Modulation of CFTR & ENaC Channel
Function By Interacting Proteins & Trafficking

By Lishuang Cao
Acta Biomedica Lovaniensia, No. 351
December 2005
Leuven University Press
ISBN: 9058675106
143 pages, Illustrated, 6 ¼” x 9 ½”
$77.50 Paper Original

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This is a Ph.D. dissertation.

Contents include:
Introduction:
1. Cystic fibrosis, a fatal genetic disease
2. CFTR, from gene to protein
3. CFTR functions as a chloride channel
4. CFTR, a regulator of other proteins
5. Classes of CFTR mutations
6. What happens to the most frequent mutant, ?F508-CFTR?
7. Rescue of ?F508-CFTR channel function: State of the art
8. ENaC, another important ion channel related to CF
Objectives:
1. Functional effect on CFTR channel activity upon MDR1 expression
2. Functional characterization of PP2A activity on the deactivation of CFTR channel
3. Functional rescue of ?F508-CFTR
4. Long-term effect of epithelial growth factor treatment on the functional expression of ENaC Channels
Materials and Methods:
1. Cell culture and DNA transfection
2. RNA analysis, vector and DNA constructs
3. Yeast two hybrid screening
4. Yeast two hybrid interaction assay
5. Biochemical techniques
6. Measurement of [Ca2+]i
7. Electrophysiological recordings
8. Solutions for patch-clamp experiments
9. Data analysis
Results:
1. Functional analysis of CFTR chloride channel activity in cells with elevated MDR1 expression
2. Interaction of PR65, a subunit of the protein phosphate 2A, with the regulatory domain of the CFTR Channel
3. Rescue of functional ?F508-CFTR channels by coexpression with truncated CFTR constructs in COS-1 cells
4. Chronic exposure to EGF affects trafficking and function of ENaC channel in cystic fibrosis cells
General Discussion and Future Prospects:
1. The interaction between CFTR and MDR1
2. The regulation of CFTR channel function by PP2A
3. Functional rescue of ?F508-CFTR
4. The regulation of ENaC channel
Summary
References
List of Publications

Biochemistry

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