ライフサイエンスコーパス: polycystic kidney

1 ogical symptoms, cardiovascular defects, and polycystic kidneys.

2 ma membrane phospholipids in human and mouse polycystic kidneys.

3 nd polycystic kidney (PCK) rats, control and polycystic kidney 2 (Pkd2(ws25/-)) mice, healthy individ

4 ted from the unaffected parent, or biallelic polycystic kidney and hepatic disease 1 (PKHD1) mutation

5 e 1 region that includes a novel mutation in polycystic kidney and hepatic disease 1 (Pkhd1).

6 ll-enriched translated proteins, we identify Polycystic Kidney and Hepatic Disease 1-Like 1 (PKHD1L1)

7 Dominantly inherited polycystic kidney and liver diseases on the ADPKD spectr

8 e inflammatory chemokines CCL5 and CXCL10 in polycystic kidneys and cultured tubular cells.

9 Polycystic kidneys are hypoxic, and oxidative stress act

10 mutant alleles of IFT complex B genes cause polycystic kidneys, but the influence of IFT complex A p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 6A (anoctamin 1), drives cyst enlargement in polycystic kidney disease (PKD).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 In polycystic kidney disease and polycystic liver disease (

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

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

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

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

185 Polycystic kidney disease did not result in different SM

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

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

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

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

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

191 Autosomal dominant polycystic kidney disease is a genetic disorder associat

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

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

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

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

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

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

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

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

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

201 Autosomal dominant polycystic kidney disease patients develop renal failure

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

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

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

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

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

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

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

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

210 Polycystic kidney disease proteins, polycystin-1 and pol

211 manipulations on quantitative parameters of polycystic kidney disease severity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

250 Subanalysis explored those with polycystic kidney disease.

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

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

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

254 3 control recipients with autosomal dominant polycystic kidney disease.

255 ated with severe developmental disorders and polycystic kidney disease.

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

257 trarenal manifestation in autosomal dominant polycystic kidney disease.

258 g therapeutic strategy in autosomal dominant polycystic kidney disease.

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

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

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

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

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

264 pathway result in deranged ciliogenesis and polycystic kidney disease.

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

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

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

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

269 Persons with early autosomal dominant polycystic kidney disease.

270 ease, focal segmental glomerulosclerosis and polycystic kidney disease.

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

272 henotype associated with autosomal recessive polycystic kidney disease.

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

274 erimental mouse models of autosomal dominant polycystic kidney disease.

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

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

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

278 in either protein causing autosomal dominant polycystic kidney disease.

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

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

281 Polycystic kidney diseases (PKD) are genetic disorders c

282 Polycystic kidney diseases (PKDs) are genetic disorders

283 Polycystic kidney diseases (PKDs) comprise a subgroup of

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

285 Polycystic kidney diseases are characterized by numerous

286 Polycystic kidney diseases are the most common genetic d

287 ivation is essential and sufficient to cause polycystic kidneys in Tuberous Sclerosis Complex (TSC) a

288 However, automatic segmentation of polycystic kidneys is a challenging task due to severe a

289 on in vitro, the bulk of STAT3 activation in polycystic kidneys occurs through an indirect mechanism

290 Polycystic kidneys of Pkd2WS25/- mice, an orthologous mo

291 In the polycystic kidney (PCK) rat model, activation of STAT3 i

292 ession was analyzed in livers of control and polycystic kidney (PCK) rats, control and polycystic kid

293 ation of both SEC63 and XBP1 exacerbated the polycystic kidney phenotype in mice by markedly suppress

294 significantly influenced the severity of the polycystic kidney phenotype in mouse models of developme

295 examined hepatic cystogenesis in OA-treated polycystic kidney rats and after genetic elimination of

296 OA increased cystogenesis in polycystic kidney rats by 35%; in contrast, hepatic cyst

297 In Wistar polycystic kidney rats with hydrocephalus, alteration of

298 All patients received general health and polycystic kidney symptom surveys.

299 neal injection is preferentially targeted to polycystic kidneys whereas injected IgG is not.

300 endent hydrocephalic phenotype in the Wistar polycystic kidney (Wpk) rat.