ライフサイエンスコーパス: sarcolemmal

1 and activates PKD that remains predominantly sarcolemmal.

2 In contrast, there are sub-sarcolemmal accumulations of vesicles in dysferlin-null

3 CO(3)(-) cotransporter (NBC) is an important sarcolemmal acid extruder in cardiac muscle.

4 ular buffering capacity, and the activity of sarcolemmal acid-extrusion proteins, Na+-H+ exchange (NH

5 ysiology themes have emerged: defects in (i) sarcolemmal and intracellular membrane remodelling and e

6 ), beta2-AR, and mu-opioid receptors in both sarcolemmal and intracellular membranes, whereas M2-mACh

7 GPCR, G-proteins, and AC with Cav-3 in both sarcolemmal and intracellular T-tubule-associated region

8 v-3 co-localized with AC5/6 and Galpha(s) in sarcolemmal and intracellular vesicles, the latter close

9 The opening of sarcolemmal and mitochondrial ATP-sensitive K(+) (KATP)

10 Evidence exists for an involvement of both sarcolemmal and mitochondrial K(ATP) channels in such pr

11 the most important pathways responsible for sarcolemmal and mitochondrial sodium movements.

12 immunolabeled with fluorescent antibodies to sarcolemmal and myofibrillar markers, and examined with

13 ROS production occurs in the sarcolemmal and t-tubule membranes where NOX2 is located

14 dynamic structures, present both at surface-sarcolemmal and transverse-tubular membranes.

15 uscle pathology compatible with targeting of sarcolemmal aquaporin-4 (AQP4) by complement-activating

16 y did not restore sarcolemmal nNOS (although sarcolemmal aquaporin-4 was restored).

17 Caveolae occupied around 50% of the sarcolemmal area predominantly assembled into multilobed

18 ed nNOSmu at similar levels does not lead to sarcolemmal association and fails to improve muscle func

19 ctin-4, and microtubules and is required for sarcolemmal association of these proteins as well as dys

20 Increased sarcolemmal ATP-sensitive K(+) (K(ATP)) channel subunit

21 bunit of metabolic-sensing, cardioprotective sarcolemmal ATP-sensitive K(+) (K(ATP)) channels.

22 tion is tightly coupled to the activation of sarcolemmal ATP-sensitive K(+) channels, hastening actio

23 tion triggered by oxidative stress activates sarcolemmal ATP-sensitive K(+) currents to form a metabo

24 bolites of arachidonic acid (AA), are potent sarcolemmal ATP-sensitive K+ (KATP) channel activators.

25 Twenty years after the discovery of sarcolemmal ATP-sensitive K+ channels and 12 years after

26 oding the Kir6.2 pore-forming subunit of the sarcolemmal ATP-sensitive potassium (K(ATP)) channel, pr

27 gen species (ROS), coupled to the opening of sarcolemmal ATP-sensitive potassium (K(ATP)) channels, c

28 ed in mice lacking the Kir6.2 subunit of the sarcolemmal ATP-sensitive potassium (sK(ATP)) channel af

29 ABSTRACT: Sarcolemmal ATP-sensitive potassium channel (KATP channe

30 Sarcolemmal ATP-sensitive potassium channels (K(ATP)) ac

31 Sarcolemmal ATP-sensitive potassium channels (KATP chann

32 tional sequelae, including redistribution of sarcolemmal beta(2)-adrenergic receptors (beta(2)AR) and

33 excitation-contraction coupling between the sarcolemmal Ca(2+) channels and mutated RyR2(R4496C+/-)

34 stolic sarcoplasmic reticulum Ca(2+) leak or sarcolemmal Ca(2+) entry may raise local [Ca(2+)]Cleft a

35 [Ca(2+)] ([Ca(2+)](rest)), increased resting sarcolemmal Ca(2+) entry, and decreased sarcoplasmic ret

36 pecific activation of A(1)AR by CCPA induced sarcolemmal Ca(2+) entry.

37 rcoplasmic reticulum Ca(2+) leak rather than sarcolemmal Ca(2+) flux.

