ライフサイエンスコーパス: cyst formation

1 ene, possibly causing haploinsufficiency and cyst formation.

2 ay explain the epithelial stratification and cyst formation.

3 ctivation of Rac1 is required for epithelial cyst formation.

4 enes, in response to tissue damage and renal cyst formation.

5 and astrocytes, lipid-laden macrophages, and cyst formation.

6 f centriole migration during female germline cyst formation.

7 as, or time-specific deletion of Pkd2 led to cyst formation.

8 rapamycin administration effectively blocks cyst formation.

9 sue pathologic features and bony microdamage/cyst formation.

10 mechanism underlying this aspect of germline cyst formation.

11 termine whether Src activity plays a role in cyst formation.

12 developmental gene expression during tissue cyst formation.

13 ty, suggesting multiple mechanisms exist for cyst formation.

14 the TNF-alpha inhibitor etanercept prevented cyst formation.

15 thought to be a major contributing factor to cyst formation.

16 aling activity is a key factor that leads to cyst formation.

17 of HNF-1beta in the mouse kidney results in cyst formation.

18 rmine the pathogenesis of Six2creFrs2alphaKO cyst formation.

19 h abnormal epithelial cell proliferation and cyst formation.

20 on factor implicated in cAMP-dependent renal cyst formation.

21 amine the pathophysiology of CNS peritumoral cyst formation.

22 bular differentiation, ultimately leading to cyst formation.

23 the two factors in angiogenesis and possibly cyst formation.

24 ls strongly supports a two-hit mechanism for cyst formation.

25 that such mutations also can play a role in cyst formation.

26 disregulation of the PKD1 gene has a role in cyst formation.

27 o a cilia biogenesis defect and rapid kidney cyst formation.

28 ve been proposed to explain the mechanism of cyst formation.

29 ability under oxidative stress and decreased cyst formation.

30 lle, the fusome, that is required for normal cyst formation.

31 even under conditions that normally promote cyst formation.

32 onous divisions of the cystoblast leading to cyst formation.

33 the epithelial proliferation associated with cyst formation.

34 lium regulates kidney tubule development and cyst formation.

35 intrafamilial phenotypic variation and focal cyst formation.

36 nse (UPR) pathway that is protective against cyst formation.

37 Entamoeba are predominantly expressed during cyst formation.

38 tion and divert excessive proliferation into cyst formation.

39 s controlling tubular diameter contribute to cyst formation.

40 taining two, four or eight cells, indicating cyst formation.

41 patients (26%) developed macular edema with cyst formation.

42 h an osmotic effect, all contributing to the cyst formation.

43 ycystic kidney disease and may contribute to cyst formation.

44 helial cells from renal tissues and delaying cyst formation.

45 lacking adenosine receptors had no defect in cyst formation.

46 wth rate, suppresses apoptosis, and prevents cyst formation.

47 promoting Wnt activation and contributing to cyst formation.

48 fails to synthesize cGMP and is defective in cyst formation.

49 downstream kinetics of renal hypertrophy and cyst formation.

50 Endosome morphology changes prior to cyst formation.

51 al hypertrophic signaling and culminating in cyst formation.

52 ral and functional hypertrophy without renal cyst formation.

53 nitiate the cell proliferation necessary for cyst formation; a paracrine mechanism may account for fo

54 Cyst formation, aberrant ductal morphology, and extensiv

55 to epithelial distension and stretch, kidney cyst formation, acute kidney injury by gentamicin, and c

56 roduce kidney cysts nor required to initiate cyst formation after mutation in Pkd1 or Pkd2.

57 ccination also severely reduced or prevented cyst formation after type II challenge infection.

58 olecular explanation for the focal nature of cyst formation and a probable mechanism whereby mutation

59 tic bile duct proliferation with progressive cyst formation and associated periportal fibrosis.

60 core PCP component, similarly led to kidney cyst formation and basal body disorganization.

61 or SKI-606 resulted in amelioration of renal cyst formation and biliary ductal abnormalities in both

62 sory signaling pathways that are involved in cyst formation and biofilms.

63 or by knocking down hdac1, suppressed kidney cyst formation and body curvature caused by pkd2 deficie

64 sion of AP2IX-9 significantly reduced tissue cyst formation and conferred alkaline pH-resistant growt

65 ts in the cyst cells resulted in a rescue of cyst formation and cyst differentiation.

