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Estimating the true stability of the prehydrolytic outward-facing state in an ABC protein. , Simon MA., Elife. October 2, 2023; 12
Asymmetry of movements in CFTR's two ATP sites during pore opening serves their distinct functions. , Sorum B., Elife. September 25, 2017; 6
Molecular Structure of the Human CFTR Ion Channel. , Liu F., Cell. March 23, 2017; 169 (1): 85-95.e8.
Cysteine accessibility probes timing and extent of NBD separation along the dimer interface in gating CFTR channels. , Chaves LA., J Gen Physiol. April 1, 2015; 145 (4): 261-83.
Comparative expression analysis of cysteine-rich intestinal protein family members crip1, 2 and 3 during Xenopus laevis embryogenesis. , Hempel A., Int J Dev Biol. January 1, 2014; 58 (10-12): 841-9.
Conformational changes in the catalytically inactive nucleotide-binding site of CFTR. , Csanády L., J Gen Physiol. July 1, 2013; 142 (1): 61-73.
Gout-causing Q141K mutation in ABCG2 leads to instability of the nucleotide-binding domain and can be corrected with small molecules. , Woodward OM., Proc Natl Acad Sci U S A. March 26, 2013; 110 (13): 5223-8.
A universally conserved residue in the SUR1 subunit of the KATP channel is essential for translating nucleotide binding at SUR1 into channel opening. , de Wet H., J Physiol. October 15, 2012; 590 (20): 5025-36.
Mutant cycles at CFTR's non-canonical ATP-binding site support little interface separation during gating. , Szollosi A., J Gen Physiol. June 1, 2011; 137 (6): 549-62.
Electrophysiological, biochemical, and bioinformatic methods for studying CFTR channel gating and its regulation. , Csanády L., Methods Mol Biol. January 1, 2011; 741 443-69.
CFTR regulation of epithelial sodium channel. , Qadri YJ., Methods Mol Biol. January 1, 2011; 742 35-50.
Involvement of F1296 and N1303 of CFTR in induced-fit conformational change in response to ATP binding at NBD2. , Szollosi A., J Gen Physiol. October 1, 2010; 136 (4): 407-23.
Strict coupling between CFTR's catalytic cycle and gating of its Cl- ion pore revealed by distributions of open channel burst durations. , Csanády L., Proc Natl Acad Sci U S A. January 19, 2010; 107 (3): 1241-6.
State-dependent inhibition of cystic fibrosis transmembrane conductance regulator chloride channels by a novel peptide toxin. , Fuller MD., J Biol Chem. December 28, 2007; 282 (52): 37545-55.
Thermodynamics of CFTR channel gating: a spreading conformational change initiates an irreversible gating cycle. , Csanády L., J Gen Physiol. November 1, 2006; 128 (5): 523-33.
In vivo phosphorylation of CFTR promotes formation of a nucleotide-binding domain heterodimer. , Mense M., EMBO J. October 18, 2006; 25 (20): 4728-39.
An energy-dependent maturation step is required for release of the cystic fibrosis transmembrane conductance regulator from early endoplasmic reticulum biosynthetic machinery. , Oberdorf J., J Biol Chem. November 18, 2005; 280 (46): 38193-202.
Functional roles of nonconserved structural segments in CFTR's NH2-terminal nucleotide binding domain. , Csanády L., J Gen Physiol. January 1, 2005; 125 (1): 43-55.
Imaging CFTR: a tail to tail dimer with a central pore. , Schillers H., Cell Physiol Biochem. January 1, 2004; 14 (1-2): 1-10.
Chromanol 293B, a blocker of the slow delayed rectifier K+ current (IKs), inhibits the CFTR Cl- current. , Bachmann A., Naunyn Schmiedebergs Arch Pharmacol. June 1, 2001; 363 (6): 590-6.
Severed molecules functionally define the boundaries of the cystic fibrosis transmembrane conductance regulator's NH(2)-terminal nucleotide binding domain. , Chan KW., J Gen Physiol. August 1, 2000; 116 (2): 163-80.
The first-nucleotide binding domain of the cystic-fibrosis transmembrane conductance regulator is important for inhibition of the epithelial Na+ channel. , Schreiber R., Proc Natl Acad Sci U S A. April 27, 1999; 96 (9): 5310-5.
Novel subunit composition of a renal epithelial KATP channel. , Ruknudin A., J Biol Chem. June 5, 1998; 273 (23): 14165-71.