Open AccessRespiratory syncytial virus (RSV) suppression of glucocorticoid receptor phosphorylation does not account for repression of transactivation
Author(s) -
Webster Marketon Jeanette I.,
Corry Jacqueline
Publication year - 2013
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1016/j.fob.2013.07.005
Subject(s) - transactivation , psychological repression , glucocorticoid receptor , bronchiolitis , phosphorylation , virology , respiratory system , virus , serine , biology , glucocorticoid , medicine , immunology , microbiology and biotechnology , gene , transcription factor , gene expression , biochemistry
Respiratory syncytial virus (RSV)‐induced bronchiolitis in infants, although inflammatory in nature, is not responsive to glucocorticoids. We have recently shown that RSV‐infected lung epithelial cells have impaired glucocorticoid receptor (GR)‐mediated transactivation. In this study, we show that the N‐terminal region of GR is required for RSV repression of GR transactivation and that RSV infection of lung epithelial cells reduces ligand‐dependent GR phosphorylation at serine 211 and serine 226. However, we also show that these changes in GR phosphorylation do not account for the RSV repression of GR transactivation suggesting other regions of the GR N‐terminus must also be involved.