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1 the first nucleotide-binding domain from the cystic fibrosis transmembrane conductance regulator.
2 lux into the lumen through activation of the cystic fibrosis transmembrane conductance regulator.
3 rhodopsins with lesser effects on misfolded cystic fibrosis transmembrane conductance regulator.
4 wn to affect function in the gene coding for cystic fibrosis transmembrane conductance regulator.
5 or cerebral resistance arteries ex vivo, the cystic fibrosis transmembrane conductance regulator (1)
6 on of Na/H exchanger regulatory factor-1 and cystic fibrosis transmembrane conductance regulator (a k
7 utation in a trypsin-controlling gene or the cystic fibrosis transmembrane conductance regulator); a
8 Because the cystic fibrosis transmembrane conductance regulator (ABC
9 umor necrosis factor-alpha downregulates the cystic fibrosis transmembrane conductance regulator acro
10 ut not forskolin/adenylyl cyclase-dependent, cystic fibrosis transmembrane conductance regulator acti
11 thelial type II cells via a reduction in the cystic fibrosis transmembrane conductance regulator acti
12 d hydrostatic pressure resulted in decreased cystic fibrosis transmembrane conductance regulator acti
13 Apical exocytosis of NHE3, CFTR (cystic fibrosis transmembrane conductance regulator), an
14 g cassette transporters (ABC), including the cystic fibrosis transmembrane conductance regulator and
16 nd synergistic effects on the degradation of cystic fibrosis transmembrane conductance regulator and
17 uodenal HCO3(-) secretion appears to require cystic fibrosis transmembrane conductance regulator and
18 induced swelling was completely dependent on cystic fibrosis transmembrane conductance regulator and
19 leads on STa/GCC-dependent activation of the cystic fibrosis transmembrane conductance regulator anio
20 ture termination codon in mRNAs encoding the cystic fibrosis transmembrane conductance regulator anio
23 from muscle fibres, at least in part through cystic fibrosis transmembrane conductance regulator-asso
24 YDR049 modestly slows the degradation of the cystic fibrosis transmembrane conductance regulator but
25 actor-1 resulted in gross mislocalization of cystic fibrosis transmembrane conductance regulator, cau
26 is (CF), which is caused by mutations of the cystic fibrosis transmembrane conductance regulator (Cft
27 Mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFT
28 Ivacaftor is a potentiator of the cystic fibrosis transmembrane conductance regulator (CFT
29 We hypothesized that cystic fibrosis transmembrane conductance regulator (CFT
30 nfection of human epithelial cells decreases cystic fibrosis transmembrane conductance regulator (CFT
31 These drugs activate cystic fibrosis transmembrane conductance regulator (CFT
32 o understanding the epithelial Cl(-) channel cystic fibrosis transmembrane conductance regulator (CFT
33 factory epithelium (OE) of mice deficient in cystic fibrosis transmembrane conductance regulator (CFT
34 vious work indicates that ivacaftor improves cystic fibrosis transmembrane conductance regulator (CFT
35 ase that is caused by defective or deficient cystic fibrosis transmembrane conductance regulator (CFT
36 The ATP-binding cassette (ABC) transporter cystic fibrosis transmembrane conductance regulator (CFT
37 The most prevalent cystic fibrosis transmembrane conductance regulator (CFT
38 cellular processing of the DeltaF508 mutant cystic fibrosis transmembrane conductance regulator (CFT
39 s in the gene encoding for the anion channel cystic fibrosis transmembrane conductance regulator (CFT
40 stic fibrosis (CF) mice with a nonfunctional cystic fibrosis transmembrane conductance regulator (CFT
41 Cystic fibrosis transmembrane conductance regulator (CFT
42 caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
43 The glucocorticoid dexamethasone increases cystic fibrosis transmembrane conductance regulator (CFT
44 eins in mediating chromatin structure at the cystic fibrosis transmembrane conductance regulator (CFT
45 tte smoke (CS) leads to an inhibition of the cystic fibrosis transmembrane conductance regulator (CFT
46 (MRPs)) and a unique ATP-gated ion channel (cystic fibrosis transmembrane conductance regulator (CFT
47 Ivacaftor, a cystic fibrosis transmembrane conductance regulator (CFT
48 organ disease caused by loss of a functional cystic fibrosis transmembrane conductance regulator (CFT
49 ABSTRACT: Cystic fibrosis transmembrane conductance regulator (CFT
50 Ivacaftor is a cystic fibrosis transmembrane conductance regulator (CFT
