ライフサイエンスコーパス: caveolae

1 tein found in plasma membrane invaginations (caveolae).

2 s were associated with enhanced formation of caveolae.

3 t bulk membrane proteins are depleted within caveolae.

4 ow these lipids contribute to the biology of caveolae.

5 ponent of cell membrane invaginations called caveolae.

6 ith cells in which cavin1 is associated with caveolae.

7 as signaling modules following release from caveolae.

8 living cells to assess the consequences for caveolae.

9 lin-1 (Cav-1), the key structural protein of caveolae.

10 ively concentrated in human and rodent tumor caveolae.

11 e which comprised sarcoplasmic reticulum and caveolae.

12 ifunctional protein and a major component of caveolae.

13 ce, indicating major importance of adipocyte caveolae.

14 olin to form membrane invaginations known as caveolae.

15 ming individual striations on the surface of caveolae.

16 ell as EHD2 and pacsin 2, are all present in caveolae.

17 o contain invaginated protein domains called caveolae.

18 lates the activity of signaling molecules in caveolae.

19 subcellular location including targeting to caveolae.

20 ormation and for maintaining the function of caveolae.

21 naling molecules in specialized areas called caveolae.

22 e size of cavin complexes, and acts to shape caveolae.

23 this induced budding and internalization of caveolae.

24 y: fenestrae, transendothelial channels, and caveolae.

25 integral membrane protein of plasma membrane caveolae.

26 carrying the c.474delA mutation form typical caveolae.

27 pendent on caveolin-1, the main component of caveolae.

28 human diseases are associated with a lack of caveolae.

29 ated caveolin-1 restored the ability to form caveolae.

30 rrying the c.474delA mutation formed typical caveolae.

31 w that EHD1, EHD2, and EHD4 are recruited to caveolae.

32 omology Domain (EHD) proteins at the neck of caveolae.

33 ated caveolin-1 restored the ability to form caveolae.

34 caveolin3 and cavin1 are sufficient to form caveolae.

35 endently of its contribution to cell surface caveolae.

36 plexes, followed by recruitment of eNOS from caveolae.

37 ular and muscle cells is partly dependent on caveolae [13-15].

38 ysates; (2) beta1 is detected in a subset of caveolae; (3) loss of Cav3 caused reduction of beta1D in

39 (CAV1), which encodes a membrane protein of caveolae abundant in the endothelium and other cells of

40 Caveolae accumulate in dystrophic muscle fibers and cave

41 enriched with cholesterol and sphingolipids, caveolae also contain a variety of fatty acids.

42 n with the membrane in both mature mammalian caveolae and a model prokaryotic system for caveola biog

43 The unique fatty acid compositions of caveolae and acylation of caveolin-1 may be important fo

44 lated EGFR via dysfunctional plasma membrane caveolae and alteration of caveolin homo-oligomerization

45 Although mild osmotic stress deforms caveolae and alters interactions between the caveolae an

46 different types of ion channels localize in caveolae and are regulated by the level of membrane chol

47 els might be attributed to partitioning into caveolae and association with caveolin-1 (Cav-1).

48 uated hypoxia-induced TRPC6 translocation to caveolae and Ca(2+) mobilization.

49 study aimed to evaluate our hypothesis that caveolae and Cav-3 are essential for AS-1-induced cardio

50 S-1 attenuates myocardial I/R injury through caveolae and Cav-3 dependent mechanism.

51 after myocardial I/R and modulated membrane caveolae and Cav-3 expression in the myocardium.

52 ed numbers and intracellular localization of caveolae and caveolar structural proteins CAV-1 and Cavi

53 The loss of caveolae and caveolin was in accordance with the decreas

54 is study, we investigated the fatty acids in caveolae and caveolin-1 bound fatty acids.

