ライフサイエンスコーパス: caveolin-3

1 internalized into caveolae (as identified by caveolin-3).

2 ng functional caveolae through expression of caveolin-3.

3 reased coprecipitation of RhoA and Rac1 with caveolin-3.

4 lular retention and degradation of wild-type caveolin-3.

5 ent of the dystrophin complex interacts with caveolin-3.

6 mbrane is not required for palmitoylation of caveolin-3.

7 act with full-length forms of caveolin-2 and caveolin-3.

8 a third member of the caveolin gene gamily, caveolin-3.

9 eNOS antiserum immunoprecipitated primarily caveolin-3.

10 which shares limited sequence identity with caveolin-3.

11 s regulated by a functional interaction with caveolin-3.

12 ns SAP97 and AKAP79/150 but are deficient in caveolin-3.

13 late sodium current compared with wild-type caveolin-3.

14 levels of myosin heavy and light chains and caveolin-3.

15 ) hearts, and NOS3 relocalized normally with caveolin-3.

16 in glycoprotein complex and normal levels of caveolin-3.

17 Abundance of caveolin-3 (0.59+/-0.08 versus 0.29+/-0.08 arbitrary uni

18 In this study, we characterized the human caveolin-3 5'-flanking region.

19 The experiments showed that cellular caveolin-3, a fraction of cellular ANP-RB, and a fractio

20 We also demonstrate that caveolin-3, a marker of caveolae, is required for the in

21 nts cofractionated on sucrose gradients with caveolin-3, a marker protein for myocyte caveolae.

22 expression; these cells also do not express caveolin-3, a muscle-specific caveolin family member.

23 Caveolin-3, a muscle-specific caveolin-related protein,

24 Caveolin-3, a muscle-specific caveolin-related protein,

25 specialized lipid microdomains that contain caveolin-3, a muscle-specific isoform of the scaffolding

26 Caveolin-3, a muscle-specific member of the caveolin fam

27 d that enhanced expression of RORa increases caveolin-3 abundance and enhances mitophagy.

28 Caveolin-3 abundance positively correlated with L-NMMA a

29 uces co-immunoprecipitation of beta(2)AR and caveolin 3 and co-migration of beta(2)AR and caveolin-3

30 zed signaling module that is associated with caveolin 3 and is essential for sympathetic stimulation

31 FAK regulation of profusion genes, including caveolin 3 and the beta1D integrin subunit, is essential

32 zation (by immunofluorescence microscopy) of caveolin-3 and alpha-tubulin; both Colch and CD decrease

33 Caveolin-3 and amphiphysin were implicated in their biog

34 determined the genomic organization of human caveolin-3 and devised a screening strategy to look for

35 y gradient fractions containing most myocyte caveolin-3 and eNOS.

36 ole for RORa in regulating mitophagy through caveolin-3 and expand our currently limited understandin

37 n rhabdomyosarcoma cell lines do not express caveolin-3 and fail to undergo myoblast fusion.

38 calization of key muscle proteins, including caveolin-3 and Fer1L5, a related ferlin protein homologo

39 th Colch and CD decreased co-localization of caveolin-3 and filamin (an F-actin cross-linking protein

40 nges can be correlated with modifications in caveolin-3 and L-Type Ca(2+) channel distributions acros

41 We isolated the gene for human caveolin-3 and mapped it to chromosome 3p25.

42 d AC6 are expressed in fractions enriched in caveolin-3 and morphologic caveolae.

43 The association between caveolin-3 and NOS3 at the sarcolemma and T tubules was

44 , in canine pacing-induced HF, expression of caveolin-3 and of sarcolemmal caveolae is increased.

45 In AD, augmented expression of caveolin-3 and presenilins in reactive astrocytes may al

46 activated Galpha(q/11) but not Galpha(i3) to caveolin-3 and prevented desensitization of the PLC-beta

47 g oxidative stress via integrated changes in caveolin-3 and stretch-activated channels (SACs).

