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Elexacaftor co-potentiates the activity of F508del and gating mutants of CFTR

Journal of cystic fibrosis, 2021-09, Vol.20 (5), p.895-898

2021

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CFTR: folding, misfolding and correcting the ΔF508 conformational defect

Trends in molecular medicine, 2012-02, Vol.18 (2), p.81-91

2012

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PINK1 autophosphorylation is required for ubiquitin recognition

EMBO reports, 2018-04, Vol.19 (4), p.n/a

2018

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From CFTR biology toward combinatorial pharmacotherapy: expanded classification of cystic fibrosis mutations

Molecular biology of the cell, 2016-02, Vol.27 (3), p.424-433

2016

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Correction of Both NBD1 Energetics and Domain Interface Is Required to Restore ΔF508 CFTR Folding and Function

Cell, 2012-01, Vol.148 (1-2), p.150-163

2012

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Cooperative assembly and misfolding of CFTR domains in vivo

Molecular biology of the cell, 2009-04, Vol.20 (7), p.1903-1915

2009

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Allosteric folding correction of F508del and rare CFTR mutants by elexacaftor-tezacaftor-ivacaftor (Trikafta) combination

JCI insight, 2020-09, Vol.5 (18)

2020

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Peripheral Protein Quality Control Removes Unfolded CFTR from the Plasma Membrane

Science (American Association for the Advancement of Science), 2010-08, Vol.329 (5993), p.805-810

2010

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The ΔF508 cystic fibrosis mutation impairs domain-domain interactions and arrests post-translational folding of CFTR

Nature structural & molecular biology, 2005-01, Vol.12 (1), p.17-25

2005

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Ubiquitin-dependent sorting in endocytosis

Cold Spring Harbor perspectives in biology, 2014-01, Vol.6 (1), p.a016808-a016808

2014

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Mechanism of PINK1 activation by autophosphorylation and insights into assembly on the TOM complex

Molecular cell, 2022-01, Vol.82 (1), p.44-59.e6

2022

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Differential Scanning Fluorimetry and Hydrogen Deuterium Exchange Mass Spectrometry to Monitor the Conformational Dynamics of NBD1 in Cystic Fibrosis

Methods in molecular biology (Clifton, N.J.), 2019, Vol.1873, p.53

2019

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Mechanism-based corrector combination restores ΔF508-CFTR folding and function

Nature chemical biology, 2013-07, Vol.9 (7), p.444

2013

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Readthrough-induced misincorporated amino acid ratios guide mutant-specific therapeutic approaches for two CFTR nonsense mutations

Frontiers in pharmacology, 2024-04, Vol.15, p.1389586-1389586

2024

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Fixing cystic fibrosis by correcting CFTR domain assembly

The Journal of cell biology, 2012-10, Vol.199 (2), p.199-204

2012

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Proteostasis: Chaperoning for hearing loss

Nature chemical biology, 2016-05, Vol.12 (6), p.388

Lukacs, Gergely L

2016

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Synergy-based small-molecule screen using a human lung epithelial cell line yields ΔF508-CFTR correctors that augment VX-809 maximal efficacy

Molecular pharmacology, 2014-07, Vol.86 (1), p.42-51

2014

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Selective Binding of HSC70 and its Co-Chaperones to Structural Hotspots on CFTR

Scientific reports, 2020-03, Vol.10 (1), p.4176-4176, Article 4176

2020

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Some gating potentiators, including VX-770, diminish ΔF508-CFTR functional expression

Science translational medicine, 2014-07, Vol.6 (246), p.246ra97

2014

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Alcohol Disrupts Levels and Function of the Cystic Fibrosis Transmembrane Conductance Regulator to Promote Development of Pancreatitis

Gastroenterology (New York, N.Y. 1943), 2015-02, Vol.148 (2), p.427-439.e16

2015

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Folding correctors can restore CFTR posttranslational folding landscape by allosteric domain-domain coupling

Nature communications, 2023-10, Vol.14 (1), p.6868-6868, Article 6868

2023

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Phosphorylation-dependent modulation of CFTR macromolecular signalling complex activity by cigarette smoke condensate in airway epithelia

Scientific reports, 2019-09, Vol.9 (1), p.12706-19, Article 12706

2019

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Structure-guided combination therapy to potently improve the function of mutant CFTRs

Nature medicine, 2018-11, Vol.24 (11), p.1732-1742

2018

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Mutation-specific downregulation of CFTR2 variants by gating potentiators

Human molecular genetics, 2017-12, Vol.26 (24), p.4873-4885

2017

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Chaperone-Independent Peripheral Quality Control of CFTR by RFFL E3 Ligase

Developmental cell, 2018-03, Vol.44 (6), p.694-708.e7

2018

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Elexacaftor co-potentiates the activity of F508del and gating mutants of CFTR

CFTR: folding, misfolding and correcting the ΔF508 conformational defect

PINK1 autophosphorylation is required for ubiquitin recognition

From CFTR biology toward combinatorial pharmacotherapy: expanded classification of cystic fibrosis mutations

Correction of Both NBD1 Energetics and Domain Interface Is Required to Restore ΔF508 CFTR Folding and Function

Cooperative assembly and misfolding of CFTR domains in vivo

Allosteric folding correction of F508del and rare CFTR mutants by elexacaftor-tezacaftor-ivacaftor (Trikafta) combination

Peripheral Protein Quality Control Removes Unfolded CFTR from the Plasma Membrane

The ΔF508 cystic fibrosis mutation impairs domain-domain interactions and arrests post-translational folding of CFTR

Ubiquitin-dependent sorting in endocytosis

Mechanism of PINK1 activation by autophosphorylation and insights into assembly on the TOM complex

Differential Scanning Fluorimetry and Hydrogen Deuterium Exchange Mass Spectrometry to Monitor the Conformational Dynamics of NBD1 in Cystic Fibrosis

Mechanism-based corrector combination restores ΔF508-CFTR folding and function

Readthrough-induced misincorporated amino acid ratios guide mutant-specific therapeutic approaches for two CFTR nonsense mutations

Fixing cystic fibrosis by correcting CFTR domain assembly

Proteostasis: Chaperoning for hearing loss

Synergy-based small-molecule screen using a human lung epithelial cell line yields ΔF508-CFTR correctors that augment VX-809 maximal efficacy

Selective Binding of HSC70 and its Co-Chaperones to Structural Hotspots on CFTR

Some gating potentiators, including VX-770, diminish ΔF508-CFTR functional expression

Alcohol Disrupts Levels and Function of the Cystic Fibrosis Transmembrane Conductance Regulator to Promote Development of Pancreatitis

Folding correctors can restore CFTR posttranslational folding landscape by allosteric domain-domain coupling

Phosphorylation-dependent modulation of CFTR macromolecular signalling complex activity by cigarette smoke condensate in airway epithelia

Structure-guided combination therapy to potently improve the function of mutant CFTRs

Mutation-specific downregulation of CFTR2 variants by gating potentiators

Chaperone-Independent Peripheral Quality Control of CFTR by RFFL E3 Ligase

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