ライフサイエンスコーパス: polycystic kidney disease

1 d to preserve renal function in experimental polycystic kidney disease.

2 Dysfunction of renal primary cilia leads to polycystic kidney disease.

3 Subanalysis explored those with polycystic kidney disease.

4 umerous disease models, including cancer and polycystic kidney disease.

5 have utility in diagnosis and monitoring of polycystic kidney disease.

6 s on renal function and favor cyst growth in polycystic kidney disease.

7 as a possible therapy for heart failure and polycystic kidney disease.

8 3 control recipients with autosomal dominant polycystic kidney disease.

9 ated with severe developmental disorders and polycystic kidney disease.

10 arget in the treatment of autosomal dominant polycystic kidney disease.

11 trarenal manifestation in autosomal dominant polycystic kidney disease.

12 g therapeutic strategy in autosomal dominant polycystic kidney disease.

13 ions to human PC2 (hPC2) are associated with polycystic kidney disease.

14 hannel that is mutated in autosomal dominant polycystic kidney disease.

15 2), respectively, lead to autosomal dominant polycystic kidney disease.

16 plains both renal and vascular phenotypes in polycystic kidney disease.

17 l diseases, such as diabetic nephropathy and polycystic kidney disease.

18 pathway result in deranged ciliogenesis and polycystic kidney disease.

19 humans and mice, nephronophthisis (NPHP) and polycystic kidney disease.

20 st, urine podocyte mRNAs did not increase in polycystic kidney disease.

21 a Ca(2+)-dependent channel with relevance to polycystic kidney disease.

22 obulin A nephropathy, and autosomal dominant polycystic kidney disease.

23 Persons with early autosomal dominant polycystic kidney disease.

24 2, the protein mutated in autosomal dominant polycystic kidney disease.

25 for approximately 15% of autosomal dominant polycystic kidney disease.

26 ice, a model that mimics autosomal recessive polycystic kidney disease.

27 C1) is the major cause of autosomal dominant polycystic kidney disease.

28 aintenance of tubule diameter correlate with polycystic kidney disease.

29 ease, focal segmental glomerulosclerosis and polycystic kidney disease.

30 ic abnormalities in a genetic mouse model of polycystic kidney disease.

31 henotype associated with autosomal recessive polycystic kidney disease.

32 in cysts of patients with autosomal dominant polycystic kidney disease.

33 erimental mouse models of autosomal dominant polycystic kidney disease.

34 sis in the kidney and in the pathogenesis of polycystic kidney disease.

35 ransduction in a model of autosomal dominant polycystic kidney disease.

36 ithelial pancreatic neoplasia, and 1 case of polycystic kidney disease.

37 in either protein causing autosomal dominant polycystic kidney disease.

38 Mutations of polycystic kidney disease 1 (PKD1) account for most ADPK

39 on to the familial mutation, variation(s) in polycystic kidney disease 1 (PKD1) or HNF1 homeobox B (H

40 ng from inherited mutations in the genes for polycystic kidney disease 1 (PKD1) or polycystic kidney

41 otentially deleterious biallelic variants in polycystic kidney disease 1 like 1 (PKD1L1), a gene asso

42 or potential (TRP) channels Trpm, NompC, and Polycystic kidney disease 2 (Pkd2) are expressed in CIII

43 The Polycystic Kidney Disease 2 (Pkd2) gene is mutated in au

44 olved in osteoblast differentiation and that polycystic kidney disease 2 (Pkd2) was a downstream targ

45 es for polycystic kidney disease 1 (PKD1) or polycystic kidney disease 2 (PKD2).

46 Here, we show that disruption of the polycystic kidney disease 2-like 1 (Pkd2l1 or Pkdl), enc

47 ociated with higher 16:1n-7, whereas PKD2L1 (polycystic kidney disease 2-like 1; P=5.7x10(-15)) and a

48 linical manifestations seen in patients with polycystic kidney disease, a cilia-associated pathology

49 oding for multiple ciliary proteins underlie polycystic kidney disease, a disorder with numerous card

50 nic kidney diseases after autosomal dominant polycystic kidney disease, accounting for ~5% of monogen

51 Autosomal dominant polycystic kidney disease (ADPKD) affects an estimated 1

52 Background Autosomal dominant polycystic kidney disease (ADPKD) affects one in 400 to

53 PKD2 mutations cause Autosomal Dominant Polycystic Kidney Disease (ADPKD) and affect many cellul

54 and comparing with IgAN, autosomal dominant polycystic kidney disease (ADPKD) and diabetic nephropat

