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1 polycystin-1 family (the protein mutated in autosomal dominant polycystic kidney disease).
2 gy, with mutations in either protein causing autosomal dominant polycystic kidney disease.
3 ons are responsible for approximately 15% of autosomal dominant polycystic kidney disease.
4 of polycystin-1 (PC1) is the major cause of autosomal dominant polycystic kidney disease.
5 flow-stimulated calcium signaling and causes autosomal dominant polycystic kidney disease.
6 annel, is frequently mutated or truncated in autosomal dominant polycystic kidney disease.
7 and PC2 are membrane proteins implicated in autosomal dominant polycystic kidney disease.
8 mediating cyst formation and enlargement in autosomal dominant polycystic kidney disease.
9 thogenesis of cystic renal disorders such as autosomal dominant polycystic kidney disease.
10 mechanism for progressive cyst formation in autosomal dominant polycystic kidney disease.
11 represents a potentially novel treatment for autosomal dominant polycystic kidney disease.
12 nsible for approximately 15% of all cases of autosomal dominant polycystic kidney disease.
13 Mutations in either PKD1 or PKD2 cause autosomal dominant polycystic kidney disease.
14 leading cause of morbidity and mortality in autosomal dominant polycystic kidney disease.
15 Mutations in polycystin-2 (PC2) cause autosomal dominant polycystic kidney disease.
16 of its function causes cystogenesis in human autosomal dominant polycystic kidney disease.
17 its function causes cyst formation in human autosomal dominant polycystic kidney disease.
18 PKD2 is mutated in 15% of patients with autosomal dominant polycystic kidney disease.
19 sensitive channel, with defects resulting in autosomal dominant polycystic kidney disease.
20 lial cells and when mutated results in human autosomal dominant polycystic kidney disease.
21 roduct of the PKD1 gene, which is mutated in autosomal dominant polycystic kidney disease.
22 in turn could contribute to the pathology of autosomal dominant polycystic kidney disease.
23 leading cause of morbidity and mortality in autosomal dominant polycystic kidney disease.
24 pithelia are associated with mouse and human autosomal dominant polycystic kidney disease.
25 ng polycystin-1 (PC1) and polycystin-2 cause autosomal dominant polycystic kidney disease.
26 ation channel that, when mutated, results in autosomal dominant polycystic kidney disease.
27 hat can be used to study the pathogenesis of autosomal dominant polycystic kidney disease.
28 2), a Ca(2+)-permeable cation channel, cause autosomal dominant polycystic kidney disease.
29 espectively, account for almost all cases of autosomal dominant polycystic kidney disease.
30 adult kidney expression of PRKX was found in autosomal dominant polycystic kidney disease.
31 KD2, genes that are mutated in most cases of autosomal dominant polycystic kidney disease.
32 pathways, and its deletion suffices to cause autosomal dominant polycystic kidney disease.
33 ne models resembles that seen in humans with autosomal dominant polycystic kidney disease.
34 iation with ACKD and one in association with autosomal dominant polycystic kidney disease.
35 nt of large cystic kidneys that characterize autosomal dominant polycystic kidney disease.
36 KD2, genes that are mutated in most cases of autosomal dominant polycystic kidney disease.
37 Germline mutations in PKD2 cause autosomal dominant polycystic kidney disease.
38 fer from that of 273 control recipients with autosomal dominant polycystic kidney disease.
39 tion may be a new target in the treatment of autosomal dominant polycystic kidney disease.
40 the most common extrarenal manifestation in autosomal dominant polycystic kidney disease.
41 erged as a promising therapeutic strategy in autosomal dominant polycystic kidney disease.
42 nselective cation channel that is mutated in autosomal dominant polycystic kidney disease.
43 nd polycystin-2 (PC2), respectively, lead to autosomal dominant polycystic kidney disease.
44 phropathy, immunoglobulin A nephropathy, and autosomal dominant polycystic kidney disease.
45 Persons with early autosomal dominant polycystic kidney disease.
46 ntry of polycystin-2, the protein mutated in autosomal dominant polycystic kidney disease.
47 2 patients and 9 of 11 Group 1 patients had autosomal-dominant polycystic kidney disease.
