Mechanisms of DNA tumor virus transformation by Leonard J. Rosenthal, Hans Wilhelm Doerr

By Leonard J. Rosenthal, Hans Wilhelm Doerr

Nearly 15 in keeping with cent of human melanoma prevalence will be attributed to virus an infection, i.e. viruses symbolize the second one most crucial threat issue (after tobacco intake) for melanoma improvement in people. this present day, 5 virus forms are identified to be serious about inflicting human melanoma: papillomaviruses, retroviruses, herpesviruses, hepadnaviruses, and flaviviruses. This quantity of "Monographs in Virology" offers a entire evaluation of a couple of DNA tumor viruses. major specialists within the box of tumor virology talk about up to date details, targeting the remodeling genes of DNA tumor viruses, the mechanisms of transformation and the in vitro technique used for his or her identity and characterization. even supposing DNA tumor viruses are a various workforce, in vitro reviews have printed a number of universal mechanisms of viral transformation. the person chapters of the publication describe the most recent learn at the id of viral oncogenes and their pursuits.

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Proc Natl Acad Sci USA 1986;83:8288–8292. Tornatore 24 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 Trapp BD, Small JA, Pulley M, Khoury G, Scangos GA: Dysmyelination in transgenic mice containing JC virus early region. Ann Neurol 1988;23:38–48. Beggs AH, Miner JH, Scangos GA: Cell type-specific expression of JC virus T antigen in primary and established cell lines from transgenic mice. J Gen Virol 1990;71:151–164. Feigenbaum L, Hinrichs SH, Jay G: JC virus and simian virus 40 enhancers and transforming proteins: Role in determining tissue specificity and pathogenicity in transgenic mice.

Our laboratory constructed a modified PDGF-R that fails to traffic to the cell surface, and thus cannot be activated by the PDGF-R ligand (PDGF BB [27, and unpubl. data]). Despite this apparent defect, this receptor cooperates with E5 to induce cellular transformation of mouse fibroblasts and IL-3-independent growth of 32D cells [D. Clarke and D. Goldstein, unpubl. data]. Reagents such as BPV-1 E5 and this modified receptor should be useful for further elucidating the downstream effects of activating receptors located within intracellular compartments, and determining whether this differs from activating receptors stationed at the cell surface.

However, several studies suggested that alternative mechanisms might exist, such as E5 perturbation of V-ATPase activity. For example, BPV E5 is capable of transforming keratinocytes, which lack PDGF-R [17]. Moreover, several E5 mutants have been shown to either fail to transform cells, despite retaining the ability to induce PDGF-R autophosphorylation, or to retain transforming ability without Goldstein/Sparkowski 38 inducing significant PDGF-R autophosphorylation [22, 35]. Alterations of Golgi pH may thus provide an alternative mechanism to account for cell transformation in situations where E5 ability to activate the PDGF-R is compromised or in cells lacking this receptor.

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