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Helenia Ansuini

Researcher at Schering-Plough

Publications -  7
Citations -  1707

Helenia Ansuini is an academic researcher from Schering-Plough. The author has contributed to research in topics: Phagemid & Receptor. The author has an hindex of 7, co-authored 7 publications receiving 1656 citations.

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The human scavenger receptor class B type I is a novel candidate receptor for the hepatitis C virus

TL;DR: It is discovered that the hepatitis C virus (HCV) envelope glycoprotein E2 binds to human hepatoma cell lines independently of the previously proposed HCV receptor CD81, and the receptor responsible for E2 binding to human hepatic cells is identified as the human scavenger receptor class B type I (SR‐BI).
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Binding of the Hepatitis C Virus E2 Glycoprotein to CD81 Is Strain Specific and Is Modulated by a Complex Interplay between Hypervariable Regions 1 and 2

TL;DR: E2 proteins from different isolates displayed a profile of binding to human hepatic cells different from that observed on Molt-4 cells or isolated recombinant CD81, indicating that additional factors are involved in viral recognition by target liver cells.
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Role of Scavenger Receptor Class B Type I in Hepatitis C Virus Entry: Kinetics and Molecular Determinants

TL;DR: A specific and direct role for the identified residues in binding HCV and mediating virus entry is suggested and the hypothesis that new therapeutic strategies aimed at interfering with virus/SR-BI recognition are feasible is supported.
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Searching for DNA–protein Interactions by Lambda Phage Display

TL;DR: The strategy described represents a powerful tool to identify proteins that bind to DNA regulatory elements and an array of multiple adjacent DNA-binding sites sharing a common consensus motif was identified.
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Biotin-tagged cDNA expression libraries displayed on lambda phage: a new tool for the selection of natural protein ligands

TL;DR: A novel lambda vector for display of exogenous peptides at the C-terminus of the capsid D protein is described, which allows efficient in vivo biotinylation of the chimeric phage during amplification.