55 TIE2 was found in caveolae and directly phosphorylated caveolin-1 at Tyr14

56 her, these results indicate that the loss of caveolae and HCN channels in ICCs-DM is important in the

57 veolin-1 (CAV1) is an essential component of caveolae and is implicated in numerous physiological pro

58 receptor within the confined surface area of caveolae and its subsequent phosphorylation in the absen

59 independently showed only few couplings with caveolae and little evidence for caveolar shapes on the

60 veolin-1 (Cav-1) ablation results in loss of caveolae and microvascular pathologies, but the role of

61 here that the apposition of plasma membrane caveolae and mitochondria (first noted in electron micro

62 ected by a cell-associated complex involving caveolae and other membrane proteins that results in end

63 hese lipids in the stability and mobility of caveolae and points the way for future work to understan

64 alent in size and caveolin density to native caveolae and reveals a possible polyhedral arrangement o

65 Yet, the functions of caveolae and the molecular mechanisms critical for shapi

66 However, the fatty acid compositions of caveolae and the type of acylation of caveolar proteins

67 caveolae and alters interactions between the caveolae and these proteins, the general structure and t

68 Conversely, the number of endothelial caveolae and transcytosis rate increase as early as 6 hr

69 d increase in H2O2 levels in the cytosol and caveolae, and a smaller increase in mitochondria.

70 grin chains localize to the plasma membrane, caveolae, and ADP-ribosylation factor-6+ (Arf6+) endocyt

71 The cavin proteins are key components of caveolae, and are expressed at varied amounts in differe

72 nternalization in the absence of clathrin or caveolae, and facilitates LDLR degradation by shuttling

73 orrespondingly, CLN3-null cells have reduced caveolae, and impaired caveolae- and MDR1-related functi

74 (Cav1) is a required structural component of caveolae, and its phosphorylation by Src is associated w

75 Membrane-raft microdomains, such as caveolae, and their constituent caveolins, modulate rece

76 nsport and that solute uptake occurs in both caveolae- and clathrin-coated vesicles.

77 ll cells have reduced caveolae, and impaired caveolae- and MDR1-related functions including endocytos

78 lar dodecahedron as structural basis for the caveolae architecture.

79 Caveolae are 50- to 80-nm membrane invaginations lined b

80 Caveolae are abundant flask-shaped invaginations of plas

81 Caveolae are abundant in endothelial cells and are thoug

82 Caveolae are abundant surface organelles implicated in a

83 Caveolae are an abundant feature of the plasma membrane

84 imaging, that endocytosis and trafficking of caveolae are associated with a Cav1 Tyr-14 phosphorylati

85 V1/2 genes that encode signature proteins of caveolae are associated with glaucoma, the second leadin

86 Caveolae are cholesterol and sphingolipids rich subcellu

87 ected to prolonged cycles of stretch forces, caveolae are destabilized and the plasma membrane is pro

88 Thus, caveolae are dynamic structures, present both at surface

89 ts for cav1, cav3, and cavin1b, we show that caveolae are essential for notochord integrity.

90 Because caveolae are found in most mammalian cells, the mechanis

91 Our data reveal that endothelial caveolae are heterogeneous, and identify cavin 2 as a de

92 The protein components that form the bulb of caveolae are increasingly well characterized, but less i

93 Furthermore, we show that caveolae are indeed likely to bud directly from the plas

94 Caveolae are invaginated plasma membrane domains involve

95 Although caveolae are likely to account for only a small proporti

96 Caveolae are lipid raft domains composed of caveolin (th

97 Caveolae are lipid raft specializations that contain an

98 Caveolae are membrane invaginations that can sequester v

99 se studies indicate that Cav-1 and/or intact caveolae are not required for cholesterol sensitivity of

100 accessory protein levels are reduced, fewer caveolae are observed, and CAV1 complexes exhibit bioche

101 Caveolae are plasma membrane structures formed from a co

102 Although caveolae are present infrequently in healthy kidneys, th

103 Caveolae are protein-dense plasma membrane domains struc

104 is reduced Ca(2+) response is also seen when caveolae are reduced by treatment with siRNA(Cav1) or by

105 Caveolae are signal transduction centers, yet their subc

106 Caveolae are small membrane invaginations important for

107 Caveolae are specialized microdomains on membranes that

108 Caveolae are strikingly abundant in endothelial cells, y

109 smotic challenge, suggesting the function of caveolae as membrane reservoir is compromised.