38 Measurements were made of trans-sarcolemmal Ca(2+) fluxes and intracellular [Ca(2+)](i)

39 reactive oxygen species (ROS) production and sarcolemmal Ca(2+) influx are early indicators of diseas

40 In addition, we demonstrate that basal sarcolemmal Ca(2+) influx is also governed by RyR1 expre

41 id), evoked a [Ca(2+)]i rise, independent of sarcolemmal Ca(2+) influx or release from mitochondria,

42 Store-operated Ca(2+) entry (SOCE) through sarcolemmal Ca(2+) selective Orai1 channels in complex w

43 (2+) leak causes an enlarged basal influx of sarcolemmal Ca(2+) that results in chronically elevated

44 nd the remaining increase was blocked by the sarcolemmal Ca2+ ATPase inhibitor carboxyeosin.

45 y membrane voltage (through its influence on sarcolemmal Ca2+ currents) and, therefore, by all ionic

46 Trans-sarcolemmal Ca2+ entries were measured fluorometrically

47 ced positive inotropic effect via inhibiting sarcolemmal Ca2+ influx and the subsequent increase in i

48 a+-Ca2+ exchanger (NCX1) is one of the major sarcolemmal Ca2+ transporters of cardiomyocytes.

49 The sodium-calcium exchanger and sarcolemmal calcium ATPase had a lower activity and the

50 r was responsible for a larger proportion of sarcolemmal calcium extrusion in smaller cells compared

51 ated cellular calcium loads due to a reduced sarcolemmal calcium extrusion reserve.

52 of the sarcoplasmic reticulum and decreased sarcolemmal calcium permeability at rest and after SOCE

53 There is increasing evidence placing the sarcolemmal calcium pump, or plasma membrane calcium/cal

54 hysiology by demonstrating that nonselective sarcolemmal cation channel activity plays a critical rol

55 Nonspecific sarcolemmal cation channels are critical for the pathoge

56 SR Ca(2+) indicator), IP(3) activated 15 pS sarcolemmal cation channels, generated a whole-cell cati

57 With time, the number of surface-sarcolemmal caveolae decreases in isolated cardiomyocyte

58 After cell isolation, the number of surface-sarcolemmal caveolae decreases significantly within a ti

59 The presence and distribution of surface-sarcolemmal caveolae in freshly isolated cells matches t

60 gests that membrane incorporation of surface-sarcolemmal caveolae underlies this, but internalization

61 rom hypoxia-induced cell death and increased sarcolemmal caveolae.

62 Sarcolemmal CD36 facilitates myocardial fatty acid (FA)

63 Thus, sarcolemmal CD36 has a key role in muscle fuel selection

64 d entry into muscle occurs via a regulatable sarcolemmal CD36-mediated mechanism.

65 ClC-1 is the dominant sarcolemmal chloride channel and plays an important role

66 myotonic discharges coupled with deficit in sarcolemmal chloride channels, required regulators of hy

67 indings are consistent with the reduction of sarcolemmal chloride conductance that occurs upon acidif

68 generation, apoptosis, inflammation, loss of sarcolemmal complexes, sarcolemmal disruption, and ultra

69 myotendinous junctions, suggesting a role at sarcolemmal contacts with extracellular matrix.

70 Concomitantly, the sarcolemmal content of the glucose transporter, GLUT4, i

71 novel pathways by which RyR2 channels engage sarcolemmal currents to produce life-threatening arrhyth

72 ot undermined by RRNYRRNY-related opening of sarcolemmal Cx43 channels.

73 lysis reveals the complex interdependence of sarcolemmal, cytoplasmic, and mitochondrial processes th

74 of the dystroglycan complex (DCG) within the sarcolemmal cytoskeleton.

75 Notably, ERRgamma did not restore sarcolemmal DAG complex, which is thus dispensable for a

76 phy-associated Caveolin-3 mutant both led to sarcolemmal damage but only in response to vigorous musc

77 Repair of skeletal muscle after sarcolemmal damage involves dysferlin and dysferlin-inte

78 n-deficient muscles, significantly preceding sarcolemmal damage that becomes evident at 7 dpf.