66 y which various biologic processes influence cyst formation and cyst growth, thereby explaining an im

67 irst time that loss of polycystin-1 leads to cyst formation and defective skeletogenesis, and indicat

68 Given the strong association between kidney cyst formation and developmental biliary defects in pati

69 armacological cAMP pathway activators induce cyst formation and diminish formation of other structure

70 By contrast, cyst formation and enlargement from HRCE cells occurred

71 OR also plays an important role in mediating cyst formation and enlargement in autosomal dominant pol

72 ed the pathophysiology of fluid secretion in cyst formation and enlargement in autosomal recessive po

73 dominant polycystic kidney disease (ADPKD), cyst formation and enlargement require proliferation of

74 unknown how defective PC2 activity leads to cyst formation and expansion in ADPKD patients.

75 The molecular mechanism of cyst formation and expansion in autosomal recessive poly

76 ial cell proliferation is a prerequisite for cyst formation and expansion in polycystic kidney diseas

77 mmon genetic disorder characterized by renal cyst formation and extrarenal complications such as hype

78 he cilium is essential for preventing kidney cyst formation and for establishing left-right asymmetry

79 tic kidney disease (ADPKD), characterized by cyst formation and growth and often leading to renal fai

80 a specific STAT3 inhibitor, S3I-201, reduces cyst formation and growth in a neonatal PKD mouse model.

81 ether miRNAs are directly involved in kidney cyst formation and growth is not known.

82 ort a contribution from threshold effects to cyst formation and growth.

83 xpression, and paralleled collecting tubular cyst formation and growth.

84 n Sec10 resulted in more efficient and rapid cyst formation and increased tubule formation upon stimu

85 The former includes induction of renal cyst formation and interstitial fibrosis while the latte

86 TgBCP1 is essential for cyst formation and is the first example of a development

87 led to a ciliary phenotype including kidney cyst formation and left-right asymmetry defects.

88 own that alpha-spectrin is also required for cyst formation and oocyte differentiation, but that its

89 pindles during mitosis and are implicated in cyst formation and oocyte differentiation.

90 hts was shown previously to be required for cyst formation and oocyte differentiation; the role of t

91 ganelle that is pre-determinative of 16-cell cyst formation and oocyte fate specification.

92 in mouse kidney tubules leads to early-onset cyst formation and postnatal lethality.

93 tion in the morphology caused by non-uniform cyst formation and presence of adjacent liver cysts.

94 the first comprehensive analysis of in situ cyst formation and progression in inv/inv kidneys.

95 nges in signaling pathways involved in liver cyst formation and progression, and their impact on chol

96 llowed by a phase of collecting tubular (CT) cyst formation and progressive enlargement leading to co

97 In conclusion, AC6 is a key mediator of cyst formation and renal injury in a model of PKD.

98 ndau associated mechanisms involved in renal cyst formation and renewed appreciation for the influenc

99 amazepine and minoxidil, markedly attenuated cyst formation and restored kidney function.

100 n Moesin dominantly suppressed seamless tube cyst formation and restored terminal branching.

101 fully penetrant phenotype, characterized by cyst formation and severe defects in renal barrier funct

102 Motivated by a variety of examples of tissue cyst formation and size control that show simultaneous g

103 at VPA was able to reduce the progression of cyst formation and slow the decline of kidney function i

104 logical changes that accompany multicellular cyst formation and specific decreased expression of the

105 models as tools to study the pathogenesis of cyst formation and the effect of various therapeutic int

106 ized that LAM nodule-derived proteases cause cyst formation and tissue damage.

107 vation of Notch1 and/or Notch2, are prone to cyst formation and tubular epithelial stratification.

108 MT, whereas DeltaNp63 fine-tunes the rate of cyst formation and tubulogenesis by maintaining an appro

109 ure, and delays but does not block MDCK cell cyst formation and tubulogenesis in 3-D culture.

110 tion leading to epidermal thickening, dermal cyst formation, and alopecia.

111 f suppurative neutrophilic bronchopneumonia, cyst formation, and alveolar damage.

112 3p LOH occurs subsequent to VHL mutation and cyst formation, and correlates with malignant progressio

113 cogen accumulation, inflammation, apoptosis, cyst formation, and impaired renal function.