51 Mutations in the cystic fibrosis transmembrane conductance regulator (CFT
52 is independent of apoptosis and involves the cystic fibrosis transmembrane conductance regulator (CFT
53 caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
54 Endocytic recycling of the cystic fibrosis transmembrane conductance regulator (CFT
55 dysfunction of the epithelial anion channel cystic fibrosis transmembrane conductance regulator (CFT
56 ve site (DHS) at kb -35 (DHS-35kb) 5' to the cystic fibrosis transmembrane conductance regulator (CFT
57 e expression, stability, and function of the cystic fibrosis transmembrane conductance regulator (CFT
58 fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFT
59 ic ducts and the function of Slc26a6 and the cystic fibrosis transmembrane conductance regulator (CFT
60 Cystic fibrosis transmembrane conductance regulator (CFT
61 In vertebrates, the chloride channel cystic fibrosis transmembrane conductance regulator (CFT
62 The cystic fibrosis transmembrane conductance regulator (CFT
63 , the deletion of Phe-508 (DeltaF508) in the cystic fibrosis transmembrane conductance regulator (CFT
64 approximately 40% compared with control) and cystic fibrosis transmembrane conductance regulator (CFT
65 CF intestines that inherently lack cystic fibrosis transmembrane conductance regulator (CFT
66 s caused by dysfunction or deficiency of the cystic fibrosis transmembrane conductance regulator (CFT
67 Cystic fibrosis transmembrane conductance regulator (CFT
68 Cystic fibrosis transmembrane conductance regulator (CFT
69 BCe1-B, and luminal HCO3(-) exit mediated by cystic fibrosis transmembrane conductance regulator (CFT
70 ot of the disease: functional defects of the cystic fibrosis transmembrane conductance regulator (CFT
71 Previous cysteine scanning studies of the cystic fibrosis transmembrane conductance regulator (CFT
72 caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
73 tested the hypothesis that disruption of the cystic fibrosis transmembrane conductance regulator (CFT
74 + channel (ENaC) and secrete Cl- through the cystic fibrosis transmembrane conductance regulator (CFT
75 Expression of the cystic fibrosis transmembrane conductance regulator (CFT
76 most common disease-causing mutation in the cystic fibrosis transmembrane conductance regulator (CFT
77 owledge accumulated since the cloning of the cystic fibrosis transmembrane conductance regulator (CFT
78 terocyte luminal membrane, which include the cystic fibrosis transmembrane conductance regulator (CFT
79 egulating the expression and function of the cystic fibrosis transmembrane conductance regulator (CFT
80 wever, the effects of low serum IGF-1 on the cystic fibrosis transmembrane conductance regulator (CFT
81 Inhibition of either cystic fibrosis transmembrane conductance regulator (CFT
82 n autosomal recessive disorder affecting the cystic fibrosis transmembrane conductance regulator (CFT
83 It is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFT
84 spiratory epithelial Cl(-) secretion via the cystic fibrosis transmembrane conductance regulator (CFT
85 Cystic fibrosis transmembrane conductance regulator (CFT
86 Golgi-localized cystic fibrosis transmembrane conductance regulator (CFT
87 p sequencing across 250 kb, encompassing the cystic fibrosis transmembrane conductance regulator (CFT
88 Smoking is reported to cause cystic fibrosis transmembrane conductance regulator (CFT
89 orylated and highly PKA-phosphorylated human cystic fibrosis transmembrane conductance regulator (CFT
90 modifies the local translation speed of the cystic fibrosis transmembrane conductance regulator (CFT
91 F508del cystic fibrosis transmembrane conductance regulator (CFT
92 Cystic fibrosis transmembrane conductance regulator (CFT
93 ing regions) of genes such as PRSS1, SPINK1, cystic fibrosis transmembrane conductance regulator (CFT
94 The F508del mutation in the cystic fibrosis transmembrane conductance regulator (Cft
95 by mutations in the apical chloride channel cystic fibrosis transmembrane conductance regulator (CFT
96 The cftr gene codes for a Cl(-) channel, the cystic fibrosis transmembrane conductance regulator (CFT
97 The cystic fibrosis transmembrane conductance regulator (CFT
98 d selectivity against other proteins such as cystic fibrosis transmembrane conductance regulator (CFT
99 Cystic fibrosis transmembrane conductance regulator (CFT
100 The cystic fibrosis transmembrane conductance regulator (CFT
101 The most common cystic fibrosis transmembrane conductance regulator (CFT