79 AAV vector is not only capable of restoring sarcolemmal DAP complexes, but can also ameliorate dystr

80 is unlikely associated with the stability of sarcolemmal DGC and integrin complexes.

81 avage-resistant dystrophin had a decrease in sarcolemmal disruption and cardiac virus titer following

82 ngth annexin A6 to the site of laser-induced sarcolemmal disruption compared to Dysf(129) myofibers,

83 inflammation, loss of sarcolemmal complexes, sarcolemmal disruption, and ultrastructural changes char

84 tight electrical coupling between different sarcolemmal domains is guaranteed only within an intact

85 trol mouse muscle, desmin is enriched at the sarcolemmal domains that lie over nearby Z lines and tha

86 pletion of ankyrin-B and resulted in loss of sarcolemmal dystrophin, dystroglycan, and microtubules.

87 ation status of dystroglycan from within the sarcolemmal dystrophin-glycoprotein complex.

88 g the balance of Ca2+ fluxes away from trans-sarcolemmal efflux toward SR accumulation.

89 ubular (t)-system of skeletal muscle couples sarcolemmal electrical excitation with contraction deep

90 Ischemia is known to inhibit the function of sarcolemmal enzymes, including the (Na+ + K+)-ATPase, bu

91 This injected biglycan restores the sarcolemmal expression of alpha-dystrobrevin-1 and -2, a

92 e using an AAV vector, resulting in specific sarcolemmal expression of micro-dystrophin in >50% of my

93 These genes encode sarcolemmal, extracellular matrix, sarcomeric, and nucle

94 During ischemia, there was a 32% decrease in sarcolemmal FAT/CD36 accompanied by a 95% decrease in fa

95 Following reperfusion, decreased sarcolemmal FAT/CD36 persisted, but fatty acid oxidation

96 ing the dystrophin-glycoprotein complex, and sarcolemmal FKRP immunofluorescence mirrors that of dyst

97 valence of Kir6.2 and SUR2 was higher in the sarcolemmal fractions of females (Kir6.2: F, 1.24 +/- 0.

98 addition, these mutant mice displayed marked sarcolemmal fragility and reduced muscle exercise tolera

99 Moreover, contraction-induced increases in sarcolemmal GLUT4 content and glucose uptake were lower

100 Elevated sarcolemmal GLUT4 persisted during reperfusion; in contr

101 ncrease abundance of alpha-DG and associated sarcolemmal glycoproteins, increase utrophin usage, and

102 k cortical actin filaments with a complex of sarcolemmal glycoproteins, yet localize to different sub

103 sistent with increased abundance of multiple sarcolemmal glycoproteins.

104 s cell-to-cell H(+) movement, while allowing sarcolemmal H(+) transporters such as Na(+)/H(+) exchang

105 er mechanisms to lower heart rate, including sarcolemmal hyperpolarization-activated current (I f) an

106 ese group of diseases is defective repair of sarcolemmal injuries, which normally requires Ca(2+) sen

107 size and repair of myofibers following focal sarcolemmal injury and lengthening contraction injury.

108 y cells other than cardiomyocytes can induce sarcolemmal injury during MI.

109 le for dysferlin in Ca2+-dependent repair of sarcolemmal injury through a process of vesicle fusion.

110 atively affects cardiac myocytes by inducing sarcolemmal injury, generating reactive aldehydes, formi

111 o and in vivo and reduced Cfb expression and sarcolemmal injury.

112 This leads to sarcolemmal instability and Ca(2+) influx, inducing cell

113 VPA-treated mice also had increased sarcolemmal integrity and decreased damage, decreased CD

114 Loss of dystrophin results in reduced sarcolemmal integrity and increased susceptibility to mu

115 tary, but nonredundant, roles in maintaining sarcolemmal integrity and protecting skeletal muscle fib

116 sal lamina contributes to the maintenance of sarcolemmal integrity and protects muscles from damage.

