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5 results on '"Kan, Sherry"'

1. Cellular Cofactors Affecting Hepatitis C Virus Infection and Replication

Author

Randall, Glenn, Panis, Maryline, Cooper, Jacob D., Tellinghuisen, Timothy L., Sukhodolets, Karen E., Pfeffer, Sebastien, Landthaler, Markus, Landgraf, Pablo, Kan, Sherry, Lindenbach, Brett D., Chien, Minchen, Weir, David B., Russo, James J., Ju, Jingyue, Brownstein, Michael J., Sheridan, Robert, Sander, Chris, Zavolan, Mihaela, Tuschl, Thomas, and Rice, Charles M.

Published
2007
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2. Identification of a ligand on the Wip1 bacteriophage highly specific for a receptor on B. anthracis

Author

Kan, Sherry, Fornelos Martins, Nadine, Schuch, Raymond, and Fischetti, Vincent

Subjects
bacteriophage, tectivirus, lysin
Abstract

Tectiviridae is a family of tailless bacteriophages with Gram-negative and Gram-positive hosts. The family model PRD1 and its close relatives all infect a broad range of enterobacteria by recognizing a plasmid-encoded conjugal transfer complex as a receptor. In contrast, tectiviruses with Gram-positive hosts are highly specific to only a few hosts within the same bacterial species. The cellular determinants that account for the observed specificity remain unknown. Here we present the genome sequence of Wip1, a tectivirus that infects the pathogen Bacillus anthracis. The Wip1 genome is related to other tectiviruses with Gram-positive hosts, notably, AP50, but displays some interesting differences in its genome organization. We identified Wip1 candidate genes for the viral spike complex, the structure located at the capsid vertices and involved in host receptor binding. Phage adsorption and inhibition tests were combined with immunofluorescence microscopy to show that the Wip1 gene product p23 is a receptor binding protein. His-p23 also formed a stable complex with p24, a Wip1 protein of unknown function, suggesting that the latter is involved with p23 in host cell recognition. The narrow host range of phage Wip1 and the identification of p23 as a receptor binding protein offer a new range of suitable tools for the rapid identification of B. anthracis. peerReviewed

Published
2013

5. Cellular cofactors affecting hepatitis C virus infection and replication.

Author

Randalla, Glenn, Panisa, Maryline, Cooper, Jacob D., Tellinghuisen, Timothy L., Sukhodoiets, Karen E., Pfeffer, Sebastien, Landthaler, Markus, Landgraf, Pablo, Kan, Sherry, Lindenbach, Brett D., Chien, Minchen, Weir, David B., Russo, James J., Jingyue Ju, Brownstein, Michael J., Sheridan, Robert, Sander, Chris, Zavolan, Mihaela, Tuschl, Thomas, and Rice, Charles M.

Subjects
HEPATITIS C virus, FLAVIVIRUSES, CELL culture, RNA, PROTEINS, GENES
Abstract

Recently identified hepatitis C virus (HCV) isolates that are infectious in cell culture provide a genetic system to evaluate the significance of virus-host interactions for HCV replication. We have completed a systematic RNAi screen wherein siRNAs were designed that target 62 host genes encoding proteins that physically interact with HCV RNA or proteins or belong to cellular pathways thought to modulate HCV infection. This includes 10 host proteins that we identify in this study to bind HCV NS5A. siRNAs that target 26 of these host genes alter infectious HCV production >3-fold. Included in this set of 26 were siRNAs that target Dicer, a principal component of the RNAi silencing pathway. Contrary to the hypothesis that RNAi is an antiviral pathway in mammals, as has been reported for subgenomic HCV replicons, siRNAs that target Dicer inhibited HCV replication. Furthermore, siRNAs that target several other components of the RNAi pathway also inhibit HCV replication. MicroRNA profiling of human liver, human hepatoma Huh-7.5 cells, and Huh-7.5 cells that harbor replicating HCV demonstrated that miR-122 is the predominant microRNA in each environment. miR-122 has been previously implicated in positively regulating the replication of HCV genotype 1 replicons. We find that 2′-O-methyl antisense oligonucleotide depletion of miR-122 also inhibits HCV genotype 2a replication and infectious virus production. Our data define 26 host genes that modulate HCV infection and indicate that the requirement for functional RNAi for HCV replication is dominant over any antiviral activity this pathway may exert against HCV. [ABSTRACT FROM AUTHOR]

Published
2007
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