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1 tide-binding domain from the cystic fibrosis transmembrane conductance regulator.
2 en through activation of the cystic fibrosis transmembrane conductance regulator.
3 lesser effects on misfolded cystic fibrosis transmembrane conductance regulator.
4 ction in the gene coding for cystic fibrosis transmembrane conductance regulator.
5 stance arteries ex vivo, the cystic fibrosis transmembrane conductance regulator (1) is critical for
6 nger regulatory factor-1 and cystic fibrosis transmembrane conductance regulator (a key player in the
7 psin-controlling gene or the cystic fibrosis transmembrane conductance regulator); a few patients hav
9 ctor-alpha downregulates the cystic fibrosis transmembrane conductance regulator across several organ
10 cells via a reduction in the cystic fibrosis transmembrane conductance regulator activity and biosynt
11 essure resulted in decreased cystic fibrosis transmembrane conductance regulator activity and liquid
13 ffects on the degradation of cystic fibrosis transmembrane conductance regulator and CPY*, which is a
14 he NHERF1-binding domains of cystic fibrosis transmembrane conductance regulator and Csk-binding prot
15 secretion appears to require cystic fibrosis transmembrane conductance regulator and electrogenic Na(
16 porters (ABC), including the cystic fibrosis transmembrane conductance regulator and P-glycoprotein.
17 was completely dependent on cystic fibrosis transmembrane conductance regulator and partially depend
18 al exocytosis of NHE3, CFTR (cystic fibrosis transmembrane conductance regulator), and GLUT5 required
19 -dependent activation of the cystic fibrosis transmembrane conductance regulator anion channel was in
21 Opening and closing of the cystic fibrosis transmembrane conductance regulator are controlled by AT
23 es, at least in part through cystic fibrosis transmembrane conductance regulator-associated channels,
24 slows the degradation of the cystic fibrosis transmembrane conductance regulator but does not impede
25 unction mutations in the chloride channel CF transmembrane conductance regulator can elevate the acti
26 in gross mislocalization of cystic fibrosis transmembrane conductance regulator, causing marked redu
27 s to the gating mutations of cystic fibrosis transmembrane conductance regulator (CFTR or ABCC7; i.e.
29 ol of cell proliferation and cystic fibrosis transmembrane conductance regulator (CFTR) -driven fluid
30 coid dexamethasone increases cystic fibrosis transmembrane conductance regulator (CFTR) abundance in
31 linone CFTRact-J027 (4) as a cystic fibrosis transmembrane conductance regulator (CFTR) activator wit
32 ates that ivacaftor improves cystic fibrosis transmembrane conductance regulator (CFTR) activity and
34 ons to the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) also cause pa
35 membrane, which include the cystic fibrosis transmembrane conductance regulator (CFTR) and Ca(2+)-ac
36 association between lack of cystic fibrosis transmembrane conductance regulator (CFTR) and ceramide
37 ainst other proteins such as cystic fibrosis transmembrane conductance regulator (CFTR) and dystrophi
38 ulated by apically expressed cystic fibrosis transmembrane conductance regulator (CFTR) and large-con
39 nal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFTR) and solute ca
40 alveolar fluid balance: the cystic fibrosis transmembrane conductance regulator (CFTR) and the amilo
41 l permeability and decreased cystic fibrosis transmembrane conductance regulator (Cftr) and the Na-K-
42 /H(+) antiporter, CLC-5, the cystic fibrosis transmembrane conductance regulator (CFTR) and the sodiu
43 g cassette (ABC) transporter cystic fibrosis transmembrane conductance regulator (CFTR) and two other
44 and secrete Cl- through the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
45 alanine 508 (F508del) in the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
47 on special properties of the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
48 in the gene that encodes the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
49 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
50 loride permeation pathway in cystic fibrosis transmembrane conductance regulator (CFTR) as a short na
51 ts in functional expression defect of the CF transmembrane conductance regulator (CFTR) at the apical
53 inclusion of the full-length cystic fibrosis transmembrane conductance regulator (CFTR) cDNA together
54 espite the importance of the cystic fibrosis transmembrane conductance regulator (CFTR) channel for e
56 F) mice with a nonfunctional cystic fibrosis transmembrane conductance regulator (CFTR) channel was r
57 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) channel, whic
59 lands are important sites of cystic fibrosis transmembrane conductance regulator (CFTR) chloride (Cl(
60 used by loss of a functional cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
61 e: functional defects of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
62 eine scanning studies of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
63 y the functional expression defect of the CF transmembrane conductance regulator (CFTR) chloride chan
65 regulatory (R) domain of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
66 s caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
67 all-molecule blockers of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