48 )AR-LTCC regulation requires the presence of caveolin-3 and the activation of the CaMKII pathway.

49 roscopy detected extensive colocalization of caveolin-3 and the major pore-forming subunit of the L-t

50 L-type Ca(2+) channel, were colocalized with caveolin-3 and the ryanodine receptor, and effectively t

51 Coimmunoprecipitations of caveolin-3 and the voltage-gated potassium channel subun

52 d in caveolar fractions, and associated with caveolin-3 and this localization was disrupted by MbetaC

53 ic oxide synthase and reduced the amounts of caveolin-3 and transforming growth factor-beta in myofib

54 igomers of a much larger size than wild type caveolin-3 and were excluded from caveolae-enriched memb

55 immunoprecipitated instead by antibodies to caveolin-3 and, conversely, eNOS antiserum immunoprecipi

56 d the hypothesis that increased abundance of caveolin-3 and/or sarcolemmal caveolae contribute to inc

57 nd important signalling proteins (e.g. nNOS, caveolin-3) and pathways are disrupted.

58 co-immunoprecipitation of the beta(2)AR and caveolin 3, and co-migration of the beta(2)AR with a cav

59 s, a fragmented T-tubule network enriched in Caveolin-3, and an impaired Ca2+ response upon mechanica

60 tissues contain the muscle-specific isoform caveolin-3, and caveolae in endothelial cells contain th

61 lpha(i), protein kinase A RIIalpha subunits, caveolin-3, and flotillins (caveolin functional homologu

62 ynthase (eNOS) associated with cardiomyocyte caveolin-3, and more neuronal NOS (nNOS) translocation t

63 triggered Ca(2+) transients, associated with caveolin-3, and supported beta-adrenergic regulation of

64 ectively repressed by caveolin-1, but not by caveolin-3, and this repression required the caveolin-1

65 ific isoform of the caveolar coating protein caveolin-3, and with a fraction of cellular ANP.

66 ted from the light membrane fractions with a caveolin-3 antibody (but not a control IgG1 antibody), c

67 However, C2C12 cells harboring caveolin-3 antisense fail to undergo myoblast fusion and

68 We show that C2C12 cells harboring caveolin-3 antisense undergo differentiation and express

69 on protein sequence homology; caveolin-1 and caveolin-3 are approximately 65% identical and approxima

70 nNOS and caveolin-3 are coimmunoprecipitated from rat skeletal mu

71 The mechanism by which LGMD-1C mutants of caveolin-3 are degraded remains unknown.

72 n alpha2 chain, all of the sarcoglycans, and caveolin 3) are separated in the lower phase.

73 y, the normal increases in the transcript of caveolin 3 as well as an integrin subunit, the beta1D is

74 Together, these data identify caveolin-3 as a critical component of the signaling mach

75 Taken together, these results propose caveolin-3 as a key player in myoblast fusion and sugges

76 othesis directly by overexpressing wild-type caveolin-3 as a transgene in mice.

77 ly of the expression of either caveolin-1 or caveolin-3 as observed using two different model cell sy

78 asma membrane, Bin1 and caveolae composed of caveolin-3 assemble into ring-like structures from which

79 t three-dimensional structural insights into caveolin-3 assembly, interactions with RyR1 suggest a no

80 Only the caveolin 3-associated Ca(v)1.2 channels are phosphorylat

81 adenylyl cyclase, PKA, and calcineurin to a caveolin 3-associated complex in ventricular myocytes th

82 fashion, causing the retention of wild type caveolin-3 at the level of the Golgi.