48 1 and polycystin-2 encoded by PKD2, underlie autosomal-dominant polycystic kidney disease.
49 protein encoded by PKD1, a gene involved in autosomal-dominant polycystic kidney disease.
51 Humans heterozygous for PKD1 or PKD2 develop autosomal dominant polycystic kidney disease, a common g
54 and those with inherited co-deletions of the autosomal dominant polycystic kidney disease (ADPKD) 1 g
57 Hypertension develops early in patients with autosomal dominant polycystic kidney disease (ADPKD) and
58 comparator groups, and comparing with IgAN, autosomal dominant polycystic kidney disease (ADPKD) and
65 not only as a novel epigenetic regulator of autosomal dominant polycystic kidney disease (ADPKD) but
66 of the PKD1 gene mutated in the majority of autosomal dominant polycystic kidney disease (ADPKD) cas
67 ancreatic cysts in a cohort of patients with autosomal dominant polycystic kidney disease (ADPKD) com
72 cation channel homologous to the human Pkd2 autosomal dominant polycystic kidney disease (ADPKD) gen
73 human genomic fragment containing the entire autosomal dominant polycystic kidney disease (ADPKD) gen
76 ated that approximately 15% of families with autosomal dominant polycystic kidney disease (ADPKD) hav
77 sms of disease causation and modification in autosomal dominant polycystic kidney disease (ADPKD) hav
78 mparable to published US criteria for type 1 autosomal dominant polycystic kidney disease (ADPKD) if
80 tility of ultrasonography (US) in diagnosing autosomal dominant polycystic kidney disease (ADPKD) in
81 similar in many respects to that seen in the autosomal dominant polycystic kidney disease (ADPKD) in
83 The principal extrarenal manifestation of autosomal dominant polycystic kidney disease (ADPKD) inv
135 hip between renal volume and hypertension in autosomal dominant polycystic kidney disease (ADPKD) occ
140 sequence similarity between a region of the autosomal dominant polycystic kidney disease (ADPKD) pro
141 ty with disease progression in patients with autosomal dominant polycystic kidney disease (ADPKD) rem
149 disease, mark a population of patients with autosomal dominant polycystic kidney disease (ADPKD) who
151 embrane proteins, which, when mutated, cause autosomal dominant polycystic kidney disease (ADPKD), a
152 Dysregulation of polycystin-1 (PC1) leads to autosomal dominant polycystic kidney disease (ADPKD), a
153 g the cilia-localized Pkd1 protein result in autosomal dominant polycystic kidney disease (ADPKD), a
154 family (polycystin-1 and -2) are mutated in autosomal dominant polycystic kidney disease (ADPKD), an
156 gene product of PKD2, whose mutations cause autosomal dominant polycystic kidney disease (ADPKD), be
157 protein mutated in the majority of cases of autosomal dominant polycystic kidney disease (ADPKD), bu
158 latory protein polycystin-1 (PC1) results in autosomal dominant polycystic kidney disease (ADPKD), ch
164 seases such as mucolipidosis type IV (MLIV), autosomal dominant polycystic kidney disease (ADPKD), fa
165 D2, the gene defective in the second form of autosomal dominant polycystic kidney disease (ADPKD), ha
166 merulonephritis and compared with those with autosomal dominant polycystic kidney disease (ADPKD), in
167 hich is encoded by a gene that is mutated in autosomal dominant polycystic kidney disease (ADPKD), is
168 rogression varies widely among patients with autosomal dominant polycystic kidney disease (ADPKD), ne
171 c Kidney Disease 2 (Pkd2) gene is mutated in autosomal dominant polycystic kidney disease (ADPKD), on
172 or almost all clinically identified cases of autosomal dominant polycystic kidney disease (ADPKD), on
177 ure of the polycystic liver that accompanies autosomal dominant polycystic kidney disease (ADPKD), we
178 progression in an orthologous mouse model of autosomal dominant polycystic kidney disease (ADPKD).
179 large multi-exon genes, PKD1 and PKD2, cause autosomal dominant polycystic kidney disease (ADPKD).
180 disease is a well described manifestation of autosomal dominant polycystic kidney disease (ADPKD).