114 on tubular cell apoptosis and proliferation, cyst formation, and renal failure in the Han:SPRD rat mo

115 of rapamycin on tubular cell proliferation, cyst formation, and renal failure in the Han:SPRD rat mo

116 induced melanoma and follicular infundibular cyst formation, and tumor-associated melanocytes display

117 thologically by bronchocentric inflammation, cyst formation, and widespread vascular abnormalities an

118 In keeping with the two-hit mechanism of cyst formation, approximately 70% of kidney cysts in Pkd

119 ycin and carbamazepine was able to attenuate cyst formation as effectively as a single treatment with

120 ht of which showed intra-insular ductular or cyst formation as seen in the pancreas of hamsters durin

121 nvolved in secretion are up-regulated during cyst formation, as are some trans-Golgi network-to-endos

122 s been extensively studied through so-called cyst-formation assays in Madin-Darby canine kidney (MDCK

123 nd to provide evidence that kidney and liver cyst formation associated with Pkd2 deficiency occurs by

124 h doses of paracetamol and decreased ovarian-cyst formation at lower doses suggest a biological basis

125 iest cellular defects occurring during renal cyst formation because its kidney (the pronephros) is si

126 Renal cyst formation begins at embryonic day 15.5 (E15.5) in p

127 Cyst formation begins in the glomerulus at 40 hpf at the

128 In mice, loss of SEC63 induces cyst formation both in liver and kidney as the result of

129 nal renal injury increased the likelihood of cyst formation but never triggered rapid PKD.

130 fore conclude that BAG1 is not essential for cyst formation, but facilitates formation of cysts in vi

131 division is a feature of Pkhd1 mutation and cyst formation, but it is neither sufficient to produce

132 , knockdown of either PC2 or InsP3R leads to cyst formation, but knockdown of InsP3R type 1 (InsP3R1)

133 ease phenotype is primarily characterized by cyst formation, but there are also prominent interstitia

134 of the tyrosine kinase c-Met contributes to cyst formation, but we do not know the downstream mediat

135 es Toxoplasma bradyzoite differentiation and cyst formation by a mechanism dependent on the generatio

136 These range from cyst formation by intermediate-sized clusters to segrega

137 Cyst formation by Madin-Darby canine kidney (MDCK) cells

138 ellular proliferation and attenuates overall cyst formation by restoring Ca(2+) signaling in these ce

139 ide compelling evidence for the influence on cyst formation by spatiotemporal gene inactivation, the

140 hypothesize that primary cilia prevent renal cyst formation by suppressing pathologic tubular cell hy

141 using short hairpin RNA results in increased cyst formation by tubular cells.

142 29 stages of germline cyst formation can be identified in D. melanogaster ooge

143 conclude that epithelial differentiation and cyst formation can occur without appreciable proliferati

144 Cyst formation correlates with inhibition of Pkhd1 expre

145 this study sought to determine whether renal cyst formation could be prevented by genetic complementa

146 Time course study of germline cyst formation demonstrates that contractile ring constr

147 ke murine ARPKD, has a transient phase of PT cyst formation during early fetal development.

148 ing collecting duct cells in early stages of cyst formation fail to properly orient their mitotic spi

149 ecome symptomatic with exponential growth or cyst formation following long periods of quiescence.

150 nvolved in biliary development and in kidney cyst formation; forced expression of vhnf1 mRNA led to r

151 ic kidney disease genes PKD1 or PKD2 induces cyst formation from kidney tubules.

152 The focal nature of cyst formation has recently been attributed to innate in

153 Recently, processes underlying cyst formation have been extensively characterized at th

154 involved the determination of lesion growth, cyst formation, homing of GFP(+)/Tie2(+) EPCs, numbers o

155 Lesion growth, cyst formation, homing of green fluorescent protein(+)/T

156 structure or motility resulted in pronephric cyst formation, hydrocephalus and left-right asymmetry d

157 rphological defects and complete ablation of cyst formation in a mouse model.

158 The disease is characterized by progressive cyst formation in a variety of organs including the kidn

159 nvestigate the role of cell proliferation in cyst formation in ADPKD and to explore further the role

160 Cyst formation in ADPKD results from numerous cellular d

161 n is both necessary and sufficient for renal cyst formation in ADPKD, suggesting that PKD2 occurs by

162 genesis may be an early initiating event for cyst formation in ADPKD.

163 that mitochondrial abnormalities facilitate cyst formation in ADPKD.

164 Acute kidney injury induced cyst formation in adult Kif3a mutant mice.

165 constitutes a 'third hit' resulting in rapid cyst formation in adulthood.

166 ration in human ADPKD cells and blocks renal cyst formation in an adult and a neonatal PKD mouse mode

167 , blocking Wnt signaling with DKK1 decreased cyst formation in an organ culture model of ADPKD.

168 D] gene) in cholangiocyte cilia; (2) biliary cyst formation in an orthologous rat model, PCK; and (3)

169 ct, the specific tubular segment involved in cyst formation in ARPKD.

