Discovery of novel potent ΔF 508‐ CFTR correctors that target the nucleotide binding domain-Reference-Cited by-同舟云学术

Discovery of novel potent ΔF 508‐ CFTR correctors that target the nucleotide binding domain

Published:2013-08-27 Issue:10 Volume:5 Page:1484-1501
ISSN:1757-4676
Container-title:EMBO Molecular Medicine
language:en
Short-container-title:EMBO Mol Med

Author:

Odolczyk Norbert¹,Fritsch Janine²³,Norez Caroline⁴,Servel Nathalie²³,da Cunha Melanie Faria²³,Bitam Sara²³,Kupniewska Anna²,Wiszniewski Ludovic⁵,Colas Julien²³,Tarnowski Krzysztof⁶,Tondelier Danielle²³,Roldan Ariel⁷,Saussereau Emilie L.²³,Melin‐Heschel Patricia⁴,Wieczorek Grzegorz¹,Lukacs Gergely L.⁷,Dadlez Michal⁶,Faure Grazyna⁸,Herrmann Harald⁹,Ollero Mario²¹⁰,Becq Frédéric⁴,Zielenkiewicz Piotr¹¹¹,Edelman Aleksander²³

Affiliation:

1. Department of BioinformaticsInstitute of Biochemistry and BiophysicsPolish Academy of SciencesWarszawaPoland

2. INSERM, U845ParisFrance

3. Faculté de MédecineUniversité Paris DescartesParisFrance

4. Université de PoitiersInstitut de Physiologie et Biologie CellulairesPoitiersFrance

5. Epithelix SARLCH‐1228 Plan‐Les‐OuatesGenevaSwitzerland

6. Laboratory of Mass SpectrometryInstitute of Biochemistry and BiophysicsPolish Academy of SciencesWarszawaPoland

7. Department of PhysiologyMcGill UniversityMontrealCanada

8. Unité Récepteurs‐Canaux; Institut PasteurCNRSParisFrance

9. Department of Molecular GeneticsGerman Cancer Research CenterHeidelbergGermany

10. INSERM, U955, Equipe 21CreteilFrance

11. Laboratory of Plant Molecular BiologyFaculty of BiologyWarsaw UniversityWarszawaPoland

Publisher

EMBO

Subject

Molecular Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/emmm.201302699

Reference54 articles.

1. Pharmacological therapy for cystic fibrosis: From bench to bedside

2. Assessment of the CFTR and ENaC association

3. Correctors of Protein Trafficking Defects Identified by a Novel High-Throughput Screening Assay

4. Phosphorylation of the R domain by cAMP-dependent protein kinase regulates the CFTR chloride channel

5. Disruption of cytokeratin-8 interaction with F508del-CFTR corrects its functional defect

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