83 We found that overexpression of caveolin-3 augmented insulin-stimulated phosphorylation

84 LGMD-1C mutants of caveolin-3 behave in a dominant negative fashion, causin

85 sion, we demonstrate that LGMD-1C mutants of caveolin-3 behave in a dominant-negative fashion, causin

86 ore, recombinant expression of caveolin-1 or caveolin-3, but not caveolin-2, in Cav-1 null cells comp

87 t recognizes the unique N-terminal region of caveolin-3, but not other members of the caveolin gene f

88 ollowed by Western blot analysis showed that caveolin-3, Ca(v)1.2, beta(2)-AR (not beta(1)-AR), G pro

89 beta-dystroglycan, we also demonstrate that caveolin-3 can effectively block the interaction of dyst

90 Our results indicate that overexpression of caveolin-3 causes severe cardiac tissue degeneration, fi

91 h cardiac myocyte-specific overexpression of caveolin-3 (Cav-3 OE) and also used an adenoviral constr

92 Caveolin-3 (Cav-3) is the only caveolin family member ex

93 Caveolae containing scaffolding protein caveolin-3 (Cav-3) localize many ion channels, signaling

94 t cardiac myocyte-specific overexpression of caveolin-3 (Cav-3), a muscle-specific caveolin, would al

95 Caveolin-3 (Cav-3), a muscle-specific caveolin-related g

96 with a reduction in the scaffolding protein caveolin-3 (Cav-3), altered Ca(2+) cycling, increased pr

97 Caveolin-3 (cav-3), an integral membrane protein, is a b

98 Caveolin-3 (Cav-3), the dominant isoform in cardiac myoc

99 However, some LTCCs are housed in caveolin-3 (Cav-3)-enriched signaling microdomains and a

100 Our objective was to determine whether caveolin 3 (Cav3) associates with Kir2.1 and whether LQT

101 Although mutations in caveolin-3 (Cav3) and dysferlin are linked to muscular d

102 stribution of ryanodine receptors (RyRs) and caveolin-3 (CAV3) in mouse ventricular myocytes.

103 the effects of an integral membrane protein, caveolin-3 (Cav3) on hERG expression levels.

104 Mutations in the CAV3 gene encoding caveolin-3 (Cav3), a scaffolding protein integral to cav

105 Caveolin-3 (Cav3), abundantly expressed in muscle cells,

106 tations in the caveolae scaffolding protein, caveolin-3 (Cav3), have been linked to the long QT type

107 rent stabilization of activated Galpha(q) by caveolin-3 (Cav3).

108 resenilins also form a physical complex with caveolin-3, caveolin-3 may provide a common platform for

109 myoblasts as a model system, we observe that caveolin-3 co-fractionates with cytoplasmic signaling mo

110 Caveolin-3 co-immunoprecipitates with antibodies directe

111 Caveolin-3 co-localizes with and affects the expression

112 Our results indicate that caveolin-3 co-localizes, co-fractionates, and co-immunop

113 We show that caveolin-3 co-purifies with dystrophin, and that a fract

114 ients as a high molecular mass complex; (ii) caveolin-3 colocalizes with caveolin-1 by immunofluoresc

115 equent movement of the insulin receptor from caveolin-3-containing domains to flotillin-1-containing

116 However, immunopurified caveolin-3-containing membranes contained no associated

117 a membrane recruitment of activated PFK-M by caveolin-3 could have important implications for underst

118 kinase C resides in caveolae and (along with caveolin-3) could represent a mechanism to target PKC is

119 Caveolin 3 deficiency was also ameliorated by the use of

120 ologous recombination techniques, to mimic a caveolin-3 deficiency.

121 ion in caveolin-3 protein expression, i.e. a caveolin-3 deficiency.

122 nes of mice, similar to that seen in mdx and caveolin-3 deficient mice.

123 LGMD-1C mutants of caveolin-3 (DeltaTFT or P --> L) were primarily retained

124 iently transfected with wild-type and mutant caveolin-3 demonstrated that mutant caveolin-3 results i

125 and cell fractionation studies; and (iii) a caveolin-3-derived polypeptide functionally suppresses t

126 Here, we demonstrate that caveolin-3 directly interacts with beta-dystroglycan, an

127 , we show that a novel WW-like domain within caveolin-3 directly recognizes the extreme C terminus of

128 in non-muscle cells, while the expression of caveolin-3 drives caveolae formation in striated muscle

129 nd more neuronal NOS (nNOS) translocation to caveolin-3 during ischemia/reperfusion.