102 tion of phenylalanine 508 (DeltaF508) in the cystic fibrosis transmembrane conductance regulator (CFT
103 The cystic fibrosis transmembrane conductance regulator (CFT
104 Despite the importance of the cystic fibrosis transmembrane conductance regulator (CFT
105 ch are homologous to the gating mutations of cystic fibrosis transmembrane conductance regulator (CFT
106 ase is caused by the loss of function of the cystic fibrosis transmembrane conductance regulator (CFT
107 ) of the unique regulatory (R) domain of the cystic fibrosis transmembrane conductance regulator (CFT
108 approximately 2.7-kb promoter region of the cystic fibrosis transmembrane conductance regulator (CFT
109 fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFT
110 Cystic fibrosis transmembrane conductance regulator (CFT
111 way submucosal glands are important sites of cystic fibrosis transmembrane conductance regulator (CFT
112 uced the ubiquitinylation and degradation of cystic fibrosis transmembrane conductance regulator (CFT
113 tissues affected by the lack of a functional cystic fibrosis transmembrane conductance regulator (CFT
114 irst nucleotide binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFT
115 Deletion of Phe508 from cystic fibrosis transmembrane conductance regulator (CFT
116 The Cystic Fibrosis Transmembrane conductance Regulator (CFT
117 Cystic fibrosis transmembrane conductance regulator (CFT
118 nce the 1989 discovery that mutations in the cystic fibrosis transmembrane conductance regulator (CFT
119 The DeltaF508 mutation in the cystic fibrosis transmembrane conductance regulator (CFT
120 tification of small-molecule blockers of the cystic fibrosis transmembrane conductance regulator (CFT
121 Cystic fibrosis transmembrane conductance regulator (CFT
122 letion of phenylalanine 508 (F508del) in the cystic fibrosis transmembrane conductance regulator (CFT
123 e expression of ABC transporters such as the cystic fibrosis transmembrane conductance regulator (CFT
124 hortening disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFT
125 ugs (phenytoin, lamotrigine), as well as the cystic fibrosis transmembrane conductance regulator (CFT
126 Cystic fibrosis transmembrane conductance regulator (CFT
127 in the biogenesis and quality control of the cystic fibrosis transmembrane conductance regulator (CFT
128 We evaluated the effects of cystic fibrosis transmembrane conductance regulator (CFT
129 epididymis, and we examined the role of the cystic fibrosis transmembrane conductance regulator (CFT
130 The cystic fibrosis transmembrane conductance regulator (CFT
131 508-CFTR over 3-fold and increased wild-type cystic fibrosis transmembrane conductance regulator (CFT
132 y of AAV limits inclusion of the full-length cystic fibrosis transmembrane conductance regulator (CFT
133 Increasing the activity of defective cystic fibrosis transmembrane conductance regulator (CFT
134 tion and proteosomal degradation of a mutant cystic fibrosis transmembrane conductance regulator (CFT
135 The cystic fibrosis transmembrane conductance regulator (CFT
136 Mutations in the cystic fibrosis transmembrane conductance regulator (CFT
137 The cystic fibrosis transmembrane conductance regulator (CFT
138 duits: the Cl(-)/H(+) antiporter, CLC-5, the cystic fibrosis transmembrane conductance regulator (CFT
139 The DeltaPhe508 mutation in the cystic fibrosis transmembrane conductance regulator (CFT
140 and maintains the steady state level of the cystic fibrosis transmembrane conductance regulator (CFT
141 The chloride channel of the cystic fibrosis transmembrane conductance regulator (CFT
142 Loss of cystic fibrosis transmembrane conductance regulator (CFT
143 slational decisions for the membrane protein cystic fibrosis transmembrane conductance regulator (CFT
144 Loss of function of the cystic fibrosis transmembrane conductance regulator (CFT
145 Cystic Fibrosis Transmembrane Conductance Regulator (CFT
146 Here we show that the cystic fibrosis transmembrane conductance regulator (CFT
147 cloning in Xenopus oocytes coexpressing the cystic fibrosis transmembrane conductance regulator (CFT
148 Cystic fibrosis transmembrane conductance regulator (CFT
149 Although an association between lack of cystic fibrosis transmembrane conductance regulator (CFT
150 in bronchial and alveolar fluid balance: the cystic fibrosis transmembrane conductance regulator (CFT
151 The cystic fibrosis transmembrane conductance regulator (CFT
152 ficking of wild-type and variant (DeltaF508) cystic fibrosis transmembrane conductance regulator (CFT