110 ral membrane protein, is a building block of caveolae as well as a regulator of a number of physiolog

111 e mechanisms by which these mutations impact caveolae assembly and contribute to disease remain uncle

112 frameshift mutation in CAV1, P158PfsX22, on caveolae assembly and function.

113 disease-associated mutations in CAV1 impair caveolae assembly.

114 adipocytokine and insulin signalling, ER-and caveolae associated activities and altered glycerolipid

115 characterized mouse and zebrafish models of caveolae-associated muscle disease.

116 show an unexpected increase the mobility of caveolae-associated proteins.

117 assembly with genomic ribonucleoproteins and caveolae-associated vesicles prior to re-insertion into

118 integrate proteomic and imaging analyses of caveolae at the blood-tumor interface to discover an act

119 2 is specifically and stably associated with caveolae at the plasma membrane and not involved in clat

120 olin-1 (CAV1) is the defining constituent of caveolae at the plasma membrane of many mammalian cells.

121 indicate that in addition to its function in caveolae biogenesis, Cavin-2 plays a critical role in en

122 bling cellular processes such as assembly of caveolae, budding of enveloped viruses, and sorting of l

123 ) have been implicated in the maintenance of caveolae, but direct evidence that these lipids are requ

124 t signaling is thought to be mediated within caveolae by a complex consisting of Na,K-ATPase, caveoli

125 In contrast, disruption of caveolae by MCD treatment or Cav-3 knockdown abolished t

126 Changes in membrane tension can flatten the caveolae, causing the release of the cavin coat and its

127 -beta-cyclodextrin) or genetic disruption of caveolae (Cav-1 knockout mice) abolished coronary FMD, w

128 he scaffolding protein and main component of caveolae, caveolin 1 (cav1), which was present in each e

129 In cells that lack caveolins and caveolae, cavin1 is cytosolic and rapidly degraded as co

130 in vitro work has shown that plasma membrane caveolae constitute a membrane reservoir that can buffer

131 Caveolae contain a variety of signaling proteins which p

132 Caveolae contained a special set of fatty acids, highly

133 With time, the number of surface-sarcolemmal caveolae decreases in isolated cardiomyocytes.

134 isolation, the number of surface-sarcolemmal caveolae decreases significantly within a time frame rel

135 ons and demonstrate reciprocal regulation of caveolae density and fat cell lipid droplet storage.

136 docytosis and LPS signaling, implicating the caveolae-dependent pathway(s) in both processes.

137 signaling utilizes isolated cells, and since caveolae-dependent pathways matter for a wide range of o

138 Given that much of the research into cardiac caveolae-dependent signaling utilizes isolated cells, an

139 ion and TLR4 agonists act preferentially via caveolae-derived endosomes.

140 have sought to determine whether endothelial caveolae disassemble under increased hemodynamic forces,

141 EHD2 by protein degradation, coincident with caveolae disassembly.

142 While caveolae do not affect cAMP signals mediated by muOR, th

143 Our data suggest that the geometry of caveolae domains gives rise to a confined diffusion of i

144 FRAP studies show that caveolae domains increase the immobile fraction of recep

145 Galpha(q) promotes localization of B(2)R to caveolae domains.

146 Mice and humans lacking caveolae due to gene knock-out or inactivating mutations

147 se fibroblasts failed to induce formation of caveolae due to retention of the mutated protein in the

148 membrane-bound state is crucial to restrict caveolae dynamics in cells.

149 avin/caveolin interplay regulating adipocyte caveolae dynamics.

150 Our previous studies have shown that caveolae enhance calcium signals generated through the G

151 storage of energy as fat are among the most caveolae-enriched cell types.

