Harvard
Luna, JM
, Scheel, TKH, Danino, T, Shaw, KS, Mele, A, Fak, JJ, Nishiuchi, E, Takacs, CN, Catanese, MT, de Jong, YP, Jacobson, IM, Rice, CM & Darnell, RB 2015, '
Hepatitis C virus RNA functionally sequesters miR-122'
Cell, bind 160, nr. 6, s. 1099-110.
https://doi.org/10.1016/j.cell.2015.02.025
APA
Luna, J. M.
, Scheel, T. K. H., Danino, T., Shaw, K. S., Mele, A., Fak, J. J., ... Darnell, R. B. (2015).
Hepatitis C virus RNA functionally sequesters miR-122.
Cell,
160(6), 1099-110.
https://doi.org/10.1016/j.cell.2015.02.025
CBE
Luna JM
, Scheel TKH, Danino T, Shaw KS, Mele A, Fak JJ, Nishiuchi E, Takacs CN, Catanese MT, de Jong YP, Jacobson IM, Rice CM, Darnell RB. 2015.
Hepatitis C virus RNA functionally sequesters miR-122.
Cell. 160(6):1099-110.
https://doi.org/10.1016/j.cell.2015.02.025
MLA
Vancouver
Author
Luna, Joseph M
; Scheel, Troels K H ; Danino, Tal ; Shaw, Katharina S ; Mele, Aldo ; Fak, John J ; Nishiuchi, Eiko ; Takacs, Constantin N ; Catanese, Maria Teresa ; de Jong, Ype P ; Jacobson, Ira M ; Rice, Charles M ; Darnell, Robert B. /
Hepatitis C virus RNA functionally sequesters miR-122. I:
Cell. 2015 ; Bind 160, Nr. 6. s. 1099-110.
Bibtex
@article{e04b70d1407346eea4492eec7330bff7,
title = "Hepatitis C virus RNA functionally sequesters miR-122",
abstract = "Hepatitis C virus (HCV) uniquely requires the liver-specific microRNA-122 for replication, yet global effects on endogenous miRNA targets during infection are unexplored. Here, high-throughput sequencing and crosslinking immunoprecipitation (HITS-CLIP) experiments of human Argonaute (AGO) during HCV infection showed robust AGO binding on the HCV 5'UTR at known and predicted miR-122 sites. On the human transcriptome, we observed reduced AGO binding and functional mRNA de-repression of miR-122 targets during virus infection. This miR-122 {"}sponge{"} effect was relieved and redirected to miR-15 targets by swapping the miRNA tropism of the virus. Single-cell expression data from reporters containing miR-122 sites showed significant de-repression during HCV infection depending on expression level and site number. We describe a quantitative mathematical model of HCV-induced miR-122 sequestration and propose that such miR-122 inhibition by HCV RNA may result in global de-repression of host miR-122 targets, providing an environment fertile for the long-term oncogenic potential of HCV.",
keywords = "Argonaute Proteins, Base Sequence, Cell Line, Tumor, Eukaryotic Initiation Factors, Hepacivirus, Hepatitis C, Humans, Liver, MicroRNAs, Molecular Sequence Data, RNA, Viral, Virus Replication",
author = "Luna, {Joseph M} and Scheel, {Troels K H} and Tal Danino and Shaw, {Katharina S} and Aldo Mele and Fak, {John J} and Eiko Nishiuchi and Takacs, {Constantin N} and Catanese, {Maria Teresa} and {de Jong}, {Ype P} and Jacobson, {Ira M} and Rice, {Charles M} and Darnell, {Robert B}",
note = "Copyright {\circledC} 2015 Elsevier Inc. All rights reserved.",
year = "2015",
month = "3",
day = "12",
doi = "10.1016/j.cell.2015.02.025",
language = "English",
volume = "160",
pages = "1099--110",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "6",
}
RIS
TY - JOUR
T1 - Hepatitis C virus RNA functionally sequesters miR-122
AU - Luna, Joseph M
AU - Scheel, Troels K H
AU - Danino, Tal
AU - Shaw, Katharina S
AU - Mele, Aldo
AU - Fak, John J
AU - Nishiuchi, Eiko
AU - Takacs, Constantin N
AU - Catanese, Maria Teresa
AU - de Jong, Ype P
AU - Jacobson, Ira M
AU - Rice, Charles M
AU - Darnell, Robert B
N1 - Copyright © 2015 Elsevier Inc. All rights reserved.
PY - 2015/3/12
Y1 - 2015/3/12
N2 - Hepatitis C virus (HCV) uniquely requires the liver-specific microRNA-122 for replication, yet global effects on endogenous miRNA targets during infection are unexplored. Here, high-throughput sequencing and crosslinking immunoprecipitation (HITS-CLIP) experiments of human Argonaute (AGO) during HCV infection showed robust AGO binding on the HCV 5'UTR at known and predicted miR-122 sites. On the human transcriptome, we observed reduced AGO binding and functional mRNA de-repression of miR-122 targets during virus infection. This miR-122 "sponge" effect was relieved and redirected to miR-15 targets by swapping the miRNA tropism of the virus. Single-cell expression data from reporters containing miR-122 sites showed significant de-repression during HCV infection depending on expression level and site number. We describe a quantitative mathematical model of HCV-induced miR-122 sequestration and propose that such miR-122 inhibition by HCV RNA may result in global de-repression of host miR-122 targets, providing an environment fertile for the long-term oncogenic potential of HCV.
AB - Hepatitis C virus (HCV) uniquely requires the liver-specific microRNA-122 for replication, yet global effects on endogenous miRNA targets during infection are unexplored. Here, high-throughput sequencing and crosslinking immunoprecipitation (HITS-CLIP) experiments of human Argonaute (AGO) during HCV infection showed robust AGO binding on the HCV 5'UTR at known and predicted miR-122 sites. On the human transcriptome, we observed reduced AGO binding and functional mRNA de-repression of miR-122 targets during virus infection. This miR-122 "sponge" effect was relieved and redirected to miR-15 targets by swapping the miRNA tropism of the virus. Single-cell expression data from reporters containing miR-122 sites showed significant de-repression during HCV infection depending on expression level and site number. We describe a quantitative mathematical model of HCV-induced miR-122 sequestration and propose that such miR-122 inhibition by HCV RNA may result in global de-repression of host miR-122 targets, providing an environment fertile for the long-term oncogenic potential of HCV.
KW - Argonaute Proteins
KW - Base Sequence
KW - Cell Line, Tumor
KW - Eukaryotic Initiation Factors
KW - Hepacivirus
KW - Hepatitis C
KW - Humans
KW - Liver
KW - MicroRNAs
KW - Molecular Sequence Data
KW - RNA, Viral
KW - Virus Replication
U2 - 10.1016/j.cell.2015.02.025
DO - 10.1016/j.cell.2015.02.025
M3 - Journal article
VL - 160
SP - 1099
EP - 1110
JO - Cell
JF - Cell
SN - 0092-8674
IS - 6
ER -