117 nges were not associated with alterations in sarcolemmal integrity as measured by muscle fiber uptake

118 taining with Evans blue dye revealed loss of sarcolemmal integrity in both lines of mice, similar to

119 Reduced sarcolemmal integrity in dystrophin-deficient muscles of

120 Compromised sarcolemmal integrity is directly shown in Large(myd) mu

121 an intact DGC is not a precondition for EOM sarcolemmal integrity, and active adaptation at the leve

122 duced serum creatine kinase levels, improved sarcolemmal integrity, fewer centralized myonuclei, incr

123 esponding deleted sarcoglycan gene preserved sarcolemmal integrity, prevented pathological dystrophy

124 h the extracellular matrix (ECM) to preserve sarcolemmal integrity.

125 ellular matrix in muscle that helps maintain sarcolemmal integrity.

126 cantly reduced cardiac fibrosis and improved sarcolemmal integrity.

127 dystrophin at costameres, and maintenance of sarcolemmal integrity.

128 At the cell level, a complex network of sarcolemmal invaginations, called the transverse-axial t

129 elopathy caused by dysfunction of one of two sarcolemmal ion channels, either the sodium channel Nav1

130 ory is associated with altered expression of sarcolemmal ion channels, the biophysical mechanisms res

131 Among the panoply of sarcolemmal ionic currents investigated (I(Na)(+)/I(CaL)

132 repolarization via LOX-1-mediated alteration sarcolemmal ionic currents.

133 Recently, the involvement of sarcolemmal K(ATP) (sarcK(ATP)) channels in ischemic and

134 in Tr5HD and Sed5HD, respectively); however, sarcolemmal K(ATP) blockade completely eradicated the tr

135 SSC is dependent upon the sarcolemmal K(ATP) channel (sarcK(ATP)), and protein kin

136 e is directly physically associated with the sarcolemmal K(ATP) channel by interacting with the Kir6.

137 ignificant increases in both subunits of the sarcolemmal K(ATP) channel following training.

138 BCC9) subunits are essential elements of the sarcolemmal K(ATP) channel in cardiac ventricular myocyt

139 Although the sarcolemmal K(ATP) channel is a multiprotein complex com

140 by 5HD; (2) pharmacological blockade of the sarcolemmal K(ATP) channel nullified the cardioprotectiv

141 nclude that M-LDH is an integral part of the sarcolemmal K(ATP) channel protein complex in vivo, wher

142 subjected to pharmacological blockade of the sarcolemmal K(ATP) channel with HMR 1098 (SedHMR and TrH

143 rise entirely from reduced expression of the sarcolemmal K(ATP) channel, but we also discuss the poss

144 time RT-PCR has demonstrated that of all six sarcolemmal K(ATP) channel-forming proteins, SUR2A was p

145 Classically, cardiac sarcolemmal K(ATP) channels are thought to be composed o

146 We demonstrate that cardiac sarcolemmal K(ATP) channels directly associate with anky

147 The role of sarcolemmal K(ATP) channels in Tr-induced protection was

148 the SUR2A subunit could change the number of sarcolemmal K(ATP) channels only if the Kir6.2 is in exc

149 An increased number of sarcolemmal K(ATP) channels seems to protect the heart b

150 riction in the wild-type and in mice lacking sarcolemmal K(ATP) channels through Kir6.2 pore knockout

151 se training; and (3) increased expression of sarcolemmal K(ATP) channels was observed following chron

152 t demonstrate gender-specific differences in sarcolemmal K(ATP) channels, we have hypothesized that t

153 limiting factor in generating fully composed sarcolemmal K(ATP) channels.

154 vels is sufficient to increase the number of sarcolemmal K(ATP) channels.

155 ue at least in part to increase in levels of sarcolemmal K(ATP) channels.

156 s an increased protein expression of cardiac sarcolemmal K(ATP) channels.

157 This suggests differential sarcolemmal K(ATP) composition in atria and ventricles,

158 and electrical excitability mediated by the sarcolemmal K(ATP) current (I(K,ATP)).

