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Grégoire Vuagniaux

Researcher at University of Lausanne

Publications -  55
Citations -  1892

Grégoire Vuagniaux is an academic researcher from University of Lausanne. The author has contributed to research in topics: Alisporivir & Inhibitor of apoptosis. The author has an hindex of 16, co-authored 52 publications receiving 1776 citations.

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Synergistic activation of ENaC by three membrane-bound channel-activating serine proteases (mCAP1, mCAP2, and mCAP3) and serum- and glucocorticoid-regulated kinase (Sgk1) in Xenopus Oocytes.

TL;DR: The synergistic effect of the two activation pathways allows a large dynamic range for ENaC-mediated sodium regulation crucial for a tight control of sodium homeostasis.
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The Isomerase Active Site of Cyclophilin A Is Critical for Hepatitis C Virus Replication

TL;DR: The respective contribution of Cyp members to HCV replication is analyzed by specifically knocking down their expression by both transient and stable small RNA interference, suggesting for the first time that HCV exploits either the isomerase or the chaperone activity of CypA to replicate in hepatocytes and that CypA is the principal mediator of the Cyp inhibitor anti-HCV activity.
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Activation of the Amiloride-Sensitive Epithelial Sodium Channel by the Serine Protease mCAP1 Expressed in a Mouse Cortical Collecting Duct Cell Line

TL;DR: Coexpression of the Xenopus, rat, or human alpha-, beta-, and gamma-ENaC subunits in Xenopus oocytes showed that mCAP1 induces a significant increase in ENaC-mediated current accompanied by a decrease of channel molecules at the cell surface, suggesting that this novel mouse channel activating protease may act as a regulator of EN aC within the kidney.
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DEB025 (Alisporivir) Inhibits Hepatitis C Virus Replication by Preventing a Cyclophilin A Induced Cis-Trans Isomerisation in Domain II of NS5A

TL;DR: It was very difficult to select resistant replicons (genotype 1b) to DEB025, requiring an average of 20 weeks (four independent experiments), compared to the typically <2 weeks with protease or polymerase inhibitors, indicating a high genetic barrier to resistance forDEB025.