Regulation of the Coxsackie and adenovirus receptor expression is dependent on cystic fibrosis transmembrane regulator in airway epithelial cells

Author:

Sharma Anurag1,Xu Yaqin1,Sung Biin2,Vincent C. Theresa34,Worgall Tilla5,Worgall Stefan12

Affiliation:

1. Department of Pediatrics; Weill Cornell Medicine; New York New York USA

2. Department of Genetic Medicine; Weill Cornell Medicine; New York New York USA

3. Department of Physiology and Biophysics; Weill Cornell Medicine; New York New York USA

4. Department of Pharmacology and Physiology; Karolinska Institute; Stockholm Sweden

5. Department of Pathology; Columbia University; New York New York USA

Funder

Cystic Fibrosis Foundation

Publisher

Hindawi Limited

Subject

Virology,Immunology,Microbiology

Reference45 articles.

1. Loss of CFTR results in reduction of histone deacetylase 2 in airway epithelial cells;Bartling;American Journal of Physiology. Lung Cellular and Molecular Physiology,2009a

2. Oxidative stress causes IL8 promoter hyperacetylation in cystic fibrosis airway cell models;Bartling;American Journal of Respiratory Cell and Molecular Biology,2009b

3. Isolation of a common receptor for Coxsackie B viruses and adenoviruses 2 and 5;Bergelson;Science,1997

4. Histone deacetylase inhibitors up-regulate the expression of tight junction proteins;Bordin;Molecular cancer research : MCR,2004

5. Correction of defective CFTR/ENaC function and tightness of cystic fibrosis airway epithelium by amniotic mesenchymal stromal (stem) cells;Carbone;Journal of Cellular and Molecular Medicine,2014

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