153 antivirals and as correctors of the F508del-cystic fibrosis transmembrane conductance regulator (CFT
154 The cystic fibrosis transmembrane conductance regulator (CFT
155 ) physically and functionally interacts with cystic fibrosis transmembrane conductance regulator (CFT
156 tin motor myosin VI regulates endocytosis of cystic fibrosis transmembrane conductance regulator (CFT
157 The cystic fibrosis transmembrane conductance regulator (CFT
158 disease caused by recessive mutations in the cystic fibrosis transmembrane conductance regulator (CFT
159 fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFT
160 Cystic fibrosis transmembrane conductance regulator (CFT
161 caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
162 The cystic fibrosis transmembrane conductance regulator (CFT
163 Because apical HCO(3)(-) exchange depends on cystic fibrosis transmembrane conductance regulator (CFT
164 DeltaF508 cystic fibrosis transmembrane conductance regulator (CFT
165 The cystic fibrosis transmembrane conductance regulator (CFT
166 The physiological role of the cystic fibrosis transmembrane conductance regulator (CFT
167 Mutations of the chloride channel cystic fibrosis transmembrane conductance regulator (CFT
168 Cystic fibrosis transmembrane conductance regulator (CFT
169 kA), the alginate transporter (AlgE) and the cystic fibrosis transmembrane conductance regulator (CFT
170 steps of folding and assembly of full-length cystic fibrosis transmembrane conductance regulator (CFT
171 serine protease inhibitor Kazal 1 (SPINK1), cystic fibrosis transmembrane conductance regulator (CFT
172 Transport of chloride through the cystic fibrosis transmembrane conductance regulator (CFT
173 deletion of three nucleotides (CTT) from the cystic fibrosis transmembrane conductance regulator (CFT
174 is involves improving the function of mutant cystic fibrosis transmembrane conductance regulator (CFT
175 CO(3)(-), HCO(3)(-) transport, or functional cystic fibrosis transmembrane conductance regulator (CFT
176 ortening disease caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFT
177 Combination treatment with the cystic fibrosis transmembrane conductance regulator (CFT
178 The cystic fibrosis transmembrane conductance regulator (CFT
179 ich is associated with failure of the mutant cystic fibrosis transmembrane conductance regulator (CFT
180 Inhibitors of the cystic fibrosis transmembrane conductance regulator (CFT
181 The cystic fibrosis transmembrane conductance regulator (CFT
182 nts involved in the allosteric regulation of cystic fibrosis transmembrane conductance regulator (CFT
183 The cystic fibrosis transmembrane conductance regulator (CFT
184 reported that gene-targeted mice lacking the cystic fibrosis transmembrane conductance regulator (Cft
185 Multiple mutations in cystic fibrosis transmembrane conductance regulator (CFT
186 Inappropriate activation of the cystic fibrosis transmembrane conductance regulator (CFT
187 Macrophages (MPhis) with mutations in cystic fibrosis transmembrane conductance regulator (CFT
188 cond nucleotide-binding domain (NBD2) of the cystic fibrosis transmembrane conductance regulator (CFT
189 ed phenylquinoxalinone CFTRact-J027 (4) as a cystic fibrosis transmembrane conductance regulator (CFT
190 Cystic fibrosis transmembrane conductance regulator (CFT
191 t is in part regulated by apically expressed cystic fibrosis transmembrane conductance regulator (CFT
192 (IL-8) secretion and decreased apical cilia, cystic fibrosis transmembrane conductance regulator (CFT
193 not dependent upon special properties of the cystic fibrosis transmembrane conductance regulator (CFT
194 e determined the amino acids inserted at the cystic fibrosis transmembrane conductance regulator (CFT
195 ism of action of modulator compounds for the cystic fibrosis transmembrane conductance regulator (CFT
196 KEY POINTS: The cystic fibrosis transmembrane conductance regulator (CFT
197 diseases.The F508 deletion (F508del) in the cystic fibrosis transmembrane conductance regulator (CFT
198 and specific domain interaction between the cystic fibrosis transmembrane conductance regulator (CFT
199 reased intestinal permeability and decreased cystic fibrosis transmembrane conductance regulator (Cft
200 More than 2000 mutations in the cystic fibrosis transmembrane conductance regulator (CFT
201 tive degradation of the common mutant of the cystic fibrosis transmembrane conductance regulator (CFT
202 Two functional abnormalities of cystic fibrosis transmembrane conductance regulator (CFT
