Selected article for: "arrest cell and cell cycle arrest"

Author: Munday, Diane C.; Emmott, Edward; Surtees, Rebecca; Lardeau, Charles-Hugues; Wu, Weining; Duprex, W. Paul; Dove, Brian K.; Barr, John N.; Hiscox, Julian A.
Title: Quantitative Proteomic Analysis of A549 Cells Infected with Human Respiratory Syncytial Virus
  • Document date: 2010_7_20
  • ID: 2zhaknbi_3
    Snippet: During infection, the virus has multiple effects on the host cell. These include (but are not limited to) cell cycle arrest through the up-regulation of transforming growth factor ␤1 (18) , alterations in the composition of lipid raft membranes (19) , decreases in members of the IFN pathways such as TRAF3 (TNF receptor-associated factor 3) and STAT2 (signal transducers and activators of transcription protein 2) (20) , activation of the NF-B sig.....
    Document: During infection, the virus has multiple effects on the host cell. These include (but are not limited to) cell cycle arrest through the up-regulation of transforming growth factor ␤1 (18) , alterations in the composition of lipid raft membranes (19) , decreases in members of the IFN pathways such as TRAF3 (TNF receptor-associated factor 3) and STAT2 (signal transducers and activators of transcription protein 2) (20) , activation of the NF-B signal transduction pathway (21, 22) , and the activation of innate immunity through Toll-like receptor 2 (23) . Many of these processes are regulated by the induction of different gene subsets (24) . The relative level of host cell proteins can have a direct effect on HRSV disease progression where secondary bacterial infections are observed. For example, aberrant expression of a mucosal ␤-defensin leads to bacterial colonization by Haemophilus influenzae in HRSV infection (25) .

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