Respiratory syncytial virus (RSV) suppression of glucocorticoid receptor phosphorylation does not account for repression of transactivation

被引:2
|
作者
Marketon, Jeanette I. Webster [1 ,2 ]
Corry, Jacqueline [1 ]
机构
[1] Ohio State Univ, Div Pulm Allergy Crit Care & Sleep Med, Dept Internal Med, Wexner Med Ctr, Columbus, OH 43210 USA
[2] Ohio State Univ, Wexner Med Ctr, Inst Behav Med Res, Columbus, OH 43210 USA
来源
FEBS OPEN BIO | 2013年 / 3卷
关键词
Respiratory syncytial virus; Glucocorticoid receptor; Transactivation; Phosphorylation; Protein phosphatase; DOUBLE-BLIND; CHILDREN; DEXAMETHASONE; INDUCTION; INFECTION; INFANTS; PP5;
D O I
10.1016/j.fob.2013.07.005
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 2013 The Authors. Published by Elsevier B.V. on behalf of Federation of European Biochemical Societies. All rights reserved.
引用
收藏
页码:305 / 309
页数:5
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