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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 tal cells and frequently coexpressed with CF transmembrane conductance regulator (CFTR) along with tr
12 ons to the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) also cause pa
13 membrane, which include the cystic fibrosis transmembrane conductance regulator (CFTR) and Ca(2+)-ac
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 regulates the biogenesis of cystic fibrosis transmembrane conductance regulator (CFTR) and the epith
18 l permeability and decreased cystic fibrosis transmembrane conductance regulator (Cftr) and the Na-K-
19 hrough the chloride channels cystic fibrosis transmembrane conductance regulator (CFTR) and TMEM16A (
20 g cassette (ABC) transporter cystic fibrosis transmembrane conductance regulator (CFTR) and two other
21 alanine 508 (F508del) in the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
22 on special properties of the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
24 fibrosis (CF) pigs, loss of 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 and secrete Cl- through the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
28 s caused by mutations of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) anion channel
29 alanine 508 (F508del) in the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel
30 loride permeation pathway in cystic fibrosis transmembrane conductance regulator (CFTR) as a short na
31 three nonsense mutations of cystic fibrosis transmembrane conductance regulator (CFTR) associated wi
32 minal truncation mutation of cystic fibrosis transmembrane conductance regulator (CFTR) associated wi
33 ts in functional expression defect of the CF transmembrane conductance regulator (CFTR) at the apical
34 ions that stabilize the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) at the apical
35 Small-molecule modulators of cystic fibrosis transmembrane conductance regulator (CFTR) biology show
37 ginine would enhance F508del-cystic fibrosis transmembrane conductance regulator (CFTR) channel activ
39 F) mice with a nonfunctional cystic fibrosis transmembrane conductance regulator (CFTR) channel was r
40 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) channel, whic
42 The role of epithelial cystic fibrosis (CF) transmembrane conductance regulator (CFTR) chloride chan
43 used by loss of a functional cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
44 e: functional defects of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
45 eine scanning studies of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
46 y the functional expression defect of the CF transmembrane conductance regulator (CFTR) chloride chan
47 of-function mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
48 ssive disease, caused by mutations in the CF transmembrane conductance regulator (CFTR) chloride chan
49 ppropriate activation of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
50 esults from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) chloride chan
51 eads to an inhibition of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel
53 tation DeltaF508 on the gene encoding the CF transmembrane conductance regulator (CFTR) Cl(-) channel
54 ability, and function of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel
55 the loss of function of the cystic fibrosis transmembrane conductance regulator (CFTR) combined with
56 of-function mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) compromise ep
58 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) disrupt epith
59 Smoking is reported to cause cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction i
60 um (OE) of mice deficient in cystic fibrosis transmembrane conductance regulator (CFTR) exhibits ion
61 els (TMEM16A), including the cystic fibrosis transmembrane conductance regulator (CFTR) expressed on
62 n epithelial cells decreases cystic fibrosis transmembrane conductance regulator (CFTR) expression an
63 arette smoke decreased AMPhi cystic fibrosis transmembrane conductance regulator (CFTR) expression, p
64 main interaction between the cystic fibrosis transmembrane conductance regulator (CFTR) first cytosol
65 as correctors of the F508del-cystic fibrosis transmembrane conductance regulator (CFTR) folding defec
66 re needed to reliably assess Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) function in v
67 e findings are directly caused by loss of CF transmembrane conductance regulator (CFTR) function or s
68 is a genetic disorder caused by defective CF Transmembrane Conductance Regulator (CFTR) function.
69 attributable to increases in cystic fibrosis transmembrane conductance regulator (CFTR) function.
