1999
DOI: 10.1006/viro.1999.9784
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A Mutational Analysis of the Transforming Functions of the E8 Protein of Bovine Papillomavirus Type 4

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Cited by 5 publications
(14 citation statements)
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“…BPV-1 infects fibroblasts and skin keratinocytes giving rise to fibropapillomas, whereas BPV-4 infects solely the epithelial cells of the mucous epithelium of the upper gastrointestinal tract [ 132 ]. Thus, while expression of BPV-1 E5 by itself is sufficient to fully transform mouse and primary human fibroblast cells [ 133 , 134 ], BPV-4 E5 contributes to the transformed phenotype of primary cells by conferring anchorage independent growth, growth in low serum, focus formation and increased cell motility but only in the presence of the other viral oncoproteins, resembling in this respect 16E5 (Table 1 ) [ 127 , 135 , 136 ]. For both proteins the hydrophobic domain, the hydrophilic residues at position 17 and the hydrophilic C-terminal tail are critical for their transforming activities [ 135 , 137 ].…”
Section: Bpv E5mentioning
confidence: 99%
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“…BPV-1 infects fibroblasts and skin keratinocytes giving rise to fibropapillomas, whereas BPV-4 infects solely the epithelial cells of the mucous epithelium of the upper gastrointestinal tract [ 132 ]. Thus, while expression of BPV-1 E5 by itself is sufficient to fully transform mouse and primary human fibroblast cells [ 133 , 134 ], BPV-4 E5 contributes to the transformed phenotype of primary cells by conferring anchorage independent growth, growth in low serum, focus formation and increased cell motility but only in the presence of the other viral oncoproteins, resembling in this respect 16E5 (Table 1 ) [ 127 , 135 , 136 ]. For both proteins the hydrophobic domain, the hydrophilic residues at position 17 and the hydrophilic C-terminal tail are critical for their transforming activities [ 135 , 137 ].…”
Section: Bpv E5mentioning
confidence: 99%
“…Unlike BPV-1 E5, BPV-4 E5 induces transformation of established cells independently from the constitutive activation of tyrosine kinase growth receptors (Table 1 ) [ 165 ]. Cell transformation by BPV-4 E5 (either of established cells by itself or of primary cells in co-operation with other viral oncoproteins) is achieved through transactivation of the cyclin A gene promoter, increased cyclin A expression and cyclin A-associated kinase activity, and inhibition of the negative regulator of cell cycle, p27 Kip1 [ 135 , 166 - 168 ]. Mutational analyses of BPV-4 E5 have demonstrate that, as is the case for BPV-1 E5, the residue at position 17 and the hydrophilic C-terminal tail are critical for its transforming activities [ 135 ].…”
Section: Bpv E5mentioning
confidence: 99%
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“…Moreover, E5 activates several protein kinases involved in the control of cell cycle, thus causing a general dysregulation of the normally tightly controlled programme of cell proliferation. [35][36][37] E5 and MHC class I down-regulation The major histocompatibility complex class I (MHC I) plays a critical role in immune surveillance as it is responsible for the presentation of antigenic peptides to effector T cells. The complex consists of heavy chain (HC), β 2-microglobulin and peptide, and is transported from the endoplasmic reticulum through the Golgi apparatus to the plasma membrane.…”
Section: E5 Oncoproteinmentioning
confidence: 99%
“…BPV-3, -4 and -6 lack the E6 ORF and contain an E8 or E5 ORF (formerly E8 ORF) in the position of the E6 ORF. The BPV-4 E5 ORF consists of 42 aa, induces anchorage-independent growth of infected cells and suppresses contact inhibition (O'Brien et al, 1999;Morgan & Campo, 2000).…”
mentioning
confidence: 99%