130 beta3-AR colocalized with caveolin-3, endothelial nitric oxide synthase (NOS) and

131 usion to multinucleated myotubes and lack of caveolin-3 enhances the fusion process.

132 AC activity and cAMP production, eliminated caveolin-3-eNOS interaction, and increased NO production

133 caveolin 3 and co-migration of beta(2)AR and caveolin-3 enriched membranes.

134 3, and co-migration of the beta(2)AR with a caveolin-3-enriched membrane fraction.

135 disrupted the distribution of Na(v)1.5 into caveolin-3-enriched microdomains, and led to redistribut

136 r, because all of these proteins copurify in caveolin-3-enriched vesicles isolated from adult cardiom

137 tein specifically co-immunoprecipitates with caveolin-3 expressed in differentiated skeletal C2C12 my

138 isorganized membrane morphology with reduced caveolin-3 expression at the sarcolemma developed coinci

139 We have shown that lack of caveolin-3 expression in skeletal muscle resembles limb-

140 atients and mdx mice have elevated levels of caveolin-3 expression in their skeletal muscle.

141 Thus, a tight regulation of caveolin-3 expression is fundamental for normal muscle f

142 ogether, these results support the idea that caveolin-3 expression is required for myoblast fusion an

143 show the widest range of expression, whereas caveolin-3 expression is restricted to muscle cell types

144 inhibitors blocks both myotube formation and caveolin-3 expression, but does not affect the expressio

145 cterized by a approximately 95% reduction of caveolin-3 expression.

146 suggest that p38 is an upstream regulator of caveolin-3 expression.

147 ta-AR blockers had no significant effects on caveolin-3 expression.

148 Caveolin-3 facilitates both caveolae formation and a ran

149 ricular myocytes using anti-Ca(v)1.2 or anti-caveolin-3 followed by Western blot analysis showed that

150 Caveolin-3 forms a disc-shaped nonamer that binds the Ca

151 ions within the coding sequence of the human caveolin-3 gene (3p25).

152 is both necessary and sufficient to control caveolin-3 gene transcription.

153 1C) in humans is due to mutations within the caveolin-3 gene: (i) a 9-base pair microdeletion that re

154 t not EP(2)R, in caveolin-rich membranes and caveolin-3 immunoprecipitates, likely explaining the obs

155 R agonist, beta(2)AR were no longer found in caveolin-3 immunoprecipitates; an effect that was blocke

156 We show dramatic upregulation of caveolin-3 immunoreactivity in astroglial cells surround

157 enylyl cyclase 5/6 no longer associates with caveolin 3 in the T-tubules, and noncaveolin 3-associate

158 in D (CD) dramatically reduced the amount of caveolin-3 in buoyant (sucrose density) fractions of adu

159 iptional regulator of the mitophagy mediator caveolin-3 in cardiomyocytes and that enhanced expressio

160 Interestingly, recombinant overexpression of caveolin-3 in cultured cells stimulated beta-secretase-m

161 ules and supported by the structural protein caveolin-3 in muscle.

162 screening strategy to look for mutations in caveolin-3 in patients with muscular dystrophy.

163 Immunolocalization of caveolin-3 in skeletal muscle fibers demonstrates that c

164 emonstrated that overexpression of wild-type caveolin-3 in skeletal muscle fibers is sufficient to in

165 we have demonstrated that overexpression of caveolin-3 in skeletal muscle tissue promotes defects si

166 ve examined whether nNOS also interacts with caveolin-3 in skeletal muscle.

167 Reintroduction of caveolin-3 in the failing myocytes is able to normalize

168 se (NOS) is down-regulated by high levels of caveolin-3 in the heart.

169 laments is associated with downregulation of caveolin-3 in the hypertrophic failing rabbit myocytes.

