- Abstract:
-
The most common mutation of Cystic Fibrosis (CF) Transmembrane Regulator (CFTR) gene, F508del, produces a misfolded protein resulting in its defective trafficking to the cell surface and an impaired chloride secretion. Pharmacological treatments partially rescue F508del CFTR activity either directly by interacting with the mutant protein and/or indirectly by altering the cellular protein homeostasis. We show that the ezrin phosphorylation together with its binding to phosphatidylinositol-4,5-...
Expand abstract - Publication status:
- Published
- Peer review status:
- Peer reviewed
- Publisher copy:
- 10.1242/jcs.177907
-
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- Publisher:
- Company of Biologists Ltd Publisher's website
- Journal:
- Journal of Cell Science Journal website
- Publication date:
- 2016-01-01
- DOI:
- EISSN:
-
1477-9137
- ISSN:
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0021-9533
- URN:
-
uuid:f1c08030-d035-415e-8f22-5f2a258357c0
- Source identifiers:
-
599424
- Local pid:
- pubs:599424
- Keywords:
- Copyright holder:
- Abbattiscianni et al.
- Copyright date:
- 2016
Journal article
Correctors of mutant CFTR enhance subcortical cAMP/PKA signaling via ezrin phosphorylation and cytoskeleton organization
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