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

This is a Ph.D. dissertation.

Contents include:
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
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
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
List of Publications


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