55 ps early in patients with autosomal dominant polycystic kidney disease (ADPKD) and is associated with

56 Hypertension is common in autosomal dominant polycystic kidney disease (ADPKD) and is associated with

57 PC-1 and PC-2, result in autosomal dominant polycystic kidney disease (ADPKD) and ultimately renal f

58 Autosomal-dominant polycystic kidney disease (ADPKD) and von Hippel-Lindau

59 idney disease (ARPKD) and autosomal dominant polycystic kidney disease (ADPKD) are genetically distin

60 anisms of cystogenesis in autosomal dominant polycystic kidney disease (ADPKD) are not fully understo

61 s and the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD) are not well understoo

62 Prenatal forms of autosomal dominant polycystic kidney disease (ADPKD) are rare but can be re

63 -Biedl syndrome (BBS) and autosomal dominant polycystic kidney disease (ADPKD) are two genetically di

64 l epigenetic regulator of autosomal dominant polycystic kidney disease (ADPKD) but also as a novel cl

65 assessment is valuable in autosomal dominant polycystic kidney disease (ADPKD) but the reference stan

66 ng molecular pathology of autosomal dominant polycystic kidney disease (ADPKD) by promoting cyst form

67 hether early diagnosis of autosomal dominant polycystic kidney disease (ADPKD) can enable earlier man

68 neys, and often liver, in autosomal dominant polycystic kidney disease (ADPKD) cause progressive incr

69 a cohort of patients with autosomal dominant polycystic kidney disease (ADPKD) compared with a contro

70 Autosomal dominant polycystic kidney disease (ADPKD) constitutes the fourth

71 Autosomal dominant polycystic kidney disease (ADPKD) constitutes the most i

72 Patients with autosomal dominant polycystic kidney disease (ADPKD) experience progressive

73 ional group of experts in autosomal dominant polycystic kidney disease (ADPKD) from paediatric and ad

74 elegans and mammals, the autosomal dominant polycystic kidney disease (ADPKD) gene products polycyst

75 ation and modification in autosomal dominant polycystic kidney disease (ADPKD) have helped to explain

76 Autosomal-dominant polycystic kidney disease (ADPKD) induces a secretory ph

77 elopment and expansion in autosomal dominant polycystic kidney disease (ADPKD) involves both fluid se