170 almitoylated to the same extent as wild type caveolin-3, indicating that targeting to the plasma memb

171 preincubation of nNOS with either of the two caveolin-3 inhibitory peptides.

172 choline receptor (nAChR), and that a lack of caveolin-3 inhibits clustering of the nAChR in myotubes.

173 We show that overexpression of caveolin-3 inhibits myoblast fusion to multinucleated my

174 Glutathiolation abolishes caveolin-3 interaction with heterotrimeric G protein alp

175 tudies have suggested that the expression of caveolin 3 is confined to striated (cardiac and skeletal

176 fies with dystrophin, and that a fraction of caveolin-3 is a dystrophin-associated protein.

177 Caveolin-3 is a member of the caveolin family of protein

178 At the molecular level, we demonstrate that caveolin-3 is a novel muscle-specific kinase (MuSK) bind

179 Caveolin-3 is a scaffolding protein, integrating many in

180 Reintroduction of caveolin-3 is able to confine beta2 adrenergic receptor

181 Since caveolin-3 is also endogenously expressed in cardiac myo

182 Expression of caveolin-3 is both necessary and sufficient for cardiac

183 We show that caveolin-3 is expressed at the neuromuscular junction, t

184 in skeletal muscle fibers demonstrates that caveolin-3 is localized to the sarcolemma (muscle cell p

185 independent lines of evidence indicate that caveolin-3 is localized to the sarcolemma, where it asso

186 Caveolin-3 is most closely related to caveolin-1 based o

187 Caveolin-3 is most closely related to caveolin-1, but ca

188 In contrast, the expression of caveolin-3 is muscle-specific.

189 The expression of caveolin-3 is muscle-specific.

190 Caveolin-3 is relatively cysteine-rich compared to caveo

191 In many respects, caveolin-3 is similar to caveolin-1: (i) caveolin-3 migr

192 Aside from the finding that caveolin-3 is specifically expressed in muscle, function

193 hese results indicate that overexpression of caveolin-3 is sufficient to induce severe cardiomyopathy

194 Caveolin-3 is the major structural protein of caveolae i

195 Caveolin-3 is the principal structural component of cave

196 Caveolin-3 is the principal structural protein of caveol

197 Caveolin-3 is the principal structural protein of caveol

198 Caveolin-3 is the structural protein component of caveol

199 es, eNOS associates with the muscle-specific caveolin-3 isoform, but whether this interaction affects

200 By using blockers of PKA and CaMKII and a Caveolin-3-knockout mouse model, we conclude that the be

201 protein and that altered nAChR clustering in caveolin-3-lacking myotubes results from inhibition of a

202 data provide a molecular explanation for why caveolin-3 levels are down-regulated in patients with th

203 2C12 cells from myoblasts to myotubes, while caveolin-3 levels are dramatically induced by this proce

204 owever, it remains unknown whether increased caveolin-3 levels in DMD patients contribute to the path

205 MD1A (myotilin), LGMD1B (lamin A/C), LGMD1C (caveolin-3), LGMD1D (desmin), LGMD1E (DNAJB6), and more

206 In these myotubes, caveolin-3 localizes to the sarcolemma (muscle cell plas

207 lso form a physical complex with caveolin-3, caveolin-3 may provide a common platform for APP and the

208 these results indicate that flotillin-1 and caveolin-3 may regulate muscle energy metabolism through

209 aveolin-3, we hypothesized that mutations in caveolin-3 may represent a novel pathogenetic mechanism

210 co-expressing wild-type and mutant forms of caveolin-3, MG-132 treatment rescued wild-type caveolin-

211 ts, caveolin-3 is similar to caveolin-1: (i) caveolin-3 migrates in velocity gradients as a high mole

212 Interestingly, caveolin-3 moves away from the plasma membrane toward th

213 Caveolin-3 mRNA and protein expression are dramatically

214 3 is most closely related to caveolin-1, but caveolin-3 mRNA is expressed only in muscle tissue types

