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1 stance arteries ex vivo, the cystic fibrosis transmembrane conductance regulator (1) is critical for
2 nger regulatory factor-1 and cystic fibrosis transmembrane conductance regulator (a key player in the
4 s to the gating mutations of cystic fibrosis transmembrane conductance regulator (CFTR or ABCC7; i.e.
6 ol of cell proliferation and cystic fibrosis transmembrane conductance regulator (CFTR) -driven fluid
7 coid dexamethasone increases cystic fibrosis transmembrane conductance regulator (CFTR) abundance in
8 linone CFTRact-J027 (4) as a cystic fibrosis transmembrane conductance regulator (CFTR) activator wit
9 ates that ivacaftor improves cystic fibrosis transmembrane conductance regulator (CFTR) activity and
11 ons to the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) also cause pa
12 membrane, which include the cystic fibrosis transmembrane conductance regulator (CFTR) and Ca(2+)-ac
13 association between lack of cystic fibrosis transmembrane conductance regulator (CFTR) and ceramide
14 ainst other proteins such as cystic fibrosis transmembrane conductance regulator (CFTR) and dystrophi
15 ulated by apically expressed cystic fibrosis transmembrane conductance regulator (CFTR) and large-con
16 nal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFTR) and solute ca
17 alveolar fluid balance: the cystic fibrosis transmembrane conductance regulator (CFTR) and the amilo
18 l permeability and decreased cystic fibrosis transmembrane conductance regulator (Cftr) and the Na-K-
19 /H(+) antiporter, CLC-5, the cystic fibrosis transmembrane conductance regulator (CFTR) and the sodiu
20 g cassette (ABC) transporter cystic fibrosis transmembrane conductance regulator (CFTR) and two other
21 and secrete Cl- through the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
22 alanine 508 (F508del) in the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
24 on special properties of the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
25 in the gene that encodes the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
26 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
27 loride permeation pathway in cystic fibrosis transmembrane conductance regulator (CFTR) as a short na
28 ts in functional expression defect of the CF transmembrane conductance regulator (CFTR) at the apical
30 inclusion of the full-length cystic fibrosis transmembrane conductance regulator (CFTR) cDNA together
31 espite the importance of the cystic fibrosis transmembrane conductance regulator (CFTR) channel for e
33 F) mice with a nonfunctional cystic fibrosis transmembrane conductance regulator (CFTR) channel was r
34 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) channel, whic
36 lands are important sites of cystic fibrosis transmembrane conductance regulator (CFTR) chloride (Cl(
37 used by loss of a functional cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
38 e: functional defects of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
39 eine scanning studies of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
40 y the functional expression defect of the CF transmembrane conductance regulator (CFTR) chloride chan
42 regulatory (R) domain of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
43 s caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
44 all-molecule blockers of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
45 ystic fibrosis (CF), a lack of functional CF transmembrane conductance regulator (CFTR) chloride chan
46 pus oocytes coexpressing the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
47 ppropriate activation of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
48 esults from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
49 eads to an inhibition of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel
50 ability, and function of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel
52 the loss of function of the cystic fibrosis transmembrane conductance regulator (CFTR) combined with
53 We evaluated the effects of cystic fibrosis transmembrane conductance regulator (CFTR) deficiency on
54 Smoking is reported to cause cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction i
56 um (OE) of mice deficient in cystic fibrosis transmembrane conductance regulator (CFTR) exhibits ion
57 n epithelial cells decreases cystic fibrosis transmembrane conductance regulator (CFTR) expression an