78 Autosomal dominant polycystic kidney disease (ADPKD) is a common cause of E

79 Autosomal dominant polycystic kidney disease (ADPKD) is a common cause of r

80 Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited

81 Autosomal-dominant polycystic kidney disease (ADPKD) is a common life-threa

82 Autosomal-dominant polycystic kidney disease (ADPKD) is a common, progressi

83 Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder

84 Autosomal dominant polycystic kidney disease (ADPKD) is a leading cause of

85 Autosomal dominant polycystic kidney disease (ADPKD) is a progressive genet

86 Autosomal dominant polycystic kidney disease (ADPKD) is an important cause

87 Autosomal dominant polycystic kidney disease (ADPKD) is an inherited monoge

88 Autosomal dominant polycystic kidney disease (ADPKD) is associated with pro

89 Autosomal dominant polycystic kidney disease (ADPKD) is caused by inactivat

90 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

91 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

92 Autosomal-dominant polycystic kidney disease (ADPKD) is caused by mutations

93 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

94 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

95 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

96 Human autosomal dominant polycystic kidney disease (ADPKD) is characterized by bi

97 Autosomal dominant polycystic kidney disease (ADPKD) is characterized by in

98 Autosomal dominant polycystic kidney disease (ADPKD) is characterized by re

99 Autosomal dominant polycystic kidney disease (ADPKD) is driven by mutations

100 Autosomal dominant polycystic kidney disease (ADPKD) is heterogeneous with

101 The course of autosomal dominant polycystic kidney disease (ADPKD) is often associated wi

102 Autosomal dominant polycystic kidney disease (ADPKD) is one of the most com

103 Autosomal dominant polycystic kidney disease (ADPKD) is one of the most com

104 Autosomal dominant polycystic kidney disease (ADPKD) is the leading genetic

105 Autosomal dominant polycystic kidney disease (ADPKD) is the most common gen

106 Autosomal dominant polycystic kidney disease (ADPKD) is the most common gen

107 Autosomal dominant polycystic kidney disease (ADPKD) is the most common her

108 Autosomal dominant polycystic kidney disease (ADPKD) is the most common her

109 Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common inh

110 Autosomal dominant polycystic kidney disease (ADPKD) is the most common lif

111 Autosomal dominant polycystic kidney disease (ADPKD) is the most common mon

112 Autosomal dominant polycystic kidney disease (ADPKD) is the most common ren

113 Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent g

114 Patients with autosomal dominant polycystic kidney disease (ADPKD) often need to undergo

115 Autosomal dominant polycystic kidney disease (ADPKD) often results in ESRD

116 gression in patients with autosomal dominant polycystic kidney disease (ADPKD) remains untested.

117 etic nephropathy (DN) and autosomal-dominant polycystic kidney disease (ADPKD) served as "external" n

118 Novel therapies in autosomal dominant polycystic kidney disease (ADPKD) signal the need for ma

119 Patients with autosomal dominant polycystic kidney disease (ADPKD) typically carry a muta

120 imaging classification of autosomal dominant polycystic kidney disease (ADPKD) uses height-adjusted t

121 The course of autosomal dominant polycystic kidney disease (ADPKD) varies among individua

122 coding for PC2 results in autosomal dominant polycystic kidney disease (ADPKD), a condition character

123 ead to the development of autosomal dominant polycystic kidney disease (ADPKD), a debilitating condit

124 lycystin-1 (PC1) leads to autosomal dominant polycystic kidney disease (ADPKD), a disorder characteri

125 olycystin-1 (PC1) lead to autosomal-dominant polycystic kidney disease (ADPKD), a leading cause of re

126 ed Pkd1 protein result in autosomal dominant polycystic kidney disease (ADPKD), a serious inherited s

127 Autosomal dominant polycystic kidney disease (ADPKD), caused by mutations i

128 Autosomal dominant polycystic kidney disease (ADPKD), characterized by the

129 In autosomal dominant polycystic kidney disease (ADPKD), cysts accumulate and

130 two main causal genes for autosomal dominant polycystic kidney disease (ADPKD), encode the multipass

131 compared with those with autosomal dominant polycystic kidney disease (ADPKD), in which the native k

132 idely among patients with autosomal dominant polycystic kidney disease (ADPKD), necessitating optimal

133 Autosomal dominant polycystic kidney disease (ADPKD), one of the most commo

134 (Pkd2) gene is mutated in autosomal dominant polycystic kidney disease (ADPKD), one of the most commo

135 cally identified cases of autosomal dominant polycystic kidney disease (ADPKD), one of the most commo

136 Autosomal dominant polycystic kidney disease (ADPKD), the most common form

137 KD1 or PKD2 cause typical autosomal dominant polycystic kidney disease (ADPKD), the most common monog

138 human genetic diseases is autosomal dominant polycystic kidney disease (ADPKD), which is caused by mu

139 function deteriorates in autosomal dominant polycystic kidney disease (ADPKD).

140 escribed manifestation of autosomal dominant polycystic kidney disease (ADPKD).

141 ed to the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD).

142 olycystin-2 (PC2) lead to autosomal dominant polycystic kidney disease (ADPKD).

143 rgement of renal cysts in autosomal dominant polycystic kidney disease (ADPKD).

144 in-2, respectively, cause autosomal dominant polycystic kidney disease (ADPKD).

145 nsion and cystogenesis in autosomal dominant polycystic kidney disease (ADPKD).

146 PKD2 gene, which leads to autosomal dominant polycystic kidney disease (ADPKD).

147 ssion to renal failure in autosomal dominant polycystic kidney disease (ADPKD).

148 or polycystin 2 leads to autosomal dominant polycystic kidney disease (ADPKD).

149 loss of renal function in autosomal dominant polycystic kidney disease (ADPKD).

150 n genetic kidney disorder autosomal dominant polycystic kidney disease (ADPKD).

151 or many clinical cases of autosomal dominant polycystic kidney disease (ADPKD).

152 uses ciliopathies such as autosomal dominant polycystic kidney disease (ADPKD).

153 ain cause of mortality in autosomal-dominant polycystic kidney disease (ADPKD).

154 t for almost all cases of autosomal dominant polycystic kidney disease (ADPKD).

155 the genes responsible for autosomal dominant polycystic kidney disease (ADPKD).

156 ses, including cancer and autosomal dominant polycystic kidney disease (ADPKD).

