ライフサイエンスコーパス: cyst formation

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

2 promoting Wnt activation and contributing to cyst formation.

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

4 downstream kinetics of renal hypertrophy and cyst formation.

5 Endosome morphology changes prior to cyst formation.

6 al hypertrophic signaling and culminating in cyst formation.

7 ral and functional hypertrophy without renal cyst formation.

8 ene, possibly causing haploinsufficiency and cyst formation.

9 ay explain the epithelial stratification and cyst formation.

10 ctivation of Rac1 is required for epithelial cyst formation.

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

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

13 f centriole migration during female germline cyst formation.

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

15 rapamycin administration effectively blocks cyst formation.

16 sue pathologic features and bony microdamage/cyst formation.

17 mechanism underlying this aspect of germline cyst formation.

18 e the importance of these cells during rapid cyst formation.

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

20 developmental gene expression during tissue cyst formation.

21 ty, suggesting multiple mechanisms exist for cyst formation.

22 monoallelic mutational mechanism that drives cyst formation.

23 the TNF-alpha inhibitor etanercept prevented cyst formation.

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

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

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

27 h abnormal epithelial cell proliferation and cyst formation.

28 lial cells, where mutations in Pkd1 initiate cyst formation.

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

30 amine the pathophysiology of CNS peritumoral cyst formation.

31 ed signaling events, and profoundly inhibits cyst formation.

32 bular differentiation, ultimately leading to cyst formation.

33 the two factors in angiogenesis and possibly cyst formation.

34 a proteins have an established role in renal cyst formation.

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

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

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

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

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

40 even under conditions that normally promote cyst formation.

41 onous divisions of the cystoblast leading to cyst formation.

42 Entamoeba are predominantly expressed during cyst formation.

43 the epithelial proliferation associated with cyst formation.

44 intrafamilial phenotypic variation and focal cyst formation.

45 ycystic kidney disease and may contribute to cyst formation.

46 rmine the pathogenesis of Six2creFrs2alphaKO cyst formation.

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

48 ability under oxidative stress and decreased cyst formation.

49 lium regulates kidney tubule development and cyst formation.

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

51 tion and divert excessive proliferation into cyst formation.

52 s controlling tubular diameter contribute to cyst formation.

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

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

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

56 helial cells from renal tissues and delaying cyst formation.

57 lacking adenosine receptors had no defect in cyst formation.

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

59 Cyst formation, aberrant ductal morphology, and extensiv

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 eveloped for cancer have shown to ameliorate cyst formation and disease progression in animal models

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 n hereditary renal disease, characterized by cyst formation and growth.

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

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

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

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

95 Abnormal cell growth leads to cyst formation and lung damage.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 3p LOH occurs subsequent to VHL mutation and cyst formation, and correlates with malignant progressio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 Loss in the basal compartment inhibits cyst formation, but has the opposite effect in the lumin

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

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

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

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

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

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

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

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

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

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

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

151 Rapid cyst formation can also be induced in conditional adult

152 29 stages of germline cyst formation can be identified in D. melanogaster ooge

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

154 g calcification result and model B recording cyst formation, classified tumor type with areas under t

155 odels, a sharp increase of proliferation and cyst formation correlates with a dramatic loss of orient

156 Cyst formation correlates with inhibition of Pkhd1 expre

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

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

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

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

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

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

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

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

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

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

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

168 es indicate that macrophages are involved in cyst formation, however the specific role and type of ma

169 before postnatal day 12-14 results in rapid cyst formation; however, cyst formation is slower when c

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

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

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

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

174 Cyst formation in ADPKD results from numerous cellular d

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

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

177 that mitochondrial abnormalities facilitate cyst formation in ADPKD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 Cyst formation in Prx1-Cre; Tsc1(f/f) and Osx-Cre; Tsc1(

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 26 treatment had no effect on progression of cyst formation in this model at doses sufficient to redu

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

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

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

229 resident macrophage accumulation, and renal cyst formation in two mouse models of cystic disease.

230 .2 (Deltaeif1.2) markedly impeded bradyzoite cyst formation in vitro and in vivo.

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

232 pharmacological inhibition of NHA2 inhibits cyst formation in vitro.

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

234 mous Hedgehog signaling in regulating kidney cyst formation in vivo in both early- and adult-onset mo

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

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

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

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

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

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

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

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

243 Minor complications included cyst formation, infection, chemosis, pyogenic granuloma,

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

245 In polycystic liver diseases, cyst formation involves cholangiocyte hyperproliferation

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

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

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

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

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

251 CNS peritumoral cyst formation is initiated by increased tumor vascular

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

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

254 14 results in rapid cyst formation; however, cyst formation is slower when cilia dysfunction is induc

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

256 ntifiable components of the living cell post cyst formation is unknown in modern investigations.

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

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

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

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

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

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

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

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

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

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

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

268 reased interstitial pressure) and subsequent cyst formation occur.

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

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

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

272 dia, sporangium formation, zoospore release, cyst formation, or appressorium formation in Ph. infesta

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

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

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

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

277 Cyst formation requires the somatic inactivation of the

278 mitotic cysts to control GSC maintenance and cyst formation, respectively, whereas IGS3 and IGS4 phys

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

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

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

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

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

284 lycystic kidney disease (ADPKD) by promoting cyst formation that, ultimately, culminates in renal fai

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

286 s switch correlates with the period in which cyst formation transitions from rapid to slow following

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

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

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

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

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

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

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

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

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

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

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

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

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

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