170 y accepted genetic mechanism for progressive cyst formation in autosomal dominant polycystic kidney d

171 oposed to explain the focal nature for renal cyst formation in autosomal dominant polycystic kidney d

172 he PKD1 or PKD2 gene, which leads to massive cyst formation in both kidneys.

173 t in a competition assay, and reduced tissue cyst formation in chronically infected mice.

174 Moreover, kidney cyst formation in ciliary mutants was blocked by the Tor

175 o suppress growth and apoptosis and leads to cyst formation in cultured renal epithelial cells.

176 eral membrane and reestablished single-lumen cyst formation in GFP-FIP2(S227E)-expressing cells in th

177 ontrol and disruption of its function causes cyst formation in human autosomal dominant polycystic ki

178 ommon human genetic disease characterized by cyst formation in kidney tubules and other ductular epit

179 a genetic disorder that is characterized by cyst formation in kidney tubules.

180 may be used as a surrogate marker for kidney cyst formation in large-scale high-throughput screens in

181 e-specific organelle that is associated with cyst formation in many insects and is likely to play an

182 structural defects in cardiac septation and cyst formation in maturing nephrons and pancreatic ducts

183 rb3 and Wwtr1/Taz, have been linked to renal cyst formation in mice before.

184 Cilia dysfunction contributes to renal cyst formation in multiple human syndromes including nep

185 on of Frem2 in adult kidneys correlated with cyst formation in my homozygotes, indicating that the ge

186 Conclusion Fibrosis and cyst formation in patients with IPF seem to start at the

187 ciliary dysfunction occurs or is relevant to cyst formation in PKD.

188 Disruption of this complex contributes to cyst formation in PKD.

189 Further analysis verified that TSA inhibited cyst formation in pkd2 knockdown animals.

190 that if a two-hit mechanism is required for cyst formation in PKD2 there is a high rate of somatic m

191 eatment with TSA, an HDAC inhibitor, reduced cyst formation in Pkd2(-/-) mouse embryos.

192 rmalities in gene expression associated with cyst formation in polycystic kidney disease, differentia

193 ts in this signaling pathway as the basis of cyst formation in polycystic kidney disease.

194 ferentiation and associates with accelerated cyst formation in polycystic kidney disease.

195 of Pkd1 and Sirt1 demonstrated delayed renal cyst formation in postnatal mouse kidneys compared with

196 edicted by a simple additive effect based on cyst formation in singly heterozygous mice.

197 Exogenous galectin-3 reduced cyst formation in suspension culture, and mice-null muta

198 pression of the long form of TgBCP1 restored cyst formation in the 38C3 mutant.

199 idney function and a substantial decrease in cyst formation in the collecting ducts.

200 on, we were able to elucidate the process of cyst formation in the developing ovary of the vertebrate

201 olycystic kidney disease is characterized by cyst formation in the kidney and other organs and result

202 pressed in cilia, linking this organelle and cyst formation in the kidney, but involvement of cilia i

203 l to an understanding of the pathogenesis of cyst formation in the liver in isolated PCLD and in ADPK

204 ical abnormalities, including curly tail and cyst formation in the pronephric kidney, caused by down-

205 stitutive absence of Nedd9 strongly promotes cyst formation in the tamoxifen-inducible Pkd1fl/fl;Cre/

206 ted by the genetic interaction and synergist cyst formation in the zebrafish pronephros model.

207 ented cell division is not a prerequisite to cyst formation in these kidneys.

208 Extensive renal cyst formation in these mice is accompanied by broadly e

209 We investigated the mechanisms of cyst formation in these two distinct processes by combin

210 26 treatment had no effect on progression of cyst formation in this model at doses sufficient to redu

211 n at P5 caused localised hypomyelination and cyst formation in this region, although cortical grey ma

212 ester activin ligands, effectively inhibited cyst formation in three distinct mouse models of PKD.

213 Prompted by kidney cyst formation in tuberous sclerosis complex (TSC) patie

214 n this work, we demonstrate the induction of cyst formation in vitro when trophozoites are starved fo

215 Cyst formation in vivo for the BAG1-complemented H7 para

216 TNF-alpha also stimulated cyst formation in vivo in Pkd2(+/-) mice.

217 whether CFTR activity is required for renal cyst formation in vivo.

218 ssion of the human PC1 tail results in renal cyst formation in zebrafish embryos.