59 main interaction between the cystic fibrosis transmembrane conductance regulator (CFTR) first cytosol
60 as correctors of the F508del-cystic fibrosis transmembrane conductance regulator (CFTR) folding defec
61 e findings are directly caused by loss of CF transmembrane conductance regulator (CFTR) function or s
64 covery that mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene cause cy
66 hesis that disruption of the cystic fibrosis transmembrane conductance regulator (CFTR) gene directly
67 of-function mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene encoding
69 ted since the cloning of the cystic fibrosis transmembrane conductance regulator (CFTR) gene is being
70 The F508del mutation in the cystic fibrosis transmembrane conductance regulator (Cftr) gene is belie
71 kb -35 (DHS-35kb) 5' to the cystic fibrosis transmembrane conductance regulator (CFTR) gene is evide
72 he DeltaF508 mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene is the m
73 ease-causing mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene is the o
76 brosis (CF) is caused by mutations in the CF transmembrane conductance regulator (CFTR) gene that imp
78 V1, expressing a full-length cystic fibrosis transmembrane conductance regulator (CFTR) gene, is capa
79 .7-kb promoter region of the cystic fibrosis transmembrane conductance regulator (CFTR) gene, we defi
80 s caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which e
88 binding domain (NBD2) of the cystic fibrosis transmembrane conductance regulator (CFTR) has lagged be
89 e than 2000 mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) have been des
90 es (MPhis) with mutations in cystic fibrosis transmembrane conductance regulator (CFTR) have blunted
91 function of Slc26a6 and the cystic fibrosis transmembrane conductance regulator (CFTR) in HeLa cells
92 rosis homozygous for F508del-cystic fibrosis transmembrane conductance regulator (CFTR) in placebo-co
93 is to efficiently and safely express the CF transmembrane conductance regulator (CFTR) in the approp
95 The role of Pseudomonas aeruginosa and CF transmembrane conductance regulator (CFTR) in Treg regul
96 used by the F508 mutation in cystic fibrosis transmembrane conductance regulator (CFTR) include a "co
106 cAMP-activated Cl(-) channel cystic fibrosis transmembrane conductance regulator (CFTR) is a major pr
107 brates, the chloride channel cystic fibrosis transmembrane conductance regulator (CFTR) is a master r
122 an DeltaF508 mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) is associated
123 Endocytic recycling of the cystic fibrosis transmembrane conductance regulator (CFTR) is blocked by
125 modulator compounds for the cystic fibrosis transmembrane conductance regulator (CFTR) is key for th
127 08 deletion (F508del) in the cystic fibrosis transmembrane conductance regulator (CFTR) is the most c
130 gamma stimulation in vivo in cystic fibrosis transmembrane conductance regulator (Cftr) knockout mice
131 binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFTR) leads to defe
132 s or dysfunction of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) leads to impa
134 s (FPOP) for footprinting of cystic fibrosis transmembrane conductance regulator (CFTR) membrane tran
135 mbination treatment with the cystic fibrosis transmembrane conductance regulator (CFTR) modulators te
137 e carrying the most frequent cystic fibrosis transmembrane conductance regulator (CFTR) mutation in h
140 The chloride channel of the cystic fibrosis transmembrane conductance regulator (CFTR) participates
141 anine 508 (DeltaF508) in the cystic fibrosis transmembrane conductance regulator (CFTR) plasma membra
142 fold and increased wild-type cystic fibrosis transmembrane conductance regulator (CFTR) plasma membra
145 ed by defective or deficient cystic fibrosis transmembrane conductance regulator (CFTR) protein activ
146 DeltaPhe508 mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) protein impai
148 ng the activity of defective cystic fibrosis transmembrane conductance regulator (CFTR) protein is a
149 and decreased apical cilia, cystic fibrosis transmembrane conductance regulator (CFTR) protein level
150 unction or deficiency of the cystic fibrosis transmembrane conductance regulator (CFTR) protein, an e
151 sing of the DeltaF508 mutant cystic fibrosis transmembrane conductance regulator (CFTR) protein.
152 is (CF) is due to a folding defect in the CF transmembrane conductance regulator (CFTR) protein.
