Julia Manzetti
University of Basel
5 Papers
2 Citations
Julia Manzetti is an academic researcher from University of Basel. The author has contributed to research in topics: Mitophagy & Viral replication. The author has an hindex of 3, co-authored 5 publications.
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Papers
BK Polyomavirus Replication in Renal Tubular Epithelial Cells Is Inhibited by Sirolimus, but Activated by Tacrolimus Through a Pathway Involving FKBP-12.
TL;DR: Sirolimus and tacrolimus exert opposite effects on BKPyV replication in renal tubular epithelial cells by a mechanism involving FKBP‐12 as common target, supporting the notion that early steps of BK PyV replication depend on mTOR activity.
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Sp1 Sites in the Noncoding Control Region of BK Polyomavirus Are Key Regulators of Bidirectional Viral Early and Late Gene Expression
Tobias Bethge,Helen A. Hachemi,Julia Manzetti,Rainer Gosert,Walter Schaffner,Hans H. Hirsch,Hans H. Hirsch +6 more
TL;DR: The results provide new insights into how BKPyV NCCR functions as a viral sensor of host cell signals and shed new light on how transcription factors like Sp1 control bidirectional viral gene expression and contribute to replication and pathology.
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BK Polyomavirus Evades Innate Immune Sensing by Disrupting the Mitochondrial Network and Promotes Mitophagy
Julia Manzetti,Fabian H. Weissbach,Fabrice E. Graf,Gunhild Unterstab,Marion Wernli,Helmut Hopfer,Cinthia B. Drachenberg,Christine Hanssen Rinaldo,Hans H. Hirsch,Hans H. Hirsch +9 more
TL;DR: It is reported that BKPyV disrupts the mitochondrial network and membrane potential when expressing the 66aa-long agnoprotein during late replication, indicating a conserved mechanism facilitating polyomavirus persistence and post-transplant disease.
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BK polyomavirus evades innate immune sensing by disrupting the mitochondrial network and membrane potential and by promoting mitophagy
Julia Manzetti,Fabian H. Weissbach,Gunhild Unterstab,Marion Wernli,Helmut Hopfer,Cinthia B. Drachenberg,Christine Hanssen Rinaldo,Hans H. Hirsch +7 more
TL;DR: It is reported that BKPyV disrupts the mitochondrial network and its membrane potential when expressing the 66aa-long agnoprotein during late replication, indicating a conserved mechanism facilitating polyomavirus persistence and post-transplant disease.
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