68 ystic fibrosis (CF), a lack of functional CF transmembrane conductance regulator (CFTR) chloride chan
69 pus oocytes coexpressing the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
70 ppropriate activation of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
71 esults from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
72 eads to an inhibition of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel
73 ability, and function of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel
75 the loss of function of the cystic fibrosis transmembrane conductance regulator (CFTR) combined with
76 We evaluated the effects of cystic fibrosis transmembrane conductance regulator (CFTR) deficiency on
77 Smoking is reported to cause cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction i
79 um (OE) of mice deficient in cystic fibrosis transmembrane conductance regulator (CFTR) exhibits ion
80 n epithelial cells decreases cystic fibrosis transmembrane conductance regulator (CFTR) expression an
82 main interaction between the cystic fibrosis transmembrane conductance regulator (CFTR) first cytosol
83 as correctors of the F508del-cystic fibrosis transmembrane conductance regulator (CFTR) folding defec
84 e findings are directly caused by loss of CF transmembrane conductance regulator (CFTR) function or s
87 covery that mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene cause cy
89 hesis that disruption of the cystic fibrosis transmembrane conductance regulator (CFTR) gene directly
90 of-function mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene encoding
92 ted since the cloning of the cystic fibrosis transmembrane conductance regulator (CFTR) gene is being
93 The F508del mutation in the cystic fibrosis transmembrane conductance regulator (Cftr) gene is belie
94 kb -35 (DHS-35kb) 5' to the cystic fibrosis transmembrane conductance regulator (CFTR) gene is evide
95 he DeltaF508 mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene is the m
96 ease-causing mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene is the o
99 brosis (CF) is caused by mutations in the CF transmembrane conductance regulator (CFTR) gene that imp
101 V1, expressing a full-length cystic fibrosis transmembrane conductance regulator (CFTR) gene, is capa
102 .7-kb promoter region of the cystic fibrosis transmembrane conductance regulator (CFTR) gene, we defi
103 s caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which e
111 binding domain (NBD2) of the cystic fibrosis transmembrane conductance regulator (CFTR) has lagged be
112 e than 2000 mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) have been des
113 es (MPhis) with mutations in cystic fibrosis transmembrane conductance regulator (CFTR) have blunted
114 function of Slc26a6 and the cystic fibrosis transmembrane conductance regulator (CFTR) in HeLa cells
115 rosis homozygous for F508del-cystic fibrosis transmembrane conductance regulator (CFTR) in placebo-co
116 is to efficiently and safely express the CF transmembrane conductance regulator (CFTR) in the approp
117 Loss of function of the cystic fibrosis transmembrane conductance regulator (CFTR) in the biliar
118 The role of Pseudomonas aeruginosa and CF transmembrane conductance regulator (CFTR) in Treg regul
119 used by the F508 mutation in cystic fibrosis transmembrane conductance regulator (CFTR) include a "co
129 cAMP-activated Cl(-) channel cystic fibrosis transmembrane conductance regulator (CFTR) is a major pr
130 brates, the chloride channel cystic fibrosis transmembrane conductance regulator (CFTR) is a master r
145 an DeltaF508 mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) is associated
146 Endocytic recycling of the cystic fibrosis transmembrane conductance regulator (CFTR) is blocked by
148 modulator compounds for the cystic fibrosis transmembrane conductance regulator (CFTR) is key for th
150 08 deletion (F508del) in the cystic fibrosis transmembrane conductance regulator (CFTR) is the most c
153 gamma stimulation in vivo in cystic fibrosis transmembrane conductance regulator (Cftr) knockout mice
154 binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFTR) leads to defe
155 s or dysfunction of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) leads to impa
157 s (FPOP) for footprinting of cystic fibrosis transmembrane conductance regulator (CFTR) membrane tran
158 mbination treatment with the cystic fibrosis transmembrane conductance regulator (CFTR) modulators te
160 e carrying the most frequent cystic fibrosis transmembrane conductance regulator (CFTR) mutation in h
163 The chloride channel of the cystic fibrosis transmembrane conductance regulator (CFTR) participates
164 anine 508 (DeltaF508) in the cystic fibrosis transmembrane conductance regulator (CFTR) plasma membra
165 fold and increased wild-type cystic fibrosis transmembrane conductance regulator (CFTR) plasma membra
168 ed by defective or deficient cystic fibrosis transmembrane conductance regulator (CFTR) protein activ
169 DeltaPhe508 mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) protein impai
171 ng the activity of defective cystic fibrosis transmembrane conductance regulator (CFTR) protein is a
172 and decreased apical cilia, cystic fibrosis transmembrane conductance regulator (CFTR) protein level
173 unction or deficiency of the cystic fibrosis transmembrane conductance regulator (CFTR) protein, an e
174 sing of the DeltaF508 mutant cystic fibrosis transmembrane conductance regulator (CFTR) protein.
