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https://athenacommons.muw.edu/urc/2021/stem/1
Department
Sciences & Mathematics
Format of Presentation
Oral Presentation
Research Category
STEM
Description
Cystic Fibrosis Transmembrane conductance Regulator (CFTR) is a protein that functions as a chloride ion channel on the plasma membrane of epithelial cells. A mutated CFTR is the cause of the genetic disease cystic fibrosis (CF), which is more common in Caucasians of northern European origin. The most common of CFTR mutations is DF508 accounting for >70% of CF cases. The aim of my proposed study is to determine the effects of certain synthetic compounds with known chloride ion channel activation properties on the expression of the DF508-CFTR protein. Dr. Heda’s laboratory has obtained five such compounds (viz., PJ-03, PJ-08, PJ-09, PJ-10, JVD alkyl) with his collaboration from an institution in India (IISER). Cystic Fibrosis Bronchial Epithelial (CFBE) cells transfected with DF508-CFTR will be treated with various concentrations (10µM-60µM) for 60 hours to increase the CFTR expression. Cell lysates will be prepared and immunoblotted. Immunoblotting is a commonly used technique for the detection of protein expression levels. This analytical technique will allow me to determine the effects of any of these compounds on the expression of DF508-CFTR. Increase in DF508-CFTR expression because of these compounds may have therapeutic properties on the CF diagnosis.
Recommended Citation
Sligh, Sara, "Effects of Chloride Ion Channel Activators on CFTR Expression" (2021). Undergraduate Research Conference. 1.
https://athenacommons.muw.edu/urc/2021/stem/1
Effects of Chloride Ion Channel Activators on CFTR Expression
Cystic Fibrosis Transmembrane conductance Regulator (CFTR) is a protein that functions as a chloride ion channel on the plasma membrane of epithelial cells. A mutated CFTR is the cause of the genetic disease cystic fibrosis (CF), which is more common in Caucasians of northern European origin. The most common of CFTR mutations is DF508 accounting for >70% of CF cases. The aim of my proposed study is to determine the effects of certain synthetic compounds with known chloride ion channel activation properties on the expression of the DF508-CFTR protein. Dr. Heda’s laboratory has obtained five such compounds (viz., PJ-03, PJ-08, PJ-09, PJ-10, JVD alkyl) with his collaboration from an institution in India (IISER). Cystic Fibrosis Bronchial Epithelial (CFBE) cells transfected with DF508-CFTR will be treated with various concentrations (10µM-60µM) for 60 hours to increase the CFTR expression. Cell lysates will be prepared and immunoblotted. Immunoblotting is a commonly used technique for the detection of protein expression levels. This analytical technique will allow me to determine the effects of any of these compounds on the expression of DF508-CFTR. Increase in DF508-CFTR expression because of these compounds may have therapeutic properties on the CF diagnosis.
https://athenacommons.muw.edu/urc/2021/stem/1