72 hesis that disruption of the cystic fibrosis transmembrane conductance regulator (CFTR) gene directly
73 of-function mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene encoding
75 ted since the cloning of the cystic fibrosis transmembrane conductance regulator (CFTR) gene is being
76 The F508del mutation in the cystic fibrosis transmembrane conductance regulator (Cftr) gene is belie
77 kb -35 (DHS-35kb) 5' to the cystic fibrosis transmembrane conductance regulator (CFTR) gene is evide
78 ease-causing mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene is the o
81 sease, caused by genetic diversity in the CF transmembrane conductance regulator (CFTR) gene, a cycli
82 s caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, encodin
83 ssive disorder caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, encodin
84 V1, expressing a full-length cystic fibrosis transmembrane conductance regulator (CFTR) gene, is capa
85 enetic disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, resulti
86 e caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, resulti
87 s caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which e
97 binding domain (NBD2) of the cystic fibrosis transmembrane conductance regulator (CFTR) has lagged be
98 e than 2000 mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) have been des
99 es (MPhis) with mutations in cystic fibrosis transmembrane conductance regulator (CFTR) have blunted
100 binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFTR) have distinct
101 2)AR)-mediated activation of cystic fibrosis transmembrane conductance regulator (CFTR) in epithelial
102 function of Slc26a6 and the cystic fibrosis transmembrane conductance regulator (CFTR) in HeLa cells
103 rosis homozygous for F508del-cystic fibrosis transmembrane conductance regulator (CFTR) in placebo-co
104 The role of Pseudomonas aeruginosa and CF transmembrane conductance regulator (CFTR) in Treg regul
105 st to assess the role of the cystic fibrosis transmembrane conductance regulator (CFTR) in urinary HC
106 used by the F508 mutation in cystic fibrosis transmembrane conductance regulator (CFTR) include a "co
107 demonstrate the efficacy of cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor (R)
113 cAMP-activated Cl(-) channel cystic fibrosis transmembrane conductance regulator (CFTR) is a major pr
114 brates, the chloride channel cystic fibrosis transmembrane conductance regulator (CFTR) is a master r
130 an DeltaF508 mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) is associated
131 Endocytic recycling of the cystic fibrosis transmembrane conductance regulator (CFTR) is blocked by
132 modulator compounds for the cystic fibrosis transmembrane conductance regulator (CFTR) is key for th
135 08 deletion (F508del) in the cystic fibrosis transmembrane conductance regulator (CFTR) is the most c
138 gamma stimulation in vivo in cystic fibrosis transmembrane conductance regulator (Cftr) knockout mice
139 s or dysfunction of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) leads to impa
141 s (FPOP) for footprinting of cystic fibrosis transmembrane conductance regulator (CFTR) membrane tran
143 mbination treatment with the cystic fibrosis transmembrane conductance regulator (CFTR) modulators te
144 o boost the response to cystic fibrosis (CF) transmembrane conductance regulator (CFTR) modulators, l
146 e carrying the most frequent cystic fibrosis transmembrane conductance regulator (CFTR) mutation in h
147 es the common human Phe508del (DeltaF508) CF transmembrane conductance regulator (CFTR) mutation, whe
150 . explored the role that the cystic fibrosis transmembrane conductance regulator (CFTR) plays in plat
153 ed by defective or deficient cystic fibrosis transmembrane conductance regulator (CFTR) protein activ
155 and decreased apical cilia, cystic fibrosis transmembrane conductance regulator (CFTR) protein level
156 unction or deficiency of the cystic fibrosis transmembrane conductance regulator (CFTR) protein, an e
157 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) protein, and
158 sing of the DeltaF508 mutant cystic fibrosis transmembrane conductance regulator (CFTR) protein.
159 is (CF) is due to a folding defect in the CF transmembrane conductance regulator (CFTR) protein.