152 lesions, we confirm the presence of LOX-1 in caveolae-enriched lipid rafts and demonstrate that lovas

153 The molecular mechanisms whereby caveolae exert control over cellular signaling have to d

154 sphotyrosine residues, promoting swelling of caveolae, followed by their release from the plasma memb

155 Caveolin-3 facilitates both caveolae formation and a range of cell signaling pathway

156 R-retention signal that inhibits ER exit and caveolae formation and accelerates CAV1 turnover in Cav1

157 -1 (Cav-1) gene inactivation interferes with caveolae formation and causes a range of cardiovascular

158 lability in vivo, thereby demonstrating that caveolae formation and downstream signaling events occur

159 acylation of caveolin-1 may be important for caveolae formation and for maintaining the function of c

160 This study was designed to separate caveolae formation from its downstream signaling effects

161 more, PLVAP knockdown prevented VEGF-induced caveolae formation in retinal explants but did not rescu

162 e 132 to leucine) has deleterious effects on caveolae formation in vivo and has been implicated in va

163 tumor exhibiting hypoxic signature triggers caveolae formation that bypasses the requirement for lig

164 The effect of VEGF on caveolae formation was studied in human retinal explants

165 iously been shown to play a critical role in caveolae formation.

166 CAV1, the principal coat protein of caveolae, has been associated with the regulation of cel

167 he muscle specific caveolin3 (Cav-3) and the caveolae have been found to be critical for cardioprotec

168 w quantitative studies on the deformation of caveolae have been reported.

169 Caveolae have been shown to provide mechanical strength

170 Caveolae have long been implicated in endocytosis.

171 ver, the in vivo mechano-protective roles of caveolae have only begun to be explored.

172 r constituent scaffolding protein of cardiac caveolae, have been associated with skeletal muscle dise

173 er increased hemodynamic forces, and whether caveolae help prevent acute rupture of the plasma membra

174 Intravital microscopy of caveolae-immunotargeted fluorophores even at low intrave

175 issue expansion underpinning the key role of caveolae in adipocyte regulation.

176 parently identical to that of humans lacking caveolae in all tissues.

177 V1 and Cavin-1, another molecular marker for caveolae in both cell phenotypes.

178 Consistent with this physiological role of caveolae in counterpoising membrane tensions, syndapin I

179 By exploiting the higher expression of caveolae in endothelial cells in comparison with epithel

180 In vivo, we demonstrate that caveolae in endothelial cells of the lung and cardiac mu

181 al cells, yet the physiological functions of caveolae in endothelium and other tissues remain incompl

182 ence and distribution of surface-sarcolemmal caveolae in freshly isolated cells matches that of intac

183 as no effect on the abundance of endothelial caveolae in heart and other tissues.

184 isolation and relate this to the presence of caveolae in intact tissue.

185 letion of cavin 2 causes loss of endothelial caveolae in lung and adipose tissue, but has no effect o

186 Approximate calculations show that caveolae in muscle tissue have the strength to handle th

187 r structural component, and by acute loss of caveolae in response to increased osmotic pressure.

188 e-dimensional reconstruction and analysis of caveolae in situ.

189 Cav-1 deficiency results in loss of caveolae in the Schlemm's canal (SC) and trabecular mesh

190 Cavin 3 is not required for making caveolae in the tissues examined.

191 rated a specific AnnA1 antibody that targets caveolae in the tumor endothelium.

192 his work reveals a novel structural role for caveolae in vertebrates and provides unique insights int

193 hat is specifically localized to endothelial caveolae in vivo and compared its effects to non-caveola

194 its initial uptake is clathrin dependent and caveolae independent.

195 The caveolae-independent rDNA transcriptional role of PTRF n

196 rofiles were revealed in tomograms of native caveolae inside cells.

197 lasses of proteins work together to generate caveolae: integral membrane proteins termed caveolins an

198 Caveolae integrity in the presence of Cav-1-F92A was mea

199 Caveolae interact with pro-inflammatory cytokines and ar

200 rst molecular components that act to cluster caveolae into a membrane ultrastructure with the potenti

201 cells: (1) the characteristic clustering of caveolae into higher-order assemblies is absent; and (2)

202 Caveolae introduce flask-shaped convolutions into the pl

203 constitutes a third structural component of caveolae involved in controlling the stability and turno

204 The generation of caveolae involves insertion of the cholesterol-binding i

205 hat mechanoprotection through disassembly of caveolae is important for endothelial function in vivo.