159 residues 1294-1358, the A-fragment, reduced sarcolemmal K(ATP) currents by over 85% after 2 days (pi

160 g mechanism responsible for NO modulation of sarcolemmal KATP (sarcKATP) channels in ventricular card

161 ntal protocol, suggested that the opening of sarcolemmal KATP channels at the beginning of sustained

162 lamp experiments that revealed activation of sarcolemmal KATP channels by preconditioning.

163 sed contracting rabbit hearts to assess when sarcolemmal KATP channels were activated during physiolo

164 ediated by the activation and trafficking of sarcolemmal KATP channels.

165 getics were tightly coupled to activation of sarcolemmal KATP currents, causing oscillations in actio

166 target of beta-adrenergic stimulation is the sarcolemmal L-type Ca(2+) channel, CaV1.2, which plays a

167 Inducible transgenic mice with enhanced sarcolemmal L-type Ca2+ channel (LTCC) activity showed p

168 EET-induced Ca2+ sparks activated nearby sarcolemmal large-conductance Ca2+-activated K+ (BKCa) c

169 ents that revealed a significantly increased sarcolemmal lateral stiffness.

170 +) release units (CaRUs) in which individual sarcolemmal LCCs interact in a stochastic manner with ne

171 mplex and the alpha7beta1 integrin are trans-sarcolemmal linkage systems that connect and transduce c

172 evidence for an ankyrin-based mechanism for sarcolemmal localization of dystrophin and beta-DG.

173 Ankyrin-B thus is an adaptor required for sarcolemmal localization of dystrophin, as well as dynac

174 mutation reduces ankyrin binding and impairs sarcolemmal localization of dystrophin-Dp71.

175 Sarcolemmal localization of gamma-SG was achieved regard

176 In the present study, we hypothesized that sarcolemmal localization of nNOS is a critical determina

177 direct role in regulating the expression and sarcolemmal localization of the intracellular signaling

178 R10-12 showed both cytosolic and sarcolemmal localization.

179 Aside from the benefits of sarcolemmal-localized NO production, NOS-M also increase

180 n skeletal muscle, where it is important for sarcolemmal maintenance.

181 Duchenne muscular dystrophy (DMD) induces sarcolemmal mechanical instability and rupture, hyperact

182 nels therefore defines whether junctional or sarcolemmal mechanisms are selected locally for the remo

183 ed to the effect that preconditioning has on sarcolemmal membrane action potential as revealed by di-

184 the couplon where L-type Ca channels in the sarcolemmal membrane adjoin ryanodine receptors in the s

185 ne or angiotensinII causes GRK5 to leave the sarcolemmal membrane and accumulate in the nucleus, whil

186 , which is associated with disruption of the sarcolemmal membrane and cleavage of dystrophin with pro

187 ifier locus on chromosome 11 associated with sarcolemmal membrane damage and heart mass.

188 MD-like zebrafish, but failed to reverse the sarcolemmal membrane damage.

189 main protein that functions to stabilize the sarcolemmal membrane during muscle contraction.

190 suggest that ANO5 plays an important role in sarcolemmal membrane dynamics.

191 We conclude that the presence of a sarcolemmal membrane either at the cell periphery or in

192 (PDE-5)-hydrolyzable cGMP undetected at the sarcolemmal membrane in contrast to cGMP stimulated by n

193 roglycan were highly overexpressed along the sarcolemmal membrane in most DG/mdx muscles.

194 of muscular dystrophy arise from compromised sarcolemmal membrane integrity, a therapeutic approach t

195 in modulating the confinement of VDCC within sarcolemmal membrane nanodomains in response to varying

196 ation, the cytokeratins are disrupted at the sarcolemmal membrane of skeletal muscle of the mdx mouse

197 -GSK-3beta to regulate mitochondrial but not sarcolemmal membrane potential.