215 Caveolin-3 mRNA is expressed predominantly in muscle tis

216 Caveolin-3 mRNA levels are dramatically increased during

217 ains by expression of a dominant-interfering caveolin 3 mutant (Cav3/DGV) inhibited the insulin stimu

218 in-1 or expression of a dystrophy-associated Caveolin-3 mutant both led to sarcolemmal damage but onl

219 In the presence of MG-132, LGMD-1C caveolin-3 mutants accumulated within the endoplasmic re

220 In accordance with these observations, caveolin-3 mutants formed oligomers of a much larger siz

221 In addition, these caveolin-3 mutants were expressed at significantly lower

222 However, caveolin-3 mutants were palmitoylated to the same extent

223 Wild type caveolin-3 or caveolin-3 mutants were transiently expressed in NIH 3T3

224 inhibitors, prevented degradation of LGMD-1C caveolin-3 mutants.

225 investigate the phenotypic behavior of these caveolin-3 mutations using heterologous expression.

226 Multiple caveolin-3 nonamers bind to a single RyR1 homotetramer.

227 Here, we created a caveolin-3 null (CAV3 -/-) mouse model, using standard h

228 veolin-3 transgenic cells and upregulated in caveolin-3 null cells.

229 In addition, we have shown that caveolin-3 null mice display mild muscle fiber degenerat

230 nalysis of skeletal muscle tissue from these caveolin-3 null mice reveals: (i) mild myopathic changes

231 Functional studies in caveolin-3 null mice show abnormal neuromuscular junctio

232 reduces insulin-stimulated glucose uptake in caveolin-3 null myotubes by inhibiting both PI3K and Akt

233 strate that microtubules are disorganized in caveolin-3 null myotubes, indicating the importance of t

234 Our results indicate that a caveolin-3 oligomer contains up to 66 palmitates, compar

235 e looked at the effects of overexpression of caveolin-3 on cardiac structure and function by characte

236 Wild type caveolin-3 or caveolin-3 mutants were transiently expres

237 Caveolin-3, or M-caveolin, was identified as a muscle-sp

238 Analysis of skeletal muscle tissue from caveolin-3- overexpressing transgenic mice reveals: (i)

239 tosis, but these defects could be rescued by caveolin-3 overexpression.

240 gy combination score was normal for isolated caveolin-3:p.T78M carriers and of LQT2 type in double he

241 Furthermore, caveolin-3:p.T78M did not exhibit a LQTS phenotype.

242 The caveolin-3:p.T78M mutation was found isolated in 3 famil

243 of a previously described missense mutation, caveolin-3:p.T78M.

244 inding was inhibited in the presence of free caveolin-3 peptides.

245 In addition, we find that caveolin-3 physically interacts and biochemically coloca

246 The multiple roles that caveolin-3 plays in cellular physiology are becoming mor

247 However, it remains unknown what role caveolin-3 plays in myoblast differentiation and myotube

248 presenilins were concomitantly increased in caveolin-3-positive astrocytes.

249 ession, whereas Id2 overexpression inhibited caveolin-3 promoter activation by myogenin.

250 ionally active heterodimers that bind to the caveolin-3 promoter and thereby mediate its transcriptio

251 We show that these mice lack caveolin-3 protein expression and sarcolemmal caveolae m

252 In addition, caveolin-3 protein expression is dramatically induced du

253 ns lead to an approximately 95% reduction in caveolin-3 protein expression, i.e. a caveolin-3 deficie

254 Here, we examine (i) the expression of caveolin-3 protein in muscle tissue types and (ii) its l

255 Caveolin-3 protein in myoblasts and myotubes was express

256 es by Western blot analysis reveals that the caveolin-3 protein is selectively expressed only in hear

257 Caveolin-3 protein is the only member of the caveolin fa

258 ble C2C12 myoblasts that fail to express the caveolin-3 protein.