157 polycystin-1 (PC1), cause autosomal-dominant polycystic kidney disease (ADPKD).

158 ng pathway is aberrant in autosomal-dominant polycystic kidney disease (ADPKD).

159 rthologous mouse model of autosomal dominant polycystic kidney disease (ADPKD).

160 in the polycystins cause autosomal dominant polycystic kidney disease (ADPKD).

161 nes, PKD1 and PKD2, cause autosomal dominant polycystic kidney disease (ADPKD).

162 trarenal manifestation of autosomal dominant polycystic kidney disease (ADPKD).

163 lving patients with early autosomal dominant polycystic kidney disease (ADPKD; estimated creatinine c

164 s of inherited disorders, autosomal dominant polycystic kidney diseases (ADPKD), a significant cause

165 kidney disease [ARPKD] or autosomal dominant polycystic kidney disease [ADPKD]).

166 a role in the pathogenesis of hypertension, polycystic kidney disease, AKI, and CKD.

167 stin-1 (PC1) give rise to autosomal dominant polycystic kidney disease, an important and common cause

168 his case involves a 54-year-old patient with polycystic kidney disease and a history of hyperacute al

169 allele significantly ameliorated the severe polycystic kidney disease and consequent runting caused

170 ve severe ventriculomegaly as well as severe polycystic kidney disease and die during the neonatal pe

171 , emphasizing CKD, transplant rejection, and polycystic kidney disease and discuss strategies to targ

172 sing for the treatment of autosomal dominant polycystic kidney disease and have been approved in Japa

173 d Safety in Management of Autosomal Dominant Polycystic Kidney Disease and Its Outcomes) trial, tolva

174 Roles of autophagy in polycystic kidney disease and kidney cancer have also be

175 vels of this eicosanoid are also elevated in polycystic kidney disease and may contribute to cyst for

176 It has a critical role in polycystic kidney disease and nephronophthisis.

177 weights and cyst growth in animal models of polycystic kidney disease and PLD, and might be develope

178 In polycystic kidney disease and polycystic liver disease (

179 The first case is a 67-year-old man with polycystic kidney disease and recipient of a zero-antige

180 tolvaptan as safe and effective therapy for polycystic kidney disease and reveal a potential new reg

181 mbryonic development to adult progression of polycystic kidney disease and some cancers.

182 s, diabetes, chronic interstitial nephritis, polycystic kidney disease, and 1-3 years of prior dialys

183 iseases such as ischemia/reperfusion injury, polycystic kidney disease, and congenital solitary kidne

184 nephropathy, albuminuria, autosomal dominant polycystic kidney disease, and ischemia/reperfusion-indu

185 therapeutic targets: TRPC6 in FSGS, PKD2 in polycystic kidney disease, and TRPM6 in familial hypomag

186 th refractory symptoms of autosomal dominant polycystic kidney disease (APKD) in need of a renal tran

187 Polycystic kidney diseases are characterized by numerous

188 Polycystic kidney diseases are the most common genetic d

189 C and PKD), identified in linkage studies of polycystic kidney disease, are candidate channels divide

190 Autosomal recessive polycystic kidney disease (ARPKD) and autosomal dominant

191 ctomies in patients with autosomal recessive polycystic kidney disease (ARPKD) and long-term clinical

192 cells from patients with autosomal recessive polycystic kidney disease (ARPKD) had significantly lowe

193 Autosomal recessive polycystic kidney disease (ARPKD) is a severe pediatric

194 Autosomal recessive polycystic kidney disease (ARPKD) is an important childh

195 rmation and expansion in autosomal recessive polycystic kidney disease (ARPKD) is poorly understood,

196 ish an in vitro model of autosomal recessive polycystic kidney disease (ARPKD), the cystic phenotype

197 Autosomal recessive polycystic kidney disease (ARPKD), the most common cilio

198 BACKGROUND & AIMS: Autosomal recessive polycystic kidney disease (ARPKD), the most common cilio

199 Autosomal recessive polycystic kidney disease (ARPKD), usually considered to

200 Caroli disease (CD), and autosomal recessive polycystic kidney disease (ARPKD).

201 codes fibrocystin, cause autosomal recessive polycystic kidney disease (ARPKD).