198 background significantly increased myofiber sarcolemmal membrane stability with greater expression a

199 ate that isoflurane modifies cardiac myocyte sarcolemmal membrane structure and composition and that

200 ociated proteins (DAPs) is reduced along the sarcolemmal membrane, but the same proteins remain conce

201 y associated with intracellular vesicles and sarcolemmal membrane.

202 nced vesicle trafficking to and budding from sarcolemmal membrane.

203 line and M-line domains at costameres at the sarcolemmal membrane.

204 etween activation of IP(3)R and RyR near the sarcolemmal membrane.

205 Adenylyl cyclase activity was blunted in sarcolemmal membranes after stretch, demonstrating beta-

206 d progressive changes in tubuloreticular and sarcolemmal membranes and mislocalized triads and mitoch

207 r were compared with muscarinic receptors in sarcolemmal membranes for the effect of guanosine 5'-[be

208 lgi apparatus, clathrin-coated vesicles, and sarcolemmal membranes were excluded from the caveolin-ri

209 s decreasing membrane excitability, injuring sarcolemmal membranes, altering calcium homeostasis due

210 ure results in mistargeting of the kinase to sarcolemmal membranes, causing severe excitation-contrac

211 With tetramers and receptors in sarcolemmal membranes, GMP-PNP effected a vertical, upwa

212 with abnormalities of intercalated discs and sarcolemmal membranes.

213 cts at tetramers in vesicles or receptors in sarcolemmal membranes.

214 Recovery of sarcolemmal microstructure correlated with functional be

215 d microtubules and also is required to align sarcolemmal microtubules with costameres.

216 se in area, diameter, and circularity of sub-sarcolemmal mitochondria, indicative of swelling.

217 rdiac myocytes is slow with respect to trans-sarcolemmal Na transport rates, although the mechanisms

218 n of enhanced IICR and increased activity of sarcolemmal Na(+)-Ca(2+) exchange depolarizing the cell

219 Inhibiting sarcolemmal Na(+)-H(+) exchange with 1 mM amiloride had

220 ty, in part through an effect on the cardiac sarcolemmal Na(+)/Ca(2+) exchanger (NCX), but little is

221 Sarcolemmal Na(+)/H(+) exchanger (NHE) activity is media

222 inical work indicates that inhibition of the sarcolemmal Na(+)/H(+) exchanger (NHE) affords significa

223 otein-coupled receptor stimulation increases sarcolemmal Na(+)/H(+) exchanger (NHE1) activity in card

224 The sarcolemmal Na+-Ca2+ exchanger (NCX) is the main Ca2+ ex

225 The cardiac sarcolemmal Na+-Ca2+ exchanger (NCX1) influences cardiac

226 entry is balanced by efflux mediated by the sarcolemmal Na+-Ca2+ exchanger.

227 ne-induced Ca2+ transient, implying impaired sarcolemmal Na+/Ca2+ exchanger function.

228 Sarcolemmal Na/Ca exchange (NCX) regulates cardiac Ca an

229 e have observed a profound activation of the sarcolemmal Na/K ATPase during cardiac ischemia, which i

230 ggest nonselective ion channel transport via sarcolemmal nanopores as a triggering mechanism.

231 e-induced inactivity correlates with loss of sarcolemmal neuronal NOS localization in mdx muscle, whe

232 -mediated phosphorylation at Ser648 inhibits sarcolemmal NHE activity during intracellular acidosis,

233 naptic nNOS but surprisingly did not restore sarcolemmal nNOS (although sarcolemmal aquaporin-4 was r

234 recapitulates the vasoregulatory actions of sarcolemmal nNOS in BMD patients, and constitutes a puta

235 chenne muscular dystrophy (DMD), the loss of sarcolemmal nNOS leads to functional ischemia and muscle

236 Sarcolemmal nNOS staining was decreased in patient biops

237 phin on the membrane does not always restore sarcolemmal nNOS.

238 , both of which are characterized by reduced sarcolemmal nNOS.

