ライフサイエンスコーパス: caveolae

1 ow these lipids contribute to the biology of caveolae.

2 living cells to assess the consequences for caveolae.

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

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

5 human diseases are associated with a lack of caveolae.

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

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

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

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

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

11 caveolin3 and cavin1 are sufficient to form caveolae.

12 endently of its contribution to cell surface caveolae.

13 in the central nervous system, have abundant caveolae.

14 plexes, followed by recruitment of eNOS from caveolae.

15 s were associated with enhanced formation of caveolae.

16 t bulk membrane proteins are depleted within caveolae.

17 ponent of cell membrane invaginations called caveolae.

18 ith cells in which cavin1 is associated with caveolae.

19 as signaling modules following release from caveolae.

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

21 ively concentrated in human and rodent tumor caveolae.

22 e which comprised sarcoplasmic reticulum and caveolae.

23 ifunctional protein and a major component of caveolae.

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

25 an accumulation of clathrin-coated pits and caveolae.

26 e, is highly concentrated in plasma membrane caveolae.

27 scription in cells with diminished levels of caveolae.

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

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

30 Caveolae act in mechanoprotection by flattening in respo

31 Caveolae activate RhoA-ROCK1/PKN2 signaling via the RhoA

32 tion, the acute dissociation of cavin-1 from caveolae allows cell membrane expansion that occurs upon

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

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

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

36 mentalization of Nox isoforms in lipid rafts/caveolae and assessed the role of these microdomains in

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

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

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

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

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

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

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

44 Ablation of both caveolae and eNOS completely abolished neurovascular cou

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

46 EphB1/Cav-1 interaction in the biogenesis of caveolae and in coordinating the signaling function of C

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

48 Cavin-1 dissociation from caveolae and membrane flattening alters the cytoskeleton

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

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

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

52 ed feedback regulation between components of caveolae and the outputs of the Hippo pathway.

53 his work provides a mechanistic link between caveolae and their ability to sense the PM lipid composi

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

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

56 important step toward a molecular picture of caveolae and vesicular endocytosis.

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

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

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

60 SHR) vessels should have a smaller number of caveolae, and that the caveolae structure should be disr

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

62 r level by increased fatty acid uptake via a caveolae- and CD36-dependent pathway that also involves

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

64 s, highlighting the concurrent activation of caveolae- and clathrin-mediated endocytosis, alongside m

65 lar dodecahedron as structural basis for the caveolae architecture.

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

67 Caveolae are abundant flask-shaped invaginations of plas

68 Caveolae are abundant surface organelles implicated in a

69 Caveolae are an abundant and characteristic surface feat

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

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

72 Caveolae are bulb-shaped invaginations of the plasma mem

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

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

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

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

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

78 Caveolae are invaginated plasma membrane domains involve

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

80 Caveolae are membrane invaginations that can sequester v

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

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

83 Caveolae are plasma membrane invaginations enriched with

84 Caveolae are protein-dense plasma membrane domains struc

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

86 Caveolae are signal transduction centers, yet their subc

87 Caveolae are small membrane invaginations important for

88 Caveolae are strikingly abundant in endothelial cells, y

89 r cholesterol-rich microdomains (lipid rafts/caveolae) are involved in these processes is unclear.

90 These findings support a role for Cav1/caveolae as a central regulator of atherosclerosis that

91 Here, we review evidence for caveolae as a specialized lipid domain and speculate on

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

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

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

95 disease-associated mutations in CAV1 impair caveolae assembly.