162 hly PKA-phosphorylated human cystic fibrosis transmembrane conductance regulator (CFTR) regulatory re
163 binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFTR) results in de
164 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) that compromi
165 ons in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) that impair i
166 ftor is a potentiator of the cystic fibrosis transmembrane conductance regulator (CFTR) that reduces
167 Misfolding of DeltaF508 cystic fibrosis (CF) transmembrane conductance regulator (CFTR) underlies pat
168 amino acids inserted at the cystic fibrosis transmembrane conductance regulator (CFTR) W1282X PTC (a
169 ons of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) which is an a
170 the apical chloride channel cystic fibrosis transmembrane conductance regulator (CFTR) with 90% of p
171 ons of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) with a preval
173 functional abnormalities of cystic fibrosis transmembrane conductance regulator (CFTR), a 25% reduct
174 f apoptosis and involves the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-regul
175 caused by mutations in the gene encoding CF transmembrane conductance regulator (CFTR), a chloride c
177 oss-of-function mutations of cystic fibrosis transmembrane conductance regulator (CFTR), a phosphoryl
179 al PDZ domains bind the cystic fibrosis (CF) transmembrane conductance regulator (CFTR), an epithelia
180 ajor anion channels, such as cystic fibrosis transmembrane conductance regulator (CFTR), anoctamin-1(
181 genes such as PRSS1, SPINK1, cystic fibrosis transmembrane conductance regulator (CFTR), chymotrypsin
182 ntify the interactome of the cystic fibrosis transmembrane conductance regulator (CFTR), demonstratin
183 of the common mutant of the cystic fibrosis transmembrane conductance regulator (CFTR), F508del, is
184 cal translation speed of the cystic fibrosis transmembrane conductance regulator (CFTR), leading to d
185 s caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), of which the
186 t VX-809, a corrector of the cystic fibrosis transmembrane conductance regulator (CFTR), reduces cyst
187 in Cl(-) extrusion, such as cystic fibrosis transmembrane conductance regulator (CFTR), should reduc
188 illustrate that disrupted function of the CF transmembrane conductance regulator (CFTR), such as that
189 ies targeting defects in the cystic fibrosis transmembrane conductance regulator (CFTR), which are li
191 the epithelial Cl(-) channel cystic fibrosis transmembrane conductance regulator (CFTR), which is def
192 smembrane channel called the cystic fibrosis transmembrane conductance regulator (CFTR), which regula
193 ts of low serum IGF-1 on the cystic fibrosis transmembrane conductance regulator (CFTR), whose defect
194 brosis (CF) is caused by mutations in the CF transmembrane conductance regulator (CFTR), with approxi
196 assessed by forskolin-induced swelling in CF transmembrane conductance regulator (CFTR)-deficient org
197 % compared with control) and cystic fibrosis transmembrane conductance regulator (CFTR)-dependent and
198 estines that inherently lack cystic fibrosis transmembrane conductance regulator (CFTR)-dependent HCO
199 s, cAMP is known to regulate cystic fibrosis transmembrane conductance regulator (CFTR)-mediated anio
200 partially restored DeltaF508-cystic fibrosis transmembrane conductance regulator (CFTR)-mediated cAMP
202 ells, motile ciliated cells, cystic fibrosis transmembrane conductance regulator (CFTR)-rich ionocyte
227 red an rAAV vector containing a truncated CF transmembrane conductance regulator (CFTRDeltaR) combine
228 TT, in deletion of Phe508 in cystic fibrosis transmembrane conductance regulator (DeltaF508 CFTR), th
229 of phenylalanine 508 of the cystic fibrosis transmembrane conductance regulator (F508 CFTR) is the m
230 zed that transgenic expression of porcine CF transmembrane conductance regulator (pCFTR) cDNA under c
231 cells via a reduction in the cystic fibrosis transmembrane conductance regulator activity and biosynt
232 essure resulted in decreased cystic fibrosis transmembrane conductance regulator activity and liquid
235 secretion appears to require cystic fibrosis transmembrane conductance regulator and electrogenic Na(
236 porters (ABC), including the cystic fibrosis transmembrane conductance regulator and P-glycoprotein.
237 was completely dependent on cystic fibrosis transmembrane conductance regulator and partially depend
238 -dependent activation of the cystic fibrosis transmembrane conductance regulator anion channel was in
240 cidic pH produced by loss of cystic fibrosis transmembrane conductance regulator anion channels or pr
241 Opening and closing of the cystic fibrosis transmembrane conductance regulator are controlled by AT
243 unction mutations in the chloride channel CF transmembrane conductance regulator can elevate the acti
244 e used mice deficient in the cystic fibrosis transmembrane conductance regulator gene (Cftr) to test
245 ate gene studies include the cystic fibrosis transmembrane conductance regulator gene (CFTR), as well
247 almost 2,000 variants in the cystic fibrosis transmembrane conductance regulator gene CFTR have empir
248 d to efficiently deliver the cystic fibrosis transmembrane conductance regulator gene to human airway
249 phils confirm a role for the cystic fibrosis transmembrane conductance regulator in maintaining HOCl
250 lucose co-transporter-1, and cystic fibrosis transmembrane conductance regulator in the jejunum.
