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1 identity to the untranslated regions of the cystic fibrosis transmembrane regulator.
2 tive cation channels, K(+) channels, and the cystic fibrosis transmembrane regulator.
3 ted by extracellular ATP and possibly by the cystic fibrosis transmembrane regulator.
4 ng motif (QDTRL) in the carboxyl terminus of cystic fibrosis transmembrane regulator.
5 ent of epithelia decreased expression of the cystic fibrosis transmembrane regulator.
6 e, further enhanced by coexpressed wild type cystic fibrosis transmembrane regulator but inhibited by
8 in these vesicles of not only AQP1 but also cystic fibrosis transmembrane regulator (CFTR) and AE2,
9 onditions known to facilitate trafficking of cystic fibrosis transmembrane regulator (CFTR) and other
14 lease and modulation of calcium channels and cystic fibrosis transmembrane regulator (CFTR) chloride
16 therefore examined the effects of BDM on the cystic fibrosis transmembrane regulator (CFTR) Cl(-) cha
17 ts in cyclic AMP-dependent activation of the cystic fibrosis transmembrane regulator (CFTR) Cl- chann
18 P-sensitive K+ (KATP) channels, also inhibit cystic fibrosis transmembrane regulator (CFTR) Cl- chann
19 ng the most common mutation (delF508) of the cystic fibrosis transmembrane regulator (CFTR) exhibit a
21 possibility, the entire coding region of the cystic fibrosis transmembrane regulator (CFTR) gene was
22 imer pairs that amplify sequences within the cystic fibrosis transmembrane regulator (CFTR) gene, mut
23 han 750 mutations have been described in the cystic fibrosis transmembrane regulator (CFTR) gene.
24 ystic fibrosis is caused by mutations in the cystic fibrosis transmembrane regulator (CFTR) gene.
26 ation and metabolic fate of WT and deltaF508 cystic fibrosis transmembrane regulator (CFTR) in the lu
28 and preaggresome particles of the misfolded cystic fibrosis transmembrane regulator (CFTR) mutant CF
30 eport the effects of gentamicin treatment on cystic fibrosis transmembrane regulator (CFTR) productio
31 ng disease including the impact of defective cystic fibrosis transmembrane regulator (CFTR) protein f
32 folding defect associated with the deltaF508 cystic fibrosis transmembrane regulator (CFTR) protein.
33 f HelA is similar to the F508 residue of the cystic fibrosis transmembrane regulator (CFTR) protein.
34 ATP-sensitive renal K+ channel (IKATP) with cystic fibrosis transmembrane regulator (CFTR) significa
36 cretin receptors (SRs) through activation of cystic fibrosis transmembrane regulator (CFTR), Cl(-) /H
37 -causing protein folding mutation, DeltaF508-cystic fibrosis transmembrane regulator (CFTR), is destr
39 t regulate tissue-specific expression of the cystic fibrosis transmembrane regulator (CFTR), we have
41 y increases Cl(-) and fluid secretion in the cystic fibrosis transmembrane regulator (CFTR)-expressin
46 omotes cyclic AMP-mediated activation of the cystic fibrosis transmembrane regulator chloride channel
47 effects of heat-stable enterotoxins via the cystic fibrosis transmembrane regulator Cl(-) channel, t
48 d (iii) de novo expressed secretin receptor, cystic fibrosis transmembrane regulator, Cl(-)/HCO(3)(-)
49 nsmembrane regulator inhibitor 172-sensitive cystic fibrosis transmembrane regulator currents were re
51 he following: (1) Strong association between cystic fibrosis transmembrane regulator dysfunction/muta
52 important for TDP-43 splicing inhibition of cystic fibrosis transmembrane regulator exon 9, and ther
53 d lower expression of chloride channel 2 and cystic fibrosis transmembrane regulator in diabetic corn
56 ed group to only those diagnosable with a 31 cystic fibrosis transmembrane regulator mutation assay a
57 ed substrates: the DeltaF-508 mutant form of cystic fibrosis transmembrane regulator, nucleotide bind
60 though definitive correction of the abnormal cystic fibrosis transmembrane regulator protein function
61 (ABC) transporter family, which includes the cystic fibrosis transmembrane regulator, the P-glycoprot
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