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

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

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

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

100 26Q mutations present a dramatic decrease of caveolae at the plasma membrane, resulting in abnormal r

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

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

103 ynamin-related ATPase located at the neck of caveolae, but its physiological function has remained un

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

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

106 gh membrane curvature in specific regions of caveolae can enrich specific lipid species, with consequ

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

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

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

110 ls shows that EphB4 controls the function of caveolae, cell-cell adhesion under mechanical stress and

111 all three lipids accumulated specifically in caveolae, cholesterol and sphingomyelin were actively se

112 r junctions, focal adhesions, primary cilia, caveolae, clathrin-coated pits, and plaques play additio

113 nce imaging revealed localization of EHD2 to caveolae, close to cell surface-associated lipid droplet

114 ippo pathway, are critical for expression of caveolae components and therefore caveolae formation in

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

116 (2020) uncover how caveolae control a PIP(2)-FMNL2 pathway that regulates t

117 Cav1 and the exact mechanisms by which Cav1/caveolae control the pathogenesis of diet-induced athero

118 binding caveolar proteins upon flattening of caveolae could allow release of specific lipids into the

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

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

121 ent relaxation could be related to decreased caveolae density in SHR vessels.

122 uggest that EHD2 controls a cell-autonomous, caveolae-dependent fatty acid uptake pathway and imply t

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

124 rom the central nervous system to SMCs via a caveolae-dependent pathway.

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

126 t and signaling molecule, through lipid raft/caveolae-dependent processes.

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

128 n-beta2 and tubulin-beta3 were necessary for caveolae-dependent TGF-beta receptor internalization.

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

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

131 EHD2 by protein degradation, coincident with caveolae disassembly.

132 Finally, caveolae disruption promotes eNOS uncoupling in normoten

133 Lipid raft/caveolae disruptors (methyl-beta-cyclodextrin (MCD) and

134 ng, distinct patterns of Cav1 expression and caveolae distribution were observed in athero-prone and

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

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

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

138 avin/caveolin interplay regulating adipocyte caveolae dynamics.

139 ne fusion and studied their acute effects on caveolae dynamics.

140 s was dominantly mediated via the lipid raft/caveolae endocytic pathway.

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

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

143 ls contain several nanoscale domains such as caveolae, fenestrations and transendothelial channels, w

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

145 uced trafficking into and out of lipid rafts/caveolae for Nox1 and Nox5 respectively.

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

147 -1 (Cav-1) gene inactivation interferes with caveolae formation and causes a range of cardiovascular

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

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

150 nique role for mTORC2-mediated regulation of caveolae formation in actively migrating cancer cells.

151 ression of caveolae components and therefore caveolae formation in both mammalian cells and zebrafish

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

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

154 biological processes such as endocytosis and caveolae formation, the cell membrane is locally deforme

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

156 Notably, caveolae function in aECs is independent of the endothel

157 propose that specific lipid accumulation in caveolae generates an intrinsically unstable domain pron

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

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

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

161 Caveolae have been shown to provide mechanical strength

162 Caveolae have long been implicated in endocytosis.

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

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

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

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

167 Acute genetic perturbations that eliminated caveolae in aECs, but not in neighbouring SMCs, impaired

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

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

170 -3 (Cav3), a scaffolding protein integral to caveolae in cardiomyocytes, have been associated with th

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

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

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

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

175 d mesenteric arteries and the role played by caveolae in endothelium-dependent relaxation.

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

177 monstrated that absence of caveolin-1 (Cav1)/caveolae in hyperlipidemic mice strongly inhibits athero

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

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

180 aveolin-3 is the major structural protein of caveolae in muscle.

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

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

183 mechanism also underlies the crucial role of caveolae in the long-term healthy expansion of the adipo

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

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

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

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

188 its initial uptake is clathrin dependent and caveolae independent.