175 is (CF) is due to a folding defect in the CF transmembrane conductance regulator (CFTR) protein.
178 hly PKA-phosphorylated human cystic fibrosis transmembrane conductance regulator (CFTR) regulatory re
179 type and variant (DeltaF508) cystic fibrosis transmembrane conductance regulator (CFTR) responsible f
181 binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFTR) results in de
182 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) that compromi
183 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) that impair i
184 brosis (CF) is caused by mutations in the CF transmembrane conductance regulator (CFTR) that prevent
185 ftor is a potentiator of the cystic fibrosis transmembrane conductance regulator (CFTR) that reduces
186 lamotrigine), as well as the cystic fibrosis transmembrane conductance regulator (CFTR) trafficking c
187 Misfolding of DeltaF508 cystic fibrosis (CF) transmembrane conductance regulator (CFTR) underlies pat
188 amino acids inserted at the cystic fibrosis transmembrane conductance regulator (CFTR) W1282X PTC (a
189 ons of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) which is an a
190 the apical chloride channel cystic fibrosis transmembrane conductance regulator (CFTR) with 90% of p
191 ons of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) with a preval
193 functional abnormalities of cystic fibrosis transmembrane conductance regulator (CFTR), a 25% reduct
194 f apoptosis and involves the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-regul
195 inylation and degradation of cystic fibrosis transmembrane conductance regulator (CFTR), a chloride c
196 we examined the role of the cystic fibrosis transmembrane conductance regulator (CFTR), a Cl(-) and
199 (CF) results from mutations that disrupt CF transmembrane conductance regulator (CFTR), an anion cha
200 al PDZ domains bind the cystic fibrosis (CF) transmembrane conductance regulator (CFTR), an epithelia
201 ajor anion channels, such as cystic fibrosis transmembrane conductance regulator (CFTR), anoctamin-1(
202 he steady state level of the cystic fibrosis transmembrane conductance regulator (CFTR), but the unde
203 genes such as PRSS1, SPINK1, cystic fibrosis transmembrane conductance regulator (CFTR), chymotrypsin
204 ntify the interactome of the cystic fibrosis transmembrane conductance regulator (CFTR), demonstratin
205 of the common mutant of the cystic fibrosis transmembrane conductance regulator (CFTR), F508del, is
206 cal translation speed of the cystic fibrosis transmembrane conductance regulator (CFTR), leading to d
207 s caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), of which the
208 illustrate that disrupted function of the CF transmembrane conductance regulator (CFTR), such as that
209 ould target the underlying defects in the CF transmembrane conductance regulator (CFTR), the Cystic F
210 shown previously that macrophages lacking CF transmembrane conductance regulator (CFTR), the gene mut
211 e caused by the DeltaF508 mutation in the CF transmembrane conductance regulator (CFTR), which disrup
212 the epithelial Cl(-) channel cystic fibrosis transmembrane conductance regulator (CFTR), which is def
214 smembrane channel called the cystic fibrosis transmembrane conductance regulator (CFTR), which regula
215 ts of low serum IGF-1 on the cystic fibrosis transmembrane conductance regulator (CFTR), whose defect
217 assessed by forskolin-induced swelling in CF transmembrane conductance regulator (CFTR)-deficient org
218 % compared with control) and cystic fibrosis transmembrane conductance regulator (CFTR)-dependent and
219 estines that inherently lack cystic fibrosis transmembrane conductance regulator (CFTR)-dependent HCO
220 s, cAMP is known to regulate cystic fibrosis transmembrane conductance regulator (CFTR)-mediated anio
221 partially restored DeltaF508-cystic fibrosis transmembrane conductance regulator (CFTR)-mediated cAMP
246 d pancreatic genes (albumin, cystic fibrosis transmembrane conductance regulator [CFTR], and insulin)
249 omal degradation of a mutant cystic fibrosis transmembrane conductance regulator (CFTRDeltaF508) was
250 red an rAAV vector containing a truncated CF transmembrane conductance regulator (CFTRDeltaR) combine
251 re of the outer mouth of the cystic fibrosis transmembrane conductance regulator channel pore: TMs 6
