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Coupling of CFTR Cl− channel gating to an ATP hydrolysis cycle
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2019, Emery and Rimoin's Principles and Practice of Medical Genetics and Genomics: Cardiovascular, Respiratory, and Gastrointestinal DisordersHow phosphorylation and ATPase activity regulate anion flux though the cystic fibrosis transmembrane conductance regulator (CFTR)
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2013, Emery and Rimoin's Principles and Practice of Medical GeneticsA unified view of cystic fibrosis transmembrane conductance regulator (CFTR) gating: Combining the allosterism of a ligand-gated channel with the enzymatic activity of an ATP-binding cassette (ABC) transporter
2011, Journal of Biological ChemistryCitation Excerpt :This could explain the higher ATP sensitivities and the slower deactivation rates upon ATP removal observed for constitutive loop mutants (i.e. mutants that bias the equilibrium toward the open channel) (51). Given that the macroscopic deactivation rate of wild-type CFTR following ATP removal is determined by the rate of ATP hydrolysis and subsequent product release from site 2 (13, 14, 16, 21), the slower deactivation of these constitutive mutants (51) could be due to a slower release of ADP and/or Pi after hydrolysis. Conceptually, this can be explained by recognizing that pore opening and NBD1-NBD2 interactions are reciprocally coupled such that mutations that affect one (gating) must also bias the equilibrium toward the other (NBD dimerization).