Full metadata record
DC Field | Value | Language |
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dc.creator | Sanchez-Quiles, V. (Virginia) | - |
dc.creator | Mora, M.I. (María I.) | - |
dc.creator | Segura, V. (Víctor) | - |
dc.creator | Greco, A. (Anna) | - |
dc.creator | Epstein, A.L. (Alberto L.) | - |
dc.creator | Foschini, M.G. (María Giovanna) | - |
dc.creator | Dayon, L. (Loïc) | - |
dc.creator | Sánchez, J.C. (Jean-Charles) | - |
dc.creator | Prieto, J. (Jesús) | - |
dc.creator | Corrales, F.J. (Fernando José) | - |
dc.creator | Santamaria, E. (Enrique) | - |
dc.date.accessioned | 2012-04-03T11:28:00Z | - |
dc.date.available | 2012-04-03T11:28:00Z | - |
dc.date.issued | 2011 | - |
dc.identifier.citation | Sanchez-Quiles V, Mora MI, Segura V, Greco A, Epstein AL, Foschini MG, et al. HSV-1 Cgal+ infection promotes quaking RNA binding protein production and induces nuclear-cytoplasmic shuttling of quaking I-5 isoform in human hepatoma cells. Mol Cell Proteomics 2011 Jun;10(6):M111.009126. | es_ES |
dc.identifier.issn | 1535-9484 | - |
dc.identifier.uri | https://hdl.handle.net/10171/21552 | - |
dc.description.abstract | Herpesvirus type 1 (HSV-1) based oncolytic vectors arise as a promising therapeutic alternative for neoplastic diseases including hepatocellular carcinoma. However, the mechanisms mediating the host cell response to such treatments are not completely known. It is well established that HSV-1 infection induces functional and structural alterations in the nucleus of the host cell. In the present work, we have used gel-based and shotgun proteomic strategies to elucidate the signaling pathways impaired in the nucleus of human hepatoma cells (Huh7) upon HSV-1 Cgal(+) infection. Both approaches allowed the identification of differential proteins suggesting impairment of cell functions involved in many aspects of host-virus interaction such as transcription regulation, mRNA processing, and mRNA splicing. Based on our proteomic data and additional functional studies, cellular protein quaking content (QKI) increases 4 hours postinfection (hpi), when viral immediate-early genes such as ICP4 and ICP27 could be also detected. Depletion of QKI expression by small interfering RNA results in reduction of viral immediate-early protein levels, subsequent decrease in early and late viral protein content, and a reduction in the viral yield indicating that QKI directly interferes with viral replication. In particular, HSV-1 Cgal(+) induces a transient increase in quaking I-5 isoform (QKI-5) levels, in parallel with an enhancement of p27(Kip1) protein content. Moreover, immunofluorescence microscopy showed an early nuclear redistribution of QKI-5, shuttling from the nucleus to the cytosol and colocalizing with nectin-1 in cell to cell contact regions at 16-24 hpi. This evidence sheds new light on mechanisms mediating hepatoma cell response to HSV-1 vectors highlighting QKI as a central molecular mediator. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | American Society for Biochemistry and Molecular Biology | es_ES |
dc.rights | info:eu-repo/semantics/closedAccess | - |
dc.subject | Cell Nucleus/metabolism | es_ES |
dc.subject | Cytoplasm/metabolism | es_ES |
dc.subject | Herpes Simplex/metabolism | es_ES |
dc.subject | Herpesvirus 1, Human/physiology | es_ES |
dc.subject | RNA-Binding Proteins/metabolism | es_ES |
dc.title | HSV-1 Cgal+ infection promotes quaking RNA binding protein production and induces nuclear-cytoplasmic shuttling of quaking I-5 isoform in human hepatoma cells | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.relation.publisherversion | http://www.mcponline.org/content/10/6/M111.009126 | es_ES |
dc.type.driver | info:eu-repo/semantics/article | es_ES |
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