155 hly PKA-phosphorylated human cystic fibrosis transmembrane conductance regulator (CFTR) regulatory re
156 type and variant (DeltaF508) cystic fibrosis transmembrane conductance regulator (CFTR) responsible f
158 binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFTR) results in de
159 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) that compromi
160 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) that impair i
161 brosis (CF) is caused by mutations in the CF transmembrane conductance regulator (CFTR) that prevent
162 ftor is a potentiator of the cystic fibrosis transmembrane conductance regulator (CFTR) that reduces
163 lamotrigine), as well as the cystic fibrosis transmembrane conductance regulator (CFTR) trafficking c
164 Misfolding of DeltaF508 cystic fibrosis (CF) transmembrane conductance regulator (CFTR) underlies pat
165 amino acids inserted at the cystic fibrosis transmembrane conductance regulator (CFTR) W1282X PTC (a
166 ons of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) which is an a
167 the apical chloride channel cystic fibrosis transmembrane conductance regulator (CFTR) with 90% of p
168 ons of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) with a preval
170 functional abnormalities of cystic fibrosis transmembrane conductance regulator (CFTR), a 25% reduct
171 f apoptosis and involves the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-regul
172 inylation and degradation of cystic fibrosis transmembrane conductance regulator (CFTR), a chloride c
173 we examined the role of the cystic fibrosis transmembrane conductance regulator (CFTR), a Cl(-) and
176 (CF) results from mutations that disrupt CF transmembrane conductance regulator (CFTR), an anion cha
177 al PDZ domains bind the cystic fibrosis (CF) transmembrane conductance regulator (CFTR), an epithelia
178 ajor anion channels, such as cystic fibrosis transmembrane conductance regulator (CFTR), anoctamin-1(
179 he steady state level of the cystic fibrosis transmembrane conductance regulator (CFTR), but the unde
180 genes such as PRSS1, SPINK1, cystic fibrosis transmembrane conductance regulator (CFTR), chymotrypsin
181 ntify the interactome of the cystic fibrosis transmembrane conductance regulator (CFTR), demonstratin
182 of the common mutant of the cystic fibrosis transmembrane conductance regulator (CFTR), F508del, is
183 cal translation speed of the cystic fibrosis transmembrane conductance regulator (CFTR), leading to d
184 s caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), of which the
185 illustrate that disrupted function of the CF transmembrane conductance regulator (CFTR), such as that
186 ould target the underlying defects in the CF transmembrane conductance regulator (CFTR), the Cystic F
187 shown previously that macrophages lacking CF transmembrane conductance regulator (CFTR), the gene mut
188 e caused by the DeltaF508 mutation in the CF transmembrane conductance regulator (CFTR), which disrup
189 the epithelial Cl(-) channel cystic fibrosis transmembrane conductance regulator (CFTR), which is def
191 smembrane channel called the cystic fibrosis transmembrane conductance regulator (CFTR), which regula
192 ts of low serum IGF-1 on the cystic fibrosis transmembrane conductance regulator (CFTR), whose defect
194 assessed by forskolin-induced swelling in CF transmembrane conductance regulator (CFTR)-deficient org
195 % compared with control) and cystic fibrosis transmembrane conductance regulator (CFTR)-dependent and
196 estines that inherently lack cystic fibrosis transmembrane conductance regulator (CFTR)-dependent HCO
197 s, cAMP is known to regulate cystic fibrosis transmembrane conductance regulator (CFTR)-mediated anio
198 partially restored DeltaF508-cystic fibrosis transmembrane conductance regulator (CFTR)-mediated cAMP
222 omal degradation of a mutant cystic fibrosis transmembrane conductance regulator (CFTRDeltaF508) was
223 red an rAAV vector containing a truncated CF transmembrane conductance regulator (CFTRDeltaR) combine
224 TT, in deletion of Phe508 in cystic fibrosis transmembrane conductance regulator (DeltaF508 CFTR), th
225 of phenylalanine 508 of the cystic fibrosis transmembrane conductance regulator (F508 CFTR) is the m
226 zed that transgenic expression of porcine CF transmembrane conductance regulator (pCFTR) cDNA under c
227 d pancreatic genes (albumin, cystic fibrosis transmembrane conductance regulator [CFTR], and insulin)
228 ctor-alpha downregulates the cystic fibrosis transmembrane conductance regulator across several organ
229 cells via a reduction in the cystic fibrosis transmembrane conductance regulator activity and biosynt
230 essure resulted in decreased cystic fibrosis transmembrane conductance regulator activity and liquid
232 ffects on the degradation of cystic fibrosis transmembrane conductance regulator and CPY*, which is a
233 he NHERF1-binding domains of cystic fibrosis transmembrane conductance regulator and Csk-binding prot
234 secretion appears to require cystic fibrosis transmembrane conductance regulator and electrogenic Na(
235 porters (ABC), including the cystic fibrosis transmembrane conductance regulator and P-glycoprotein.