206 Dysfunction of caveolae is involved in human muscle disease, although t

207 find that around 5% of the cellular pool of caveolae is present on dynamic endosomes, and is deliver

208 The level of FRET between B(2)R and caveolae is reduced by downregulation of Galpha(q) or by

209 Caveolin-1 (Cav-1), a major component of caveolae, is a known Src phosphorylation target, and bot

210 EHD2, which has been previously detected at caveolae, is absent.

211 Cav-1, the principal structural component of caveolae, is overexpressed in the cancers noted above th

212 growth involves the isotropic flattening of caveolae (known for their mechanical buffering role) ass

213 or 1 and 2 that accentuates the formation of caveolae, leading to increased dimerization of EGF recep

214 Both clathrin- and caveolae/lipid raft-mediated endocytosis pathways are in

215 e that LXRbeta has nonnuclear function in EC caveolae/lipid rafts that entails crosstalk with ERalpha

216 d functionally coupled in EC plasma membrane caveolae/lipid rafts.

217 Here, we quantify caveolae located within 100 nm of the outer cell surface

218 te which contained a variety of fatty acids, caveolae mainly contained three types of fatty acids, 0.

219 To test the hypothesis that SOD delivery to caveolae may specifically inhibit this pathological path

220 tic pathways: clathrin-mediated endocytosis, caveolae-mediated endocytosis, and clathrin-independent

221 ion by Src is associated with an increase in caveolae-mediated endocytosis.

222 the skeletal muscle cells by an energy- and caveolae-mediated endocytosis.

223 g to internalization of NPs via clathrin and caveolae-mediated endocytosis.

224 sis while decreasing those for clathrin- and caveolae-mediated endocytosis.

225 th alveolar Type I cells, and dose-dependent caveolae-mediated in vitro uptake by lung cancer cells.

226 on of filamentous actin, focal adhesions and caveolae-mediated membrane trafficking, resulting in imp

227 by active transport and that inhibiting the caveolae-mediated pathway significantly reduced cellular

228 ly internalize these nanoparticles using the caveolae-mediated pathway.

229 and endocytosis via a lipid-raft-dependent, caveolae-mediated pathway.

230 lipid composition specifically inhibits the caveolae-mediated transcytotic route readily used in the

231 uces endocytosis of injured membrane through caveolae, membrane invaginations from lipid rafts.

232 oted in electron micrographs >50 yr ago) and caveolae-mitochondria interaction regulates adaptation t

233 report that cavin-1, a structural protein of caveolae, modulates the oncogenic function of caveolin-1

234 hours postinvasion, replaced by distinctive caveolae nanostructures.

235 act heart illustrate the regular presence of caveolae not only at the surface sarcolemma, but also on

236 caveolae, whereas exogenous ONOO(-) reduced caveolae number.

237 Caveolae occupied around 50% of the sarcolemmal area pre

238 2Y2R interaction with Cav-1 in membrane-raft caveolae of 1321N1 cells modulates receptor coupling to

239 inuous population with the caveolin-1 in the caveolae of cells under isotonic culture.

240 ified by real-time fluorescence imaging, and caveolae of endothelial cells were isolated and probed f

241 acid backbone exhibit specific affinity for caveolae of endothelial cells.

242 es of PTX are not dependent upon endothelial caveolae or endothelial nitric oxide synthase.

243 Our data establish that caveolae participate in a unique cell response connected

244 However, how caveolae participate in fat cell functions is poorly und

245 e to plasma membrane rupture indicating that caveolae play a role in mechanoprotection.

246 We have therefore explored the role caveolae play in modulating Ras signaling.

247 nduced the dispersion of caveolin-1 from the caveolae, possibly through flattened caveolar intermedia

248 crog stearic acid and 0.83 microg oleic acid/caveolae preparation/5 x 10(7) cells.

249 We hypothesized that the high density of caveolae present in vacuolated cells [5, 6] could buffer

250 Loss of caveolae produces lipodystrophic diabetes in humans, whi

251 in accord with the idea that the presence of caveolae prolongs Galpha(q) activation.

252 We localize caveolae proteins to human and murine conventional drain

253 uscle pathology associated with mutations in caveolae proteins.

