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Content archived on 2022-12-23

Molecular mechanisms of cell transformation by viral and cellular oncogenes

Objective



Oncogenes may transform cells by affecting many components of the signal transduction pathway and/or inactivating tumour suppressor functions of cellular genes (Rb, p53). Activated Ha-ras oncogenes and tyrosine kinase oncogenes have been shown to affect the activity of transcription factors regulated through phosphorylation by MAP kinases. Viral oncogenes, like the adenovirus (Ad) E1A + E1B and the SV40 large T are supposed to transform cells mainly by binding to and inactivation of the Rb and p53 tumour suppressor activity.

The laboratory in Leiden will investigate what effect cell-transformation by the E1A gene has on the repertoire of active AP-1/ATF transcription factors. The Karlsruhe laboratory is involved in studies on the AP-1 transcription factors and the signal transduction pathways leading to the activation of these factors.

The laboratory in St. Petersburg has transformed rat embryo fibroblasts by various cytoplasmic and nuclear oncogenes which will be used to study whether these different types of oncogenes utilise to some extent common or non-overlapping mechanisms of cell transformation. The effects of the various oncogenes on the expression, activity, composition and regularity of transcription factors will lead to insight in the unique and the general pathways involved in cell-transformation. The cellular components used by these various pathways will be investigated for their effects on each other.

Call for proposal

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Funding Scheme

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Coordinator

Rijksuniversiteit Leiden
EU contribution
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Address
Wassenaarseweg 72
2333 AL Leiden
Netherlands

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Total cost
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Participants (2)