236 was completely dependent on cystic fibrosis transmembrane conductance regulator and partially depend
237 -dependent activation of the cystic fibrosis transmembrane conductance regulator anion channel was in
239 Opening and closing of the cystic fibrosis transmembrane conductance regulator are controlled by AT
241 slows the degradation of the cystic fibrosis transmembrane conductance regulator but does not impede
242 unction mutations in the chloride channel CF transmembrane conductance regulator can elevate the acti
243 re of the outer mouth of the cystic fibrosis transmembrane conductance regulator channel pore: TMs 6
244 ary Cl(-) conductance in the cystic fibrosis transmembrane conductance regulator Cl(-) channel requir
245 egments line the pore of the cystic fibrosis transmembrane conductance regulator Cl(-) channel; howev
246 tance is mediated by altered cystic fibrosis transmembrane conductance regulator expression and activ
247 e used mice deficient in the cystic fibrosis transmembrane conductance regulator gene (Cftr) to test
248 ate gene studies include the cystic fibrosis transmembrane conductance regulator gene (CFTR), as well
250 almost 2,000 variants in the cystic fibrosis transmembrane conductance regulator gene CFTR have empir
251 d to efficiently deliver the cystic fibrosis transmembrane conductance regulator gene to human airway
252 ) cells after treatment with cystic fibrosis transmembrane conductance regulator inhibitor CFTR(inh)-
253 ence factors alkaline protease (AprA) and CF transmembrane conductance regulator inhibitory factor (C
254 eruginosa epoxide hydrolase, cystic fibrosis transmembrane conductance regulator inhibitory factor (C
256 n of our editase can correct cystic fibrosis transmembrane conductance regulator mRNA, restore full-l
258 ts of the disease-associated cystic fibrosis transmembrane conductance regulator mutant F508del.
260 the threshold, whereas, the cystic fibrosis transmembrane conductance regulator only contributes to
262 ch was partially reversed by cystic fibrosis transmembrane conductance regulator potentiation with iv
263 e the feasibility of using a cystic fibrosis transmembrane conductance regulator potentiator, ivacaft
265 ny missense mutations in the cystic fibrosis transmembrane conductance regulator protein (CFTR) resul
266 he loss of chloride transport through the CF transmembrane conductance regulator protein (CFTR).
267 -length plasmid encoding the cystic fibrosis transmembrane conductance regulator protein was achieved
268 bed in CF including disabled cystic fibrosis transmembrane conductance regulator recruitment to phago
270 ficient degradation of human cystic fibrosis transmembrane conductance regulator requires function of
271 ) lung disease, the absence of functional CF transmembrane conductance regulator results in Cl(-)/HCO
272 estigation proposes that the cystic fibrosis transmembrane conductance regulator transports extracell
274 creased levels of functional cystic fibrosis transmembrane conductance regulator were associated with
275 veolar macrophages from cystic fibrosis (CF) transmembrane conductance regulator(-/-) mice have impai
276 y the retention of the CFTR (cystic fibrosis transmembrane conductance regulator) mutant protein in t
277 ngle residue (F508) in CFTR (cystic fibrosis transmembrane conductance regulator) that disrupts the f
278 ease the level of functional cystic fibrosis transmembrane conductance regulator) with the need for m
279 al exocytosis of NHE3, CFTR (cystic fibrosis transmembrane conductance regulator), and GLUT5 required
280 psin-controlling gene or the cystic fibrosis transmembrane conductance regulator); a few patients hav
281 in gross mislocalization of cystic fibrosis transmembrane conductance regulator, causing marked redu
284 ation with and activation of cystic fibrosis transmembrane conductance regulator, one of its binding
285 ngiocyte functions including cystic fibrosis transmembrane conductance regulator, secretin receptor,
286 cretion via up-regulation of cystic fibrosis transmembrane conductance regulator, suggesting an impor
287 embrane K(ATP) channels, the cystic fibrosis transmembrane conductance regulator, the transient recep
288 ing functional defect in the cystic fibrosis transmembrane conductance regulator, there is still an u
289 romone, Ste6* (sterile), and cystic fibrosis transmembrane conductance regulator, undergo Ubr1-depend
290 including the anion channel cystic fibrosis transmembrane conductance regulator, which shunt the tra
291 -fibrosis-associated protein cystic fibrosis transmembrane conductance regulator, which upon deletion
292 es, at least in part through cystic fibrosis transmembrane conductance regulator-associated channels,
293 These findings link loss of cystic fibrosis transmembrane conductance regulator-dependent alkaliniza
294 oncentration of bicarbonate, which mimics CF transmembrane conductance regulator-mediated anion secre
299 denosine 3',5'-monophosphate/cystic fibrosis transmembrane conductance regulator/chloride bicarbonate
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