259 ed that overexpression of myogenin activates caveolin-3 reporter gene expression, whereas Id2 overexp

260 tides corresponding to the membrane-proximal caveolin-3 residues 65-84 and 109-130 and homologous cav

261 d mutant caveolin-3 demonstrated that mutant caveolin-3 results in a 2- to 3-fold increase in late so

262 es with an oligopeptide corresponding to the caveolin-3 scaffolding domain.

263 In developing myotubes, amphiphysin 2 and caveolin-3 segregated in tubular and vesicular portions

264 An antibody against caveolin-3 shows a strong signal at the stratum granulos

265 In fact, we demonstrate that lack of caveolin-3 significantly reduces insulin-stimulated gluc

266 ific caveolin antibodies to reveal prominent caveolin-3 staining in myocyte sarcolemmal membranes and

267 es map to a functionally important domain in caveolin-3, suggesting that these are not benign polymor

268 of cardiomyocytes adenylyl cyclase V/VI and caveolin-3, suggesting their in vivo association.

269 f eNOS and nNOS by the scaffolding domain of caveolin-3 suggests that eNOS in cardiac myocytes and nN

270 lead to formation of unstable aggregates of caveolin-3 that are retained intracellularly and are rap

271 f unstable high molecular mass aggregates of caveolin-3 that are retained within the Golgi complex an

272 identified 4 novel mutations in CAV3-encoded caveolin-3 that were absent in >1000 control alleles.

273 (including ankyrins, yotiao, syntrophin, and caveolin-3) that regulate the activities of key membrane

274 sates and coimmunoprecipitation of erbB4 and caveolin-3, the caveolin isoform expressed in cardiac my

275 Mutations in CAV3, coding for caveolin-3, the major constituent scaffolding protein of

276 Caveolin-3, the most recently recognized member of the c

277 The additional palmitoylation sites in caveolin-3 therefore provide a mechanistic basis by whic

278 Interactions between nNOS and caveolin-3, therefore, appear to be direct and to involv

279 The addition of antibodies against caveolin-3 to the cell's cytoplasm via the pipette solut

280 Determination of caveolin-3 transcript distribution patterns in vivo reve

281 Thus, caveolin-3 transgenic and null mice represent valid mous

282 talized precursor skeletal muscle cells from caveolin-3 transgenic and null mice.

283 we show that M-cadherin is downregulated in caveolin-3 transgenic cells and upregulated in caveolin-

284 sociated glycoproteins are down-regulated in caveolin-3 transgenic heart.

285 We have recently generated caveolin-3 transgenic mice and demonstrated that overexp

286 In addition, these findings suggest that caveolin-3 transgenic mice may represent a valid mouse m

287 The Duchenne-like phenotype of caveolin-3 transgenic mice will provide an important mou

288 iac structure and function by characterizing caveolin-3 transgenic mice.

289 Here, we show that LGMD-1C mutants of caveolin-3 undergo ubiquitination-proteasomal degradatio

290 In striking contrast, caveolin 3 was predominantly expressed in brain astrogli

291 double-labeling experiments, while wild type caveolin-3 was efficiently targeted to the plasma membra

292 ment rescued wild-type caveolin-3; wild-type caveolin-3 was not degraded and reached the plasma membr

293 se inhibitor p21(Cip1/Waf1), caveolin-1, and caveolin-3 was reduced in carotid arteries obtained from

294 of TT-associated proteins junctophilin-2 and caveolin-3 was significantly changed, correlating with n

295 se major component in the striated muscle is caveolin-3, we hypothesized that mutations in caveolin-3

296 or by small interfering RNA directed against caveolin-3, whereas beta(1)-AR stimulation (norepinephri

297 veolin-3, MG-132 treatment rescued wild-type caveolin-3; wild-type caveolin-3 was not degraded and re

298 ments demonstrate that PFK-M associates with caveolin-3 with a significant time lag after the biosynt

299 her demonstrate that the interaction between caveolin-3 with ACV and phosphodiesterase is responsible

300 In this regard, interaction of caveolin-3 with beta-dystroglycan may competitively regu