252 denosine 3',5'-monophosphate/cystic fibrosis transmembrane conductance regulator/chloride bicarbonate
253 ary Cl(-) conductance in the cystic fibrosis transmembrane conductance regulator Cl(-) channel requir
254 egments line the pore of the cystic fibrosis transmembrane conductance regulator Cl(-) channel; howev
255 TT, in deletion of Phe508 in cystic fibrosis transmembrane conductance regulator (DeltaF508 CFTR), th
256 These findings link loss of cystic fibrosis transmembrane conductance regulator-dependent alkaliniza
257 tance is mediated by altered cystic fibrosis transmembrane conductance regulator expression and activ
258 of phenylalanine 508 of the cystic fibrosis transmembrane conductance regulator (F508 CFTR) is the m
259 e used mice deficient in the cystic fibrosis transmembrane conductance regulator gene (Cftr) to test
260 ate gene studies include the cystic fibrosis transmembrane conductance regulator gene (CFTR), as well
262 almost 2,000 variants in the cystic fibrosis transmembrane conductance regulator gene CFTR have empir
263 d to efficiently deliver the cystic fibrosis transmembrane conductance regulator gene to human airway
264 ) cells after treatment with cystic fibrosis transmembrane conductance regulator inhibitor CFTR(inh)-
265 ence factors alkaline protease (AprA) and CF transmembrane conductance regulator inhibitory factor (C
266 eruginosa epoxide hydrolase, cystic fibrosis transmembrane conductance regulator inhibitory factor (C
268 oncentration of bicarbonate, which mimics CF transmembrane conductance regulator-mediated anion secre
269 veolar macrophages from cystic fibrosis (CF) transmembrane conductance regulator(-/-) mice have impai
270 n of our editase can correct cystic fibrosis transmembrane conductance regulator mRNA, restore full-l
272 ts of the disease-associated cystic fibrosis transmembrane conductance regulator mutant F508del.
273 y the retention of the CFTR (cystic fibrosis transmembrane conductance regulator) mutant protein in t
275 ation with and activation of cystic fibrosis transmembrane conductance regulator, one of its binding
276 the threshold, whereas, the cystic fibrosis transmembrane conductance regulator only contributes to
277 zed that transgenic expression of porcine CF transmembrane conductance regulator (pCFTR) cDNA under c
279 ch was partially reversed by cystic fibrosis transmembrane conductance regulator potentiation with iv
280 e the feasibility of using a cystic fibrosis transmembrane conductance regulator potentiator, ivacaft
282 ny missense mutations in the cystic fibrosis transmembrane conductance regulator protein (CFTR) resul
283 he loss of chloride transport through the CF transmembrane conductance regulator protein (CFTR).
284 -length plasmid encoding the cystic fibrosis transmembrane conductance regulator protein was achieved
285 bed in CF including disabled cystic fibrosis transmembrane conductance regulator recruitment to phago
287 ficient degradation of human cystic fibrosis transmembrane conductance regulator requires function of
288 ) lung disease, the absence of functional CF transmembrane conductance regulator results in Cl(-)/HCO
289 ngiocyte functions including cystic fibrosis transmembrane conductance regulator, secretin receptor,
290 cretion via up-regulation of cystic fibrosis transmembrane conductance regulator, suggesting an impor
291 ngle residue (F508) in CFTR (cystic fibrosis transmembrane conductance regulator) that disrupts the f
292 embrane K(ATP) channels, the cystic fibrosis transmembrane conductance regulator, the transient recep
293 ing functional defect in the cystic fibrosis transmembrane conductance regulator, there is still an u
294 estigation proposes that the cystic fibrosis transmembrane conductance regulator transports extracell
295 romone, Ste6* (sterile), and cystic fibrosis transmembrane conductance regulator, undergo Ubr1-depend
297 creased levels of functional cystic fibrosis transmembrane conductance regulator were associated with
298 including the anion channel cystic fibrosis transmembrane conductance regulator, which shunt the tra
299 -fibrosis-associated protein cystic fibrosis transmembrane conductance regulator, which upon deletion
300 ease the level of functional cystic fibrosis transmembrane conductance regulator) with the need for m
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