203 with cystic fibrosis homozygous for F508del-cystic fibrosis transmembrane conductance regulator (CFT
204 ector, rAAV2/HBoV1, expressing a full-length cystic fibrosis transmembrane conductance regulator (CFT
205 ent protein kinase (PKG), and opening of the cystic fibrosis transmembrane conductance regulator (CFT
206 cessfully to identify the interactome of the cystic fibrosis transmembrane conductance regulator (CFT
207 n genetic disease caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFT
208 irway epithelia partially restored DeltaF508-cystic fibrosis transmembrane conductance regulator (CFT
209 ng (PDE1), control of cell proliferation and cystic fibrosis transmembrane conductance regulator (CFT
210 caused by loss-of-function mutations of the cystic fibrosis transmembrane conductance regulator (CFT
211 (MRPs), and an ATP-gated anion channel, the cystic fibrosis transmembrane conductance regulator (CFT
212 The cystic fibrosis transmembrane conductance regulator (CFT
213 The cystic fibrosis transmembrane conductance regulator (CFT
214 The cystic fibrosis transmembrane conductance regulator (CFT
215 In the airways, cAMP is known to regulate cystic fibrosis transmembrane conductance regulator (CFT
216 ed by mutations in the gene that encodes the cystic fibrosis transmembrane conductance regulator (CFT
217 The cAMP-activated Cl(-) channel cystic fibrosis transmembrane conductance regulator (CFT
218 -conducting transmembrane channel called the cystic fibrosis transmembrane conductance regulator (CFT
219 caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
220 ystic fibrosis results from mutations in the cystic fibrosis transmembrane conductance regulator (CFT
221 al analyses of major anion channels, such as cystic fibrosis transmembrane conductance regulator (CFT
222 The cystic fibrosis transmembrane conductance regulator (CFT
223 The virulence factor cystic fibrosis transmembrane conductance regulator (CFT
224 endosomes in cells expressing the misfolded cystic fibrosis transmembrane conductance regulator (CFT
225 caused by mutations of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
226 The cystic fibrosis transmembrane conductance regulator (CFT
227 The cystic fibrosis transmembrane conductance regulator (CFT
228 The cystic fibrosis transmembrane conductance regulator (CFT
229 correctors rescue the trafficking mutant of cystic fibrosis transmembrane conductance regulator (CFT
230 The cystic fibrosis transmembrane conductance regulator (CFT
231 icture of the chloride permeation pathway in cystic fibrosis transmembrane conductance regulator (CFT
232 Malfunction of the cystic fibrosis transmembrane conductance regulator (CFT
233 Cystic fibrosis transmembrane conductance regulator (CFT
234 effect of PPAR-gamma stimulation in vivo in cystic fibrosis transmembrane conductance regulator (Cft
235 rosis (CF) is the result of mutations in the cystic fibrosis transmembrane conductance regulator (CFT
236 nstrate that mice carrying the most frequent cystic fibrosis transmembrane conductance regulator (CFT
237 mmonly caused by the F508del mutation in the cystic fibrosis transmembrane conductance regulator (CFT
238 ation of proteins (FPOP) for footprinting of cystic fibrosis transmembrane conductance regulator (CFT
239 irst nucleotide-binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFT
240 he prevalent human DeltaF508 mutation in the cystic fibrosis transmembrane conductance regulator (CFT
241 Alterations to the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
242 stic fibrosis caused by the F508 mutation in cystic fibrosis transmembrane conductance regulator (CFT
243 Using 20 variants from cystic fibrosis transmembrane conductance regulator (CFT
244 caused by mutations of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFT
245 id transporter, secretin receptor, cilia and cystic fibrosis transmembrane conductance regulator (CFT
246 The cystic fibrosis transmembrane-conductance regulator (CFT
247 r, bile duct, and pancreatic genes (albumin, cystic fibrosis transmembrane conductance regulator [CFT
248 ven lung expansion through activation of the cystic fibrosis transmembrane conductance regulator, CFT
249 is arises from an amino acid deletion in the cystic fibrosis transmembrane conductance regulator, CFT
250 ensional structure of the outer mouth of the cystic fibrosis transmembrane conductance regulator chan
251 ate (cAMP)-stimulated secretion depends on a cystic fibrosis transmembrane conductance regulator chan
