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Modulation of signaling pathways by RNA virus capsid proteins

Capsid proteins are structural components of virus particles. They are nucleic acid-binding proteins whose main recognized function is to package viral genomes into protective structures called nucleocapsids. Research over the last 10 years indicates that in addition to their role as genome guardian...

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Detalles Bibliográficos
Autores principales: Urbanowski, Matthew D., Ilkow, Carolina S., Hobman, Tom C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier Inc. 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7127581/
https://www.ncbi.nlm.nih.gov/pubmed/18258415
http://dx.doi.org/10.1016/j.cellsig.2007.12.018
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author Urbanowski, Matthew D.
Ilkow, Carolina S.
Hobman, Tom C.
author_facet Urbanowski, Matthew D.
Ilkow, Carolina S.
Hobman, Tom C.
author_sort Urbanowski, Matthew D.
collection PubMed
description Capsid proteins are structural components of virus particles. They are nucleic acid-binding proteins whose main recognized function is to package viral genomes into protective structures called nucleocapsids. Research over the last 10 years indicates that in addition to their role as genome guardians, viral capsid proteins modulate host cell signaling networks. Disruption or alteration of intracellular signaling pathways by viral capsids may benefit replication of the virus by affecting innate immunity and in some cases, may underlie disease progression. In this review, we describe how the capsid proteins from medically relevant RNA viruses interact with host cell signaling pathways.
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spelling pubmed-71275812020-04-08 Modulation of signaling pathways by RNA virus capsid proteins Urbanowski, Matthew D. Ilkow, Carolina S. Hobman, Tom C. Cell Signal Article Capsid proteins are structural components of virus particles. They are nucleic acid-binding proteins whose main recognized function is to package viral genomes into protective structures called nucleocapsids. Research over the last 10 years indicates that in addition to their role as genome guardians, viral capsid proteins modulate host cell signaling networks. Disruption or alteration of intracellular signaling pathways by viral capsids may benefit replication of the virus by affecting innate immunity and in some cases, may underlie disease progression. In this review, we describe how the capsid proteins from medically relevant RNA viruses interact with host cell signaling pathways. Elsevier Inc. 2008-07 2008-01-04 /pmc/articles/PMC7127581/ /pubmed/18258415 http://dx.doi.org/10.1016/j.cellsig.2007.12.018 Text en Copyright © 2007 Elsevier Inc. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Article
Urbanowski, Matthew D.
Ilkow, Carolina S.
Hobman, Tom C.
Modulation of signaling pathways by RNA virus capsid proteins
title Modulation of signaling pathways by RNA virus capsid proteins
title_full Modulation of signaling pathways by RNA virus capsid proteins
title_fullStr Modulation of signaling pathways by RNA virus capsid proteins
title_full_unstemmed Modulation of signaling pathways by RNA virus capsid proteins
title_short Modulation of signaling pathways by RNA virus capsid proteins
title_sort modulation of signaling pathways by rna virus capsid proteins
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7127581/
https://www.ncbi.nlm.nih.gov/pubmed/18258415
http://dx.doi.org/10.1016/j.cellsig.2007.12.018
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