M
Miklós Bagdány
Researcher at McGill University
Publications - 22
Citations - 1840
Miklós Bagdány is an academic researcher from McGill University. The author has contributed to research in topics: Cystic fibrosis transmembrane conductance regulator & Förster resonance energy transfer. The author has an hindex of 12, co-authored 20 publications receiving 1626 citations. Previous affiliations of Miklós Bagdány include University of Debrecen.
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Journal ArticleDOI
Peripheral Protein Quality Control Removes Unfolded CFTR from the Plasma Membrane
Tsukasa Okiyoneda,Herve Barriere,Miklós Bagdány,Wael M. Rabeh,Kai Du,Jörg Höhfeld,Jason C. Young,Gergely L. Lukacs +7 more
TL;DR: Using functional small-interfering RNA screens in cells expressing the common cystic fibrosis mutation F508CFTR, the authors identified a pair of chaperones that promoted clearance of defective proteins from the plasma membrane that will also need to be overcome to increase the effectiveness of strategies to overcome protein misfolding disorders.
Journal ArticleDOI
Mechanism-based corrector combination restores ΔF508-CFTR folding and function
Tsukasa Okiyoneda,Guido Veit,Johanna F. Dekkers,Miklós Bagdány,Naoto Soya,Haijin Xu,Ariel Roldan,Alan S. Verkman,Mark J. Kurth,Ágnes Simon,Tamás Hegedus,Jeffrey M. Beekman,Gergely L. Lukacs +12 more
TL;DR: The molecular targets of available correctors are elucidated: class I stabilizes the NBD1-MSD1 and N BD1- MSD2 interfaces, and class II targets NBD2, which stabilizes human ΔF508-NBD1.
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Correction of both NBD1 energetics and domain interface is required to restore ΔF508 CFTR folding and function
Wael M. Rabeh,Florian Bossard,Haijin Xu,Tsukasa Okiyoneda,Miklós Bagdány,Cory M. Mulvihill,Kai Du,Salvatore di Bernardo,Yu-Hong Liu,Lars Konermann,Ariel Roldan,Gergely L. Lukacs +11 more
TL;DR: It is shown that ΔF508 destabilizes NBD1 both thermodynamically and kinetically, but correction of either defect alone is insufficient to restore Δf508 CFTR biogenesis, suggesting a synergistic role of NBD 1 energetics and topology in CFTR-coupled domain assembly.
Journal ArticleDOI
Some gating potentiators, including VX-770, diminish ΔF508-CFTR functional expression
Guido Veit,Radu G. Avramescu,Doranda Perdomo,Puay Wah Phuan,Miklós Bagdány,Pirjo M. Apaja,Florence Borot,Daniel Szollosi,Yu Sheng Wu,Walter E. Finkbeiner,Tamás Hegedus,Tamás Hegedus,Alan S. Verkman,Gergely L. Lukacs +13 more
TL;DR: Combining the two types of drugs does not work effectively because potentiators make CFTR less stable, accelerating the removal of this channel from the cell membrane, suggesting the need for further optimization of potentiator to maximize the clinical benefit of corrector-potentiator combination therapy in CF.
Journal ArticleDOI
Kv1.3 potassium channels are localized in the immunological synapse formed between cytotoxic and target cells
Gyorgy Panyi,György Vámosi,Zsolt Bacsó,Miklós Bagdány,Andrea Bodnár,Zoltan Varga,Rezsö Gáspár,László Mátyus,Sándor Damjanovich +8 more
TL;DR: This paper investigated the redistribution of Kv1.3 channels, which are the dominant voltage-gated potassium channels, in the plasma membrane of allogen-activated human cytotoxic T lymphocytes (CTLs) on interacting with their specific target cells.