202 eral cystic disease (eg, autosomal recessive polycystic kidney disease [ARPKD] or autosomal dominant

203 ed in cancer cells, ciliopathies such as the polycystic kidney disease, as well as in the genetic dis

204 Furthermore, autosomal dominant polycystic kidney disease-associated TRPP2 mutant T448K

205 laying an important role in the formation of polycystic kidney disease, but not for Rab8 another cili

206 hannel protein PKD2 cause autosomal dominant polycystic kidney disease, but the function of PKD2 in c

207 s the juvenile cystic kidneys (jck) model of polycystic kidney disease, but the functions of Nek8 are

208 dentical to those seen in autosomal dominant polycystic kidney disease, but without clinically releva

209 G protein-coupled receptors (GPCRs) and the polycystic kidney disease-causing polycystin 1/2 complex

210 ascular manifestations of autosomal dominant polycystic kidney disease derive directly from myocardiu

211 Polycystic kidney disease did not result in different SM

212 acterized internal domain is a member of the polycystic kidney disease domain family but also how the

213 erties of PC2 are lost in autosomal dominant polycystic kidney disease, emphasizing the importance of

214 APK activation, all of which are features of polycystic kidney disease, especially nephronophthisis.

215 riched miRNA family, and upregulation of the polycystic kidney disease gene Pkd1.

216 ozygous mutations in the autosomal recessive polycystic kidney disease gene PKHD1, indicating that ad

217 Knockout of the polycystic kidney disease genes PKD1 or PKD2 induces cys

218 uires lov-1 and pkd-2 (homologs of the human polycystic kidney disease genes, PKD1 and PKD2), which a

219 Deletion of Lgr4 in mouse led to aniridia, polycystic kidney disease, genitourinary anomalies, and

220 Ectopic cAMP signaling is pathologic in polycystic kidney disease; however, its spatiotemporal a

221 or down-regulation of PKD1 or PKD2 leads to polycystic kidney disease in animal models, but their in

222 Autosomal dominant polycystic kidney disease is a genetic disorder associat

223 Autosomal dominant polycystic kidney disease is caused by mutations in the

224 Recent evidence suggests that polycystic kidney disease is characterized by defects in

225 iography in patients with autosomal dominant polycystic kidney disease is cost-effective.

226 ssues, the relationship between Hedgehog and polycystic kidney disease is not known.

227 Autosomal dominant polycystic kidney disease is the most common inherited k

228 man homologues are associated with autosomal polycystic kidney disease, is an essential protein whose

229 a suspected diagnosis of autosomal dominant polycystic kidney disease, medullary cystic kidney disea

230 Using human ADPKD tissues and polycystic kidney disease mouse models, we show that the

231 The most severe form of autosomal dominant polycystic kidney disease occurs in patients with mutati

232 fective for patients with autosomal dominant polycystic kidney disease or polycystic liver disease; e

233 m that may play a role in autosomal dominant polycystic kidney disease pathogenesis.

234 Autosomal dominant polycystic kidney disease patients develop renal failure

235 ls (NL, 42 vs. 17; US, 40 vs. 13 points) and polycystic kidney disease patients without PLD (22 point

236 es of PLD patients with general controls and polycystic kidney disease patients without PLD.

237 Cysts and aneurysms from polycystic kidney disease patients, Pkd mouse, and zebra

238 ectomies exist for patients with symptomatic polycystic kidney disease (PCKD).

239 in a disruption of renal ciliogenesis and a polycystic kidney disease phenotype in zebrafish and mic

240 unction by re-expressing survivin can rescue polycystic kidney disease phenotypes.

241 ious studies report a cross-talk between the polycystic kidney disease (PKD) and tuberous sclerosis c

242 insulinemic hypoglycemia (HI) and congenital polycystic kidney disease (PKD) are rare, genetically he

243 denosine monophosphate (cAMP) drives genetic polycystic kidney disease (PKD) cystogenesis.

244 s to drive the aggregation of the downstream polycystic kidney disease (PKD) domain into a melanosoma

245 ncluding the leucine-rich repeats, the first polycystic kidney disease (PKD) domain, and the C-type l

246 s structure reveals that of the five Ig-like polycystic kidney disease (PKD) domains in AAVR, PKD2 bi

247 Polycystic kidney disease (PKD) exhibits an inflammatory

248 sease progression in autosomal-dominant (AD) polycystic kidney disease (PKD) exhibits high intra-fami

249 Polycystic kidney disease (PKD) family proteins associat

250 nd their disruption has been associated with polycystic kidney disease (PKD) genes, the majority of w

251 Polycystic kidney disease (PKD) is a leading cause of ES

252 Autosomal-dominant (AD) polycystic kidney disease (PKD) is a leading cause of re

253 Polycystic kidney disease (PKD) is a life-threatening di

254 Polycystic kidney disease (PKD) is one of the most commo

255 and interstitial fibrosis, similar to known polycystic kidney disease (PKD) models.

