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Vincent Piguet

Researcher at University of Toronto

Publications -  273
Citations -  10487

Vincent Piguet is an academic researcher from University of Toronto. The author has contributed to research in topics: Medicine & Hidradenitis suppurativa. The author has an hindex of 45, co-authored 241 publications receiving 9102 citations. Previous affiliations of Vincent Piguet include University Hospital of Basel & Salk Institute for Biological Studies.

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The dendritic cell-specific adhesion receptor DC-SIGN internalizes antigen for presentation to T cells.

TL;DR: It is demonstrated that on DCs DC-SIGN is rapidly internalized upon binding of soluble ligand, which points to a novel function of the adhesion receptor DC- SIGN as an efficient DC-specific Ag receptor that can be used as a target to induce viral and antitumor immunity.
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Langerin is a natural barrier to HIV-1 transmission by Langerhans cells.

TL;DR: Langerin is a natural barrier to HIV-1 infection, and strategies to combat infection must enhance, preserve or, at the very least, not interfere with Langerin expression and function.
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Melanomas require HEDGEHOG-GLI signaling regulated by interactions between GLI1 and the RAS-MEK/AKT pathways.

TL;DR: The data uncover an unsuspected role of HH-GLI signaling in melanocytes and melanomas, demonstrate a role for this pathway in RAS-induced tumors, suggest a general integration of the RAS/AKT and HH- GLI pathways, and open a therapeutic approach for human melanomas.
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HIV-1 Nef protein binds to the cellular protein PACS-1 to downregulate class I major histocompatibility complexes

TL;DR: These results support a model in which Nef relocalizes MHC-I by acting as a connector between M HC-I’s cytoplasmic tail and the PACS-1-dependent protein-sorting pathway.
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HIV-1 Vpu neutralizes the antiviral factor Tetherin/BST-2 by binding it and directing its beta-TrCP2-dependent degradation.

TL;DR: It is shown that HIV-1 Vpu induces the depletion of tetherin from cells and interacts with tetherin to direct its β-TrCP2-dependent proteasomal degradation, thereby alleviating the blockade to the release of infectious virions.