181 tations in PKD1 are the most common cause of autosomal dominant polycystic kidney disease (ADPKD).
182 stin-1 (PC1), contribute to >85% of cases of autosomal dominant polycystic kidney disease (ADPKD).
183 on are a continuous concern in patients with autosomal dominant polycystic kidney disease (ADPKD).
184 D1 and TRPP2 account for nearly all cases of autosomal dominant polycystic kidney disease (ADPKD).
185 f Src has been linked to the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD).
186 the focal nature for renal cyst formation in autosomal dominant polycystic kidney disease (ADPKD).
187 ics of sensory behavior, cilia function, and autosomal dominant polycystic kidney disease (ADPKD).
188 mplicated in mediating disease escalation in autosomal dominant polycystic kidney disease (ADPKD).
189 nction, and human genetic diseases including autosomal dominant polycystic kidney disease (ADPKD).
190 werful model to study the molecular basis of autosomal dominant polycystic kidney disease (ADPKD).
191 tic entity that can occur independently from autosomal dominant polycystic kidney disease (ADPKD).
192 the disease as it manifests in patients with autosomal dominant polycystic kidney disease (ADPKD).
193 d fluid secretion by the cystic epithelia in autosomal dominant polycystic kidney disease (ADPKD).
194 is detected in kidneys of all patients with autosomal dominant polycystic kidney disease (ADPKD).
195 luid filled cysts in MDCK cells and in human autosomal dominant polycystic kidney disease (ADPKD).
196 of unknown function that is responsible for autosomal dominant polycystic kidney disease (ADPKD).
197 umulation are responsible for cyst growth in autosomal dominant polycystic kidney disease (ADPKD).
199 in infants with a family history of classic, autosomal dominant polycystic kidney disease (ADPKD).
200 he progressive enlargement of renal cysts in autosomal dominant polycystic kidney disease (ADPKD).
201 elopment of hypertension and cystogenesis in autosomal dominant polycystic kidney disease (ADPKD).
202 ion in the PKD1 or PKD2 gene, which leads to autosomal dominant polycystic kidney disease (ADPKD).
203 t growth and progression to renal failure in autosomal dominant polycystic kidney disease (ADPKD).
204 C2) cause the common genetic kidney disorder autosomal dominant polycystic kidney disease (ADPKD).
205 ciliary function causes ciliopathies such as autosomal dominant polycystic kidney disease (ADPKD).
206 r PKD2 (15%) account for almost all cases of autosomal dominant polycystic kidney disease (ADPKD).
207 entified as one of the genes responsible for autosomal dominant polycystic kidney disease (ADPKD).
208 a variety of diseases, including cancer and autosomal dominant polycystic kidney disease (ADPKD).
210 previous trial involving patients with early autosomal dominant polycystic kidney disease (ADPKD; est
211 , between two groups of inherited disorders, autosomal dominant polycystic kidney diseases (ADPKD), a
213 This adaptive response is blocked when the autosomal-dominant polycystic kidney disease (ADPKD) gen
219 uggests that some vascular manifestations of autosomal-dominant polycystic kidney disease (ADPKD) res
220 Patients with diabetic nephropathy (DN) and autosomal-dominant polycystic kidney disease (ADPKD) ser
223 cilia are implicated in the pathogenesis of autosomal-dominant polycystic kidney disease (ADPKD), wh
224 of its function causes cystogenesis in human autosomal-dominant polycystic kidney disease (ADPKD).
225 ts of rigorous versus standard BP control on autosomal-dominant polycystic kidney disease (ADPKD).
226 disorders are the main cause of mortality in autosomal-dominant polycystic kidney disease (ADPKD).
227 in Pkd1, encoding polycystin-1 (PC1), cause autosomal-dominant polycystic kidney disease (ADPKD).
228 ycin (mTOR) signaling pathway is aberrant in autosomal-dominant polycystic kidney disease (ADPKD).