256 of AQP3 in cyst development, we generated 2 polycystic kidney disease (PKD) mouse models: kidney-spe

257 olysis Site (GPS) of cell-adhesion GPCRs and polycystic kidney disease (PKD) proteins constitutes a h

258 ptor potential channel polycystin (TRPP) and polycystic kidney disease (PKD) proteins, play key roles

259 eracts predominantly with the second Ig-like polycystic kidney disease (PKD) repeat domain (PKD2) pre

260 be an underlying cause of autosomal dominant polycystic kidney disease (PKD), and ciliary-EV interact

261 ney disease (ADPKD), the most common form of polycystic kidney disease (PKD), is a disorder with char

262 In polycystic kidney disease (PKD), renal parenchyma is des

263 Polycystic kidney disease (PKD), the most common genetic

264 is challenging for chronic diseases such as polycystic kidney disease (PKD), the most common heredit

265 P signaling contribute to the development of polycystic kidney disease (PKD).

266 tro and in vivo models of autosomal dominant polycystic kidney disease (PKD).

267 is an important mediator of cystogenesis in polycystic kidney disease (PKD).

268 indicates the importance of elevated cAMP in polycystic kidney disease (PKD).

269 ding the kidney, liver and pancreas features polycystic kidney disease (PKD).

270 6A (anoctamin 1), drives cyst enlargement in polycystic kidney disease (PKD).

271 ouse kidney results in polycystin-1-mediated polycystic kidney disease (PKD).

272 shows beneficial effects in animal models of polycystic kidney disease (PKD); however, two clinical t

273 Polycystic kidney diseases (PKD) are genetic disorders c

274 e (Pu-Py) mirror repeat tract from the human polycystic kidney disease (PKD1) intron 21 forms non-B D

275 However, in polycystic kidney disease (pkd1)-knockout mice, CFTR was

276 Polycystic kidney diseases (PKDs) are genetic disorders

277 Polycystic kidney diseases (PKDs) comprise a subgroup of

278 Genetic forms of polycystic kidney diseases (PKDs), including nephronopht

279 In contrast to many models of polycystic kidney disease, precystic Ift140-deleted coll

280 f a 21-year-old man with autosomal recessive polycystic kidney disease, presenting with subarachnoid

281 may predict and/or effect autosomal dominant polycystic kidney disease progression.

282 vels of the cluster in three disease models: polycystic kidney disease, prostate cancer, and breast c

283 Furthermore, the polycystic kidney disease protein IFT88 binds IFT52281-3

284 GPS is also shared by polycystic kidney disease proteins and it precedes the f

285 Polycystic kidney disease proteins, polycystin-1 and pol

286 ne that is mutated in the autosomal dominant polycystic kidney disease, regulates a number of process

287 , and ciliary dysfunction is associated with polycystic kidney disease, retinal degeneration, polydac

288 manipulations on quantitative parameters of polycystic kidney disease severity.

289 who participated in the Halt Progression of Polycystic Kidney Disease Study A were categorized on th

290 For patients with autosomal dominant polycystic kidney disease that progressed more slowly, t

291 tin 2 are responsible for autosomal dominant polycystic kidney disease, the most common heritable hum

292 rize for Advancement in the Understanding of Polycystic Kidney Disease to participate in a forward-th

293 h G proteins are regulated in the context of polycystic kidney disease to promote abnormal epithelial

294 enal disease secondary to autosomal dominant polycystic kidney disease was referred to a quaternary c

295 om GPCRs and fibrocystin (also implicated in polycystic kidney disease), we demonstrate these motifs

296 To gain insights into autosomal dominant polycystic kidney disease, we performed yeast two-hybrid

297 , recipient employment, and the diagnosis of polycystic kidney disease were significantly associated

298 originally identified in autosomal dominant polycystic kidney disease where it regulates the calcium

299 ferral before dialysis were the diagnosis of polycystic kidney disease, white recipient race, referra

300 to identify patients with autosomal dominant polycystic kidney disease who are most likely to benefit