219 in the kidney of transgenic mice results in cysts formation in distal nephron structures consistent

220 This syndrome, in addition to renal cyst formation, includes the presence of an invariably a

221 fied in a number of diseases associated with cyst formation, including autosomal dominant and recessi

222 The timing of cyst formation indicates that full-length polycystin is

223 ruption of the AP2IX-9 gene increased tissue cyst formation, indicating AP2IX-9 operates as a repress

224 ey disease (ADPKD) is characterized by renal cyst formation, inflammation, and fibrosis.

225 In polycystic liver diseases, cyst formation involves cholangiocyte hyperproliferation

226 re and manifesting the most rapid and severe cyst formation involving the glomerulus, tubule and duct

227 Temporary cyst formation is a well-known physiological response of

228 In zebrafish, kidney cyst formation is closely associated with laterality def

229 ysts indicating that the process of germline cyst formation is conserved in the mouse.

230 ided for the concept that the probability of cyst formation is determined by functional PKD protein l

231 CNS peritumoral cyst formation is initiated by increased tumor vascular

232 ther polarity is established during or after cyst formation is not clear.

233 hich cilia loss was induced, suggesting that cyst formation is not simply caused by impaired mechanos

234 rexpression of polycystin-1 is necessary for cyst formation is still unclear.

235 ng from primary ciliary dysfunction to renal cyst formation is unknown.

236 Although encystation (or cyst formation) is an important step of the life cycle o

237 Although encystation (cyst formation) is important for the survival of Giardia

238 interface, signal intensity of graft marrow, cyst formation, joint effusion, articular cartilage defe

239 nockout of polycystin-1 caused massive renal cyst formation, kidney enlargement, and severe kidney fa

240 ased renal hypertrophy and accelerated renal cyst formation, leading to renal dysfunction.

241 Because the primary cilium suppresses renal cyst formation, loss of the cilium may be an initiating

242 he importance of the primary cilium in renal cyst formation may guide potential therapy for cystic ki

243 ng skeletal fusome components prevent proper cyst formation, mutations in the bag-of-marbles gene dis

244 otentially governing sexual reproduction and cyst formation, novel promoter elements, and a microRNA

245 ins that are required in germ-line cells for cyst formation, nurse cell chromosome structure and egg

246 reased interstitial pressure) and subsequent cyst formation occur.

247 nib had strong inhibitory effects on biliary cyst formation of PCK rats.

248 Embryonic kidney cyst formation of Sclt1-/- mice was effectively reduced

249 polycystic kidney disease may contribute to cyst formation or expansion.

250 s gene product(s) into ring canals following cyst formation, polarized microtubule networks do not fo

251 Although the mechanisms of cyst formation remain incompletely defined for all DCLDs

252 atory periapical lesions and with periapical cyst formation represents an interesting but poorly unde

253 ce and locations of the cysts suggested that cyst formation required increased rates of cell prolifer

254 Cyst formation requires the somatic inactivation of the

255 tin-1 also serves to sensitize the kidney to cyst formation resulting from mutations in Pkhd1, the re

256 ft-right asymmetry and for preventing kidney cyst formation; seahorse transcript is highly enriched i

257 lls and suggest a possible mechanism for the cyst formation seen in ADPKD2.

258 Furthermore, aneurysm formation and cyst formation share a common cellular and molecular pat

259 njury can also markedly accelerate the renal cyst formation that occurs after disruption of cilia in

260 s described here highlight the importance of cyst formation to the subsequent development of function

261 onents can dramatically increase or decrease cyst formation, unveiling a critical role for microenvir

262 Germline cyst formation via incomplete cytokinesis (IC) is necess

263 activation effect on cell proliferation and cyst formation was assessed in cholangiocytes derived fr

264 ugh the degree of cartilage damage and joint cyst formation was comparable between the groups, the de

265 een largely based on postnatal specimens, PT cyst formation was hypothesized to be a characteristic f

266 raflagellar transport protein (IFT) mutants, cyst formation was not associated with cilia defects and

267 Cyst formation was rescued in CD73(-/-) astrocytes suppl

268 contribution of the PDE1A subfamily to renal cyst formation, we examined the expression and function

269 erstand the molecular mechanisms involved in cyst formation, we have cloned the swt mutation and find

270 irectly part of the disease pathway of renal cyst formation, we used a genetic approach to introduce

271 mline heterozygous Pkd1 mutation facilitated cyst formation when a somatic Pkd1 mutation was induced.

272 VEGF resulted in extensive angiogenesis and cyst formation when delivered in the ovary.

273 ronal loss and demyelination, with prominent cyst formation, which is generally absent in mouse SCI.

274 ssive liver enlargement results from massive cyst formation while liver parenchymal volume remains un