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Emmy W. Verschuren

Researcher at University of Helsinki

Publications -  36
Citations -  1354

Emmy W. Verschuren is an academic researcher from University of Helsinki. The author has contributed to research in topics: Lung cancer & Internal medicine. The author has an hindex of 16, co-authored 31 publications receiving 1224 citations. Previous affiliations of Emmy W. Verschuren include University of Groningen & University of California, San Francisco.

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Temporal dissection of p53 function in vitro and in vivo.

TL;DR: It is shown here that both tissues in vivo and cells in vitro derived from such mice can be rapidly toggled between wild-type and p53 knockout states, the first example of a new class of genetic model that allows the specific, rapid and reversible perturbation of the function of a single endogenous gene in vivo.
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The oncogenic potential of Kaposi's sarcoma-associated herpesvirus cyclin is exposed by p53 loss in vitro and in vivo.

TL;DR: It is shown that K cyclin expression in primary cells sensitizes to apoptosis and induces growth arrest, both of which are dependent on p53 but independent of E2F1 or p19(ARF); DNA synthesis, but not cytokinesis, continues in K Cyclin-expressing cells, leading to multinucleation and polyploidy.
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The cell cycle and how it is steered by Kaposi's sarcoma-associated herpesvirus cyclin.

TL;DR: Some of the major structural and functional properties of mammalian cyclin/Cdk complexes, some of which are phenocopied by v-cyclin, and the molecular events leading to orderly progression through the G(1)/S and G/M cell cycle phases are reviewed.
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The Evi5 Oncogene Regulates Cyclin Accumulation by Stabilizing the Anaphase-Promoting Complex Inhibitor Emi1

TL;DR: It is proposed that the balance of Evi5 and Polo-like kinase activities determines the timely accumulation of Emi1 and cyclin, ensuring mitotic fidelity.
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Prophase I arrest and progression to metaphase I in mouse oocytes are controlled by Emi1-dependent regulation of APC(Cdh1).

TL;DR: A novel mechanism for the control of entry into the first meiotic division is revealed: an Emi1-dependent inhibition of APCCdh1, which requires the presence of Cdh1.