189 The caveolae-independent rDNA transcriptional role of PTRF n

190 Instead, we find that the absence of Cav1/caveolae inhibited low-density lipoprotein transport acr

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

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

193 Therefore, we aimed to investigate caveolae integrity and density in SHR aortas and mesente

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

195 CAV1, a key component of caveolae, interacted with strumpellin in cells, and stru

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

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

198 These exosomes were endocytosed through caveolae into primary microglial cells, thereby mounting

199 Caveolae introduce flask-shaped convolutions into the pl

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

201 Additionally, a smaller number of caveolae is associated with hypertension.

202 The uniform shape of caveolae is characterized by a bulb with consistent curv

203 tress the regulation of mechanoprotection by caveolae is directly coupled with the regulation of IL6/

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

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

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

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

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

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

210 We have been able to show the presence of caveolae-like structures in SHR aortas and mesenteric ar

211 We speculate that the caveolae-lipid system has evolved to function as a gener

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

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

214 Consistent with the idea that Cav1/caveolae may play a role in early flow-dependent inflamm

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

216 The resulting cationic conjugate undergoes caveolae-mediated endocytosis and transcytosis, which en

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

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

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

220 lesterol-lowering drug, was used to modulate caveolae-mediated HER2 endocytosis.

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

222 esses such as production of nitric oxide and caveolae-mediated intracellular trafficking.

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

224 bited partial impairment, revealing that the caveolae-mediated pathway in aECs is a major contributor

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

226 They further examine caveolae-mediated tensional dysregulation and its functi

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

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

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

230 hours postinvasion, replaced by distinctive caveolae nanostructures.

231 to scission if not restrained by EHD2 at the caveolae neck.

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

233 o observed that Cav-1 protein expression and caveolae numbers were markedly reduced in ECs from EphB1

234 ss of Cav-1 was responsible for reducing the caveolae numbers.

235 ere greatly reduced and so was the number of caveolae observed in SCs.

236 Caveolae occupied around 50% of the sarcolemmal area pre

237 2Y2R interaction with Cav-1 in membrane-raft caveolae of 1321N1 cells modulates receptor coupling to

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

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

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

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

242 (EHD2) has previously been shown to regulate caveolae, plasma membrane-specific domains that are invo

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

244 s a dynamic molecule whose dissociation from caveolae plays an important role in mechanoprotection an

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

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

247 We localize caveolae proteins to human and murine conventional drain

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

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

250 Because caveolae regulate endothelial function and vascular perm

251 The expression of Cav1 and distribution of caveolae regulated by flow were analyzed by immunofluore

252 ether these Cav3 LQT9 mutations impact other caveolae related ion channels remains unknown.

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

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

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

256 Caveolae respond to membrane stress by releasing cavins

257 Mutations in the caveolae scaffolding protein, caveolin-3 (Cav3), have be

258 eas cholesterol and glycosphingolipids drive caveolae scission from the PM.

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

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

261 Caveolae, small (60-100 nm) bulb-like invaginations of t

262 se factor (PTRF) is a requisite component of caveolae, small plasma membrane invaginations that are h

263 Caveolae, specific lipid rafts which concentrate caveoli

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

265 All these results showed that caveolae structure and integrity are essential for endot

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

267 e a smaller number of caveolae, and that the caveolae structure should be disrupted in these vessels.

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

269 wever, the influence of lipid composition on caveolae surface stability is not well described or unde

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

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

272 e identify an important role for lipid rafts/caveolae that act as signaling platforms for Nox1 and No

273 Caveolins (CAVs) are structural proteins of caveolae that function as signaling platforms to regulat

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

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

276 Caveolae, the cave-like structures abundant in endotheli

277 re fully reversed by reassembling functional caveolae through expression of caveolin-3.

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

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

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

281 These data link caveolae to Hippo signaling in the context of cellular r

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

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

284 We demonstrate that sphingomyelin stabilizes caveolae to the cell surface, whereas cholesterol and gl

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

286 Similarly, caveolae transduce mechanical stress into PM lipid alter

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

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

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

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

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

292 Concomitantly, elevated numbers of detached caveolae were found in brown and white adipose tissue la

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

294 hat Caveolin-1 (Cav-1), a major component of caveolae which regulates cell signaling and endocytosis,

295 ivity by mTORC2 also alters the abundance of caveolae, which are specialized lipid raft invaginations

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

297 ion in 3D matrix and durotaxis controlled by caveolae, which form in response to low membrane tension

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

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