252 ivating cyclic adenosine 3',5'-monophosphate/cystic fibrosis transmembrane conductance regulator/chlo
254 smembrane (TM) segments line the pore of the cystic fibrosis transmembrane conductance regulator Cl(-
255 as I507-ATC-->ATT, in deletion of Phe508 in cystic fibrosis transmembrane conductance regulator (Del
256 These findings link loss of cystic fibrosis transmembrane conductance regulator-depe
257 ystic fibrosis is caused by mutations in the cystic fibrosis transmembrane conductance regulator (enc
258 ted Cl(-) conductance is mediated by altered cystic fibrosis transmembrane conductance regulator expr
259 Deletion of phenylalanine 508 of the cystic fibrosis transmembrane conductance regulator (F50
260 n or pulmonary inflammation and that loss of cystic fibrosis transmembrane conductance regulator func
261 Few of the almost 2,000 variants in the cystic fibrosis transmembrane conductance regulator gene
262 ings from candidate gene studies include the cystic fibrosis transmembrane conductance regulator gene
263 g-range regulatory elements that control the cystic fibrosis transmembrane conductance regulator gene
264 We used mice deficient in the cystic fibrosis transmembrane conductance regulator gene
265 as been developed to efficiently deliver the cystic fibrosis transmembrane conductance regulator gene
267 ; and 16HBE14o(-) cells after treatment with cystic fibrosis transmembrane conductance regulator inhi
268 a secreted P. aeruginosa epoxide hydrolase, cystic fibrosis transmembrane conductance regulator inhi
270 n the first nucleotide binding domain of the cystic fibrosis transmembrane conductance regulator is d
271 acilitates B. cenocepacia infection in mice, cystic fibrosis transmembrane conductance regulator knoc
272 Na(+) channel-mediated Na(+) absorption and cystic fibrosis transmembrane conductance regulator-medi
273 y encoded version of our editase can correct cystic fibrosis transmembrane conductance regulator mRNA
274 As an ion channel, the cystic fibrosis transmembrane conductance regulator must
275 quently caused by the retention of the CFTR (cystic fibrosis transmembrane conductance regulator) mut
276 ed folding defects of the disease-associated cystic fibrosis transmembrane conductance regulator muta
277 namic co-localization with and activation of cystic fibrosis transmembrane conductance regulator, one
278 above and below the threshold, whereas, the cystic fibrosis transmembrane conductance regulator only
279 n, an effect which was partially reversed by cystic fibrosis transmembrane conductance regulator pote
280 Cystic fibrosis transmembrane conductance regulator pote
281 To determine the feasibility of using a cystic fibrosis transmembrane conductance regulator pote
282 livery of a full-length plasmid encoding the cystic fibrosis transmembrane conductance regulator prot
283 The Cystic Fibrosis Transmembrane Conductance Regulator prot
284 Many missense mutations in the cystic fibrosis transmembrane conductance regulator prot
285 have been described in CF including disabled cystic fibrosis transmembrane conductance regulator recr
286 The cystic fibrosis transmembrane conductance regulator regu
287 e observed in normal AT2 cells an absence of cystic fibrosis transmembrane conductance regulator regu
288 l ER ligases, efficient degradation of human cystic fibrosis transmembrane conductance regulator requ
289 ortant for cholangiocyte functions including cystic fibrosis transmembrane conductance regulator, sec
290 al cell Cl(-) secretion via up-regulation of cystic fibrosis transmembrane conductance regulator, sug
291 deletion of a single residue (F508) in CFTR (cystic fibrosis transmembrane conductance regulator) tha
292 of the plasma membrane K(ATP) channels, the cystic fibrosis transmembrane conductance regulator, the
293 come the underlying functional defect in the cystic fibrosis transmembrane conductance regulator, the
294 The present investigation proposes that the cystic fibrosis transmembrane conductance regulator tran
295 ating type a pheromone, Ste6* (sterile), and cystic fibrosis transmembrane conductance regulator, und
297 to result in decreased levels of functional cystic fibrosis transmembrane conductance regulator were
298 plasma membrane, including the anion channel cystic fibrosis transmembrane conductance regulator, whi
299 escue the cystic-fibrosis-associated protein cystic fibrosis transmembrane conductance regulator, whi
300 nt known to decrease the level of functional cystic fibrosis transmembrane conductance regulator) wit
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