed that there are many, previously unidentified, cellular proteins subjected to degradation by adenovirus utilizing pathways independent of E1B-55k expression. Moreover, we found that ALCAM, EPHA2 and PTPRF, three cellular proteins that function in the regulation of cell\u2013cell contacts, appeared to be degraded by E1B-55k\/E4orf3 and\/or E1B-55k\/E4orf6 complexes. These molecules, like integrin \u03b13 (a known substrate of E1B-55k\/E4orf6), are critical regulators of cell signalling, cell adhesion and cell surface modulation, and their degradation during infection is, potentially, pertinent to adenovirus propagation. The data presented in this study illustrate the broad nature of protein down-regulation mediated by adenovirus.<\/jats:p>","DOI":"10.1099\/jgv.0.000781","type":"journal-article","created":{"date-parts":[[2017,6,20]],"date-time":"2017-06-20T11:12:25Z","timestamp":1497957145000},"page":"1377-1388","source":"Crossref","is-referenced-by-count":12,"title":["Comparison of protein expression during wild-type, and E1B-55k-deletion, adenovirus infection using quantitative time-course proteomics"],"prefix":"10.1099","volume":"98","author":[{"given":"Yen Rong","family":"Fu","sequence":"first","affiliation":[{"name":"School of Cellular and Molecular Medicine, University Walk, University of Bristol, Bristol BS8 1TD, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew S.","family":"Turnell","sequence":"additional","affiliation":[{"name":"Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, 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