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As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.Articles
Unraveling the Mechanism of Action, Binding Sites, and Therapeutic Advances of CFTR Modulators: A Narrative Review
All articles published by MDPI are made immediately available worldwide under an open access license. No special permission is required to reuse all or part of the article published by MDPI, including figures and tables. For articles published under an open access Creative Common CC BY license, any part of the article may be reused without permission provided that the original article is clearly cited. For more information, please refer to https://www.mdpi.com/openaccess.
In Silico and In Vitro Evaluation of the Mechanism of Action of Three VX809-Based Hybrid Derivatives as Correctors of the F508del CFTR Protein
All articles published by MDPI are made immediately available worldwide under an open access license. No special permission is required to reuse all or part of the article published by MDPI, including figures and tables. For articles published under an open access Creative Common CC BY license, any part of the article may be reused without permission provided that the original article is clearly cited. For more information, please refer to https://www.mdpi.com/openaccess.
Elexacaftor Mediates the Rescue of F508del CFTR Functional Expression Interacting with MSD2
1. Introduction Cystic fibrosis (CF) is an autosomal recessive disease caused by variants in the cystic fibrosis transmembrane conductance regulator (CFTR) protein, a chloride and bicarbonate channel located on the apical side of epithelia, where it plays a critical role in maintaining the electrolyte and fluid balance of the surface liquid layer [1,2]. The lack or dysfunction of CFTR results in thick secretions that cause gastrointestinal, reproductive, and respiratory system defects.
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