254 rategy reveals a unique target, antibody and caveolae pumping system for solid tumor penetration.

255 Finally, we describe the caveolae pumping system, a promising active transport al

256 Because caveolae regulate endothelial function and vascular perm

257 ndapin III KO mice show severe reductions of caveolae reminiscent of human caveolinopathies.

258 Thus, we postulate that caveolae remotely regulate Ras nanoclustering and signal

259 conventional drainage tissues and show that caveolae respond to mechanical stimulation.

260 Caveolae respond to membrane stress by releasing cavins

261 oportion of total endocytosis, cells lacking caveolae show fundamentally altered patterns of membrane

262 ne-binding protein and critical organizer of caveolae (small microdomains in the plasma membrane), as

263 olin-1 is an essential structural protein of caveolae, specialized plasma membrane organelles highly

264 Caveolae, specific lipid rafts which concentrate caveoli

265 t caveolin, the main structural component of caveolae, specifically binds Galphaq and stabilizes its

266 her the mechanisms and relationships between caveolae structure and intracellular signaling.

267 his study shows that mutant Cav-1-F92A forms caveolae structures similar to WT but leads to increases

268 a(2+) transients were eliminated by either a caveolae-targeted LTCC antagonist or disrupting caveolae

269 hypertrophic signaling, which was reliant on caveolae targeting of TRPCs.

270 primary structural component of endothelial caveolae that is essential for transcellular trafficking

271 mbrane curvature and drives the formation of caveolae that participate in many crucial cell functions

272 flask-shaped membrane invaginations known as caveolae that participate in signaling, clathrin-indepen

273 the cavin-3 linkage reduces the abundance of caveolae, thereby separating this ERK activation module

274 Release of cavin1 from caveolae thus leads to exposure of key lysine residues i

275 Increasing the number of caveolae to enhance the function of HCN channels may rep

276 esults connect the mechanical deformation of caveolae to Galphaq-mediated Ca(2+) signals.

277 This deformation eliminates the ability of caveolae to stabilize calcium signals mediated through G

278 2) is a dynamin-related ATPase that confines caveolae to the cell surface by restricting the scission

279 ates signal transduction to ERK by anchoring caveolae to the membrane skeleton of the plasma membrane

280 ll lines and in mice to raise the density of caveolae, to increase adipocyte ability to accommodate l

281 Similarly, caveolae transduce mechanical stress into PM lipid alter

282 embrane incorporation of surface-sarcolemmal caveolae underlies this, but internalization and/or micr

283 lines, to assay the subcellular dynamics of caveolae using tagged proteins expressed at endogenous l

284 ding to Caveolin-1, the main coat protein of caveolae, using a highly specific peptide, CavNOxin.

285 d periphery, which underlie a suppression of caveolae vesicle formation and trafficking in brain endo

286 ish a unique lipid environment that inhibits caveolae vesicle formation in CNS endothelial cells to s

287 g to marked accumulation of intraendothelial caveolae vesicles.

288 golipid-enriched plasma membrane microdomain caveolae were also observed.

289 Caveolae were detected in the basolateral membranes of p

290 Caveolae were isolated from Chinese hamster ovary (CHO)

291 ma membrane capacitance, and in fixed cells, caveolae were quantified by transmission electron micros

292 exhibited a decreased number of endothelial caveolae, whereas exogenous ONOO(-) reduced caveolae num

293 one is dynamin-dependent and likely involves caveolae, whereas the other is dynamin- and small GTPase

294 major component of the coating structure of caveolae, which can serve as a lipid binding adaptor pro

295 selectively targets and disrupts endothelial caveolae, which contributes to NOS uncoupling, and, henc

296 of specialized membrane microdomains called caveolae, which functions in both membrane protein turno

297 es with the function of coronary endothelial caveolae, which plays an important role in nitric oxide

298 veolin-1 (Cav1) is an essential component of caveolae whose Src kinase-dependent phosphorylation on t

299 eolae-targeted LTCC antagonist or disrupting caveolae with methyl-beta-cyclodextrin, with an associat

300 half reversibly changes the configuration of caveolae without releasing a significant portion of cave