229 Mutations in polycystin-1 (PC1) give rise to autosomal dominant polycystic kidney disease, an importa
231 quaretics are promising for the treatment of autosomal dominant polycystic kidney disease and have be
232 lvaptan Efficacy and Safety in Management of Autosomal Dominant Polycystic Kidney Disease and Its Out
233 hibit hepatorenal pathology resembling human autosomal dominant polycystic kidney disease and represe
234 cultured cells from patients who suffer from autosomal dominant polycystic kidney disease, and this P
235 el of HIVAN, in HIVAN biopsy samples, and in autosomal dominant polycystic kidney disease, another re
236 sial in patients with refractory symptoms of autosomal dominant polycystic kidney disease (APKD) in n
239 ers of patients with autosomal recessive and autosomal dominant polycystic kidney disease (ARPKD and
241 2, the product of the gene mutated in type 2 autosomal dominant polycystic kidney disease, belongs to
242 nd pathologically identical to those seen in autosomal dominant polycystic kidney disease, but withou
243 ate that Pkd2ws25/- mice, an animal model of autosomal dominant polycystic kidney disease, developed
244 attern is unchanged in orthologous models of autosomal dominant polycystic kidney disease due to muta
245 These properties of PC2 are lost in autosomal dominant polycystic kidney disease, emphasizin
246 e for renal and systemic diseases, including autosomal dominant polycystic kidney disease, Gitelman s
248 in encoded by the principal gene involved in autosomal dominant polycystic kidney disease, has been i
249 oduct of the gene most frequently mutated in autosomal dominant polycystic kidney disease, has reveal
250 specific Pkd1(flox/-);Ksp-Cre mouse model of autosomal dominant polycystic kidney disease, in which t
260 D2) responsible for the majority of cases of autosomal dominant polycystic kidney disease is unknown.
262 ein defective in a majority of patients with autosomal dominant polycystic kidney disease, is a ubiqu
263 the gene responsible for the second form of autosomal dominant polycystic kidney disease, is highly
264 mology to human polycystins, products of the autosomal dominant polycystic kidney-disease loci PKD1 a
265 ysregulation of these or similar channels in autosomal dominant polycystic kidney disease may contrib
266 ients referred with a suspected diagnosis of autosomal dominant polycystic kidney disease, medullary
268 ogues is equally effective for patients with autosomal dominant polycystic kidney disease or polycyst
269 rats, normal human beings, and patients with autosomal-dominant polycystic kidney disease or ARPKD.
270 a control mechanism that may play a role in autosomal dominant polycystic kidney disease pathogenesi
271 ssion in the livers of PCK rats and ARPKD or autosomal-dominant polycystic kidney disease patients.
272 identification of the genes responsible for autosomal dominant polycystic kidney disease (PKD) and a
275 m of Radiologic Imaging Study of PKD (CRISP) autosomal dominant polycystic kidney disease (PKD) popul
276 icking defects may be an underlying cause of autosomal dominant polycystic kidney disease (PKD), and
278 gene responsible for the most common form of autosomal dominant polycystic kidney disease ( PKD1 ) is
279 of renal cystic disease in the major form of autosomal dominant polycystic kidney disease (PKD1) is h
280 function and its role in the development of autosomal dominant polycystic kidney disease (PKD1) requ
281 ncluding the gene most frequently mutated in autosomal dominant polycystic kidney disease (PKD1).
282 The gene responsible for the second form of autosomal dominant polycystic kidney disease, PKD2, has
283 uates factors that may predict and/or effect autosomal dominant polycystic kidney disease progression
284 2 forms a calcium-sensitive complex with the autosomal dominant polycystic kidney disease protein pol
285 A common inherited cause of renal failure, autosomal dominant polycystic kidney disease results fro
286 several of the most severe complications of autosomal-dominant polycystic kidney disease, such as in
288 s a genetic modifier for disease severity in autosomal dominant polycystic kidney disease that result
290 ystin 1 and polycystin 2 are responsible for autosomal dominant polycystic kidney disease, the most c
292 ast 85% of the mutations present in affected autosomal dominant polycystic kidney disease type 1 pedi
294 an with end-stage renal disease secondary to autosomal dominant polycystic kidney disease was referre
296 tations in pkd2 result in the type 2 form of autosomal dominant polycystic kidney disease, which acco
299 nd others may help to identify patients with autosomal dominant polycystic kidney disease who are mos
300 which are the principal proteins involved in autosomal dominant polycystic kidney disease, with polar
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