ライフサイエンスコーパス: caveolin-3

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

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

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

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

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

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

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

8 eNOS antiserum immunoprecipitated primarily caveolin-3.

9 which shares limited sequence identity with caveolin-3.

10 levels of myosin heavy and light chains and 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 ) hearts, and NOS3 relocalized normally with caveolin-3.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

31 Caveolin-3 and amphiphysin were implicated in their biog

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 Caveolin-3 co-immunoprecipitates with antibodies directe

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

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

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

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

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

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

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

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

110 Caveolin 3 deficiency was also ameliorated by the use of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 3, and co-migration of the beta(2)AR with a caveolin-3-enriched membrane fraction.

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

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

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

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

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

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

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

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

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

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

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

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

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

139 Caveolin-3 facilitates both caveolae formation and a ran

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

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

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

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

144 1C) in humans is due to mutations within the caveolin-3 gene: (i) a 9-base pair microdeletion that re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 Caveolin-3 is the principal structural component of cave

182 Caveolin-3 is the principal structural protein of caveol

183 Caveolin-3 is the principal structural protein of caveol

184 Caveolin-3 is the structural protein component of caveol

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

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

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

188 2C12 cells from myoblasts to myotubes, while caveolin-3 levels are dramatically induced by this proce

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

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

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

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

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

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

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

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

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

198 Caveolin-3 mRNA and protein expression are dramatically

199 3 is most closely related to caveolin-1, but caveolin-3 mRNA is expressed only in muscle tissue types

200 Caveolin-3 mRNA is expressed predominantly in muscle tis

201 Caveolin-3 mRNA levels are dramatically increased during

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 Caveolin-3 protein in myoblasts and myotubes was express

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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