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Extensive studies on viral‐mediated oncogenic transformation by human adenoviruses have revealed much of our current understanding on the molecular mechanisms that are involved in the process. To date, these studies have shown that cell transformation is a multistep process regulated by the cooperation of several adenoviral gene products encoded in the early regions 1 (E1) and 4 (E4). Early region 1A immortalizes primary rodent cells, whereas co‐expression of early region protein 1B induces full manifestation of the transformed phenotype. Beside E1 proteins, also some E4 proteins have partial transforming activities through regulating many cellular pathways. Here, we summarize recent data of how adenoviral oncoproteins may contribute to viral transformation and discuss the challenge of pinpointing the underlying mechanisms. [ABSTRACT FROM AUTHOR]

The adenovirus E1B 55K (E1B) protein plays major roles in productive adenoviral infection and cellular transformation. Interest in E1B increased because of the potential of adenoviruses as therapeutic vectors, and the E1B gene is commonly deleted from adenovirus vectors for anticancer therapy. E1B activities are spatiotemporally regulated through SUMOylation and phosphorylation, and through interactions with multiple partners that occur presumably at different intracellular sites and times postinfection. E1B is implicated in the formation of viral replication compartments and regulates viral genome replication and transcription, transcriptional repression, degradation of cellular proteins, and several intranuclear steps of viral late mRNA biogenesis. Here, we review advances in our understanding of E1B during productive adenovirus replication and discuss fundamental aspects that remain unresolved. [ABSTRACT FROM AUTHOR]