251 ) cells after treatment with cystic fibrosis transmembrane conductance regulator inhibitor CFTR(inh)-
252 ence factors alkaline protease (AprA) and CF transmembrane conductance regulator inhibitory factor (C
253 eruginosa epoxide hydrolase, cystic fibrosis transmembrane conductance regulator inhibitory factor (C
254 n of our editase can correct cystic fibrosis transmembrane conductance regulator mRNA, restore full-l
258 ch was partially reversed by cystic fibrosis transmembrane conductance regulator potentiation with iv
259 e the feasibility of using a cystic fibrosis transmembrane conductance regulator potentiator, ivacaft
261 he loss of chloride transport through the CF transmembrane conductance regulator protein (CFTR).
262 -length plasmid encoding the cystic fibrosis transmembrane conductance regulator protein was achieved
263 bed in CF including disabled cystic fibrosis transmembrane conductance regulator recruitment to phago
264 ficient degradation of human cystic fibrosis transmembrane conductance regulator requires function of
265 ) lung disease, the absence of functional CF transmembrane conductance regulator results in Cl(-)/HCO
267 creased levels of functional cystic fibrosis transmembrane conductance regulator were associated with
268 veolar macrophages from cystic fibrosis (CF) transmembrane conductance regulator(-/-) mice have impai
269 ed by mutations in the CFTR (cystic fibrosis transmembrane conductance regulator) gene that encodes a
270 toxemia, unaffected by CFTR (cystic fibrosis transmembrane conductance regulator) modulation, and res
271 acaftor-ivacaftor is a CFTR (cystic fibrosis transmembrane conductance regulator) modulator combinati
272 y the retention of the CFTR (cystic fibrosis transmembrane conductance regulator) mutant protein in t
273 icate a human-relevant CFTR (cystic fibrosis transmembrane conductance regulator) variant.Objectives:
274 al exocytosis of NHE3, CFTR (cystic fibrosis transmembrane conductance regulator), and GLUT5 required
275 tionale: Enhancing non-CFTR (cystic fibrosis transmembrane conductance regulator)-mediated anion secr
277 ociliary function in the absence of CFTR (CF transmembrane conductance regulator).Objectives: To test
278 egion Y-box 9+) to a mature (cystic fibrosis transmembrane conductance regulator+/secretin receptor+)
279 cellular adhesion molecule, cystic fibrosis transmembrane conductance regulator, and anion exchanger
280 in gross mislocalization of cystic fibrosis transmembrane conductance regulator, causing marked redu
283 ation with and activation of cystic fibrosis transmembrane conductance regulator, one of its binding
284 ngiocyte functions including cystic fibrosis transmembrane conductance regulator, secretin receptor,
285 embrane K(ATP) channels, the cystic fibrosis transmembrane conductance regulator, the transient recep
286 ing functional defect in the cystic fibrosis transmembrane conductance regulator, there is still an u
287 romone, Ste6* (sterile), and cystic fibrosis transmembrane conductance regulator, undergo Ubr1-depend
288 including the anion channel cystic fibrosis transmembrane conductance regulator, which shunt the tra
289 -fibrosis-associated protein cystic fibrosis transmembrane conductance regulator, which upon deletion
290 es, at least in part through cystic fibrosis transmembrane conductance regulator-associated channels,
291 These findings link loss of cystic fibrosis transmembrane conductance regulator-dependent alkaliniza
292 oncentration of bicarbonate, which mimics CF transmembrane conductance regulator-mediated anion secre
293 TEER) (>400 Ohms.cm(2)), and cystic fibrosis transmembrane conductance regulator-mediated short-circu
298 denosine 3',5'-monophosphate/cystic fibrosis transmembrane conductance regulator/chloride bicarbonate
300 ciated degradation (ERAD) of Cystic fibrosis transmembrane-conductance regulator (CFTR) is largely un