Cell cycle arrest during measles virus infection: a G0-like block leads to suppression of retinoblastoma protein expression.
about
Measles virus infects and suppresses proliferation of T lymphocytes from transgenic mice bearing human signaling lymphocytic activation moleculeCD150 (SLAM) is a receptor for measles virus but is not involved in viral contact-mediated proliferation inhibition.The paramyxovirus simian virus 5 V protein slows progression of the cell cycle.Evasion of host defenses by measles virus: wild-type measles virus infection interferes with induction of Alpha/Beta interferon production.Measles virus-induced suppression of immune responses.Murine coronavirus replication induces cell cycle arrest in G0/G1 phase.Quantitative proteomic analysis of A549 cells infected with human respiratory syncytial virusQuantitative Proteomics Reveals the Roles of Peroxisome-associated Proteins in Antiviral Innate Immune Responses.Expression of the NS5 (VPg) Protein of Murine Norovirus Induces a G1/S Phase Arrest.Immune containment and consequences of measles virus infection in healthy and immunocompromised individuals.Involvement of miR-15a in G0/G1 Phase Cell Cycle Arrest Induced by Porcine Circovirus Type 2 Replication.Measles virus interacts with human SLAM receptor on dendritic cells to cause immunosuppression.Making it to the synapse: measles virus spread in and among neurons.Measles virus hemagglutinin triggers intracellular signaling in CD150-expressing dendritic cells and inhibits immune response.Cell cycle arrest by transforming growth factor beta1 enhances replication of respiratory syncytial virus in lung epithelial cellsMurine coronavirus nonstructural protein p28 arrests cell cycle in G0/G1 phase.Characterization of the interaction between human respiratory syncytial virus and the cell cycle in continuous cell culture and primary human airway epithelial cells.The coronavirus endoribonuclease Nsp15 interacts with retinoblastoma tumor suppressor protein.Proteolytic cleavage of the fusion protein but not membrane fusion is required for measles virus-induced immunosuppression in vitro.Measles virus-induced immunosuppression in vitro is independent of complex glycosylation of viral glycoproteins and of hemifusion.Localization to the nucleolus is a common feature of coronavirus nucleoproteins, and the protein may disrupt host cell division.Inhibition of in vitro leukocyte proliferation by morbilliviruses.Cell cycle status affects coxsackievirus replication, persistence, and reactivation in vitroInhibition of ubiquitination and stabilization of human ubiquitin E3 ligase PIRH2 by measles virus phosphoproteinGrowth arrest of epithelial cells during measles virus infection is caused by upregulation of interferon regulatory factor 1.MiRNA-124 is a link between measles virus persistent infection and cell division of human neuroblastoma cells.Quantitative Analysis of Cellular Proteome Alterations in CDV-Infected Mink Lung Epithelial Cells.Inducing controlled cell cycle arrest and re-entry during asexual proliferation of Plasmodium falciparum malaria parasites
P2860
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P2860
Cell cycle arrest during measles virus infection: a G0-like block leads to suppression of retinoblastoma protein expression.
description
1999 nî lūn-bûn
@nan
1999 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի մարտին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Cell cycle arrest during measl ...... noblastoma protein expression.
@ast
Cell cycle arrest during measl ...... noblastoma protein expression.
@en
type
label
Cell cycle arrest during measl ...... noblastoma protein expression.
@ast
Cell cycle arrest during measl ...... noblastoma protein expression.
@en
prefLabel
Cell cycle arrest during measl ...... noblastoma protein expression.
@ast
Cell cycle arrest during measl ...... noblastoma protein expression.
@en
P2093
P2860
P1433
P1476
Cell cycle arrest during measl ...... inoblastoma protein expression
@en
P2093
P2860
P304
P577
1999-03-01T00:00:00Z