Combination of Selective PARP3 and PARP16 Inhibitory Analogues of Latonduine A Corrects F508del-CFTR Trafficking-Reference-Cited by-同舟云学术

Combination of Selective PARP3 and PARP16 Inhibitory Analogues of Latonduine A Corrects F508del-CFTR Trafficking

Published:2020-09-29 Issue:40 Volume:5 Page:25593-25604
ISSN:2470-1343
Container-title:ACS Omega
language:en
Short-container-title:ACS Omega

Author:

Centko Ryan M.,Carlile Graeme W.¹,Barne Isabel,Patrick Brian O.,Blagojevic Polina,Thomas David Y.¹,Andersen Raymond J.^ORCID

Affiliation:

1. Departments of Biochemistry and Human Genetics and The Cystic Fibrosis Translational Research Centre, McGill University, Montréal, Québec, Canada H3G 1Y6

Funder

Canadian Institutes of Health Research

Cystic Fibrosis Canada

Natural Sciences and Engineering Research Council of Canada

Publisher

American Chemical Society (ACS)

Subject

General Chemical Engineering,General Chemistry

Link

http://pubs.acs.org/doi/pdf/10.1021/acsomega.0c02467

Reference43 articles.

1. Correctors of the basic trafficking defect of the mutant F508del-CFTR that causes cystic fibrosis

2. Multiple proteolytic systems, including the proteasome, contribute to CFTR processing

3. Degradation of CFTR by the ubiquitin-proteasome pathway

4. Processing of mutant cystic fibrosis transmembrane conductance regulator is temperature-sensitive

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

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