239 We have previously shown that sarcolemmal nNOSmu matches the blood supply to the metab

240 ere, we investigated the effect of restoring sarcolemmal nNOSmu on muscle contractile function in mdx

241 When healthy skeletal muscle is exercised, sarcolemmal nNOSmu-derived nitric oxide (NO) attenuates

242 ith SIT or ET, while neither endothelial nor sarcolemmal NOX2 was changed.

243 rmally triggered by Ca(2+) influx across the sarcolemmal or transverse tubule membrane neighboring th

244 ), the respective blockers of mitochondrial, sarcolemmal, or both types of K(ATP) channels prior to S

245 ther aspects of the synaptic and nonsynaptic sarcolemmal organization of EOM fiber types may underlie

246 -/-) muscle fibers showed a striking loss of sarcolemmal organization, aberrant T-tubule structures,

247 inflammatory cell infiltration and increased sarcolemmal permeability.

248 that phospholemman (PLM), a 15-kDa integral sarcolemmal phosphoprotein, inhibits the cardiac Na+/Ca2

249 that phospholemman (PLM), a 15-kDa integral sarcolemmal phosphoprotein, is a novel endogenous protei

250 Phosphorylation of sarcolemmal PKC was reduced by Chel (p-PKC/PKC: control,

251 s entirely PKD-dependent, involving fleeting sarcolemmal PKD translocation (for activation) and very

252 from proteasomal degradation, an increase in sarcolemmal plectin appeared to confer protection on Dag

253 tion potential as revealed by di-8-ANEPPS, a sarcolemmal-potential sensitive dye, and laser confocal

254 These results suggest that sarcolemmal processes are responsible for the reduced sp

255 matory molecules and augmented the levels of sarcolemmal protein beta-dystroglycan and neuronal nitri

256 The sarcolemmal protein phospholemman (PLM) was found associ

257 Dystrophin is a large sub-sarcolemmal protein.

258 postulated that changes in cytoskeletal and sarcolemmal proteins provide a final common pathway for

259 acids in mice to study acute changes in the sarcolemmal proteome in early phase of myofiber injury.

260 We have implemented an improved sarcolemmal proteomics approach together with in vivo la

261 es in cell morphology, impaired formation of sarcolemmal protrusions, and defective cell motility.

262 omyocytes (NRCMs) transduced with GFP showed sarcolemmal, punctate Cx43 expression.

263 rotocols recruit a complex signal cascade of sarcolemmal receptor activation, intracellular enzyme ac

264 Nedd4 protein localized to the sarcolemmal region of muscle fibers.

265 heral muscle and cardiac tissue, with robust sarcolemmal relocalization of the dystrophin-associated

266 ily, glucocorticoid steroid regimen promotes sarcolemmal repair and muscle recovery from injury while

267 Here we examine sarcolemmal repair in live zebrafish embryos by real-tim

268 le pulse of glucocorticoid steroids improved sarcolemmal repair through increased expression of annex

269 e assessed the efficacy of steroid dosing on sarcolemmal repair, muscle function, histopathology, and

270 emma, whereas isoproterenol triggered faster sarcolemmal responses than cytosolic, likely due to rest

271 Sarcolemmal rupture was evident in 10.9% of fibers in LV

272 In adult VCMs, sarcolemmal (sarc) and mitochondrial (mito) ATP-sensitiv

273 and a subset of microtubules disappear from sarcolemmal sites in ankyrin-B-depleted muscle.

274 pattern in which nerves terminate at select sarcolemmal sites often localized to the central region

275 sed to investigate whether inhibition of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1)

276 Inhibition of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1)

277 Activation of the sarcolemmal sodium-hydrogen exchanger isoform-1 (NHE-1)

278 This results in improved sarcolemmal stability and prevents dystrophic pathology

279 uscle pathology, reduced fibrosis, increased sarcolemmal stability, and promoted muscle regeneration

280 ate for the primary defects of DMD restoring sarcolemmal stability.

281 expression improves dystrophic pathology and sarcolemmal stability.

282 d) Ca2+ sparks occurred within 1 microm of a sarcolemmal structure (cell periphery or TATS), and 33 %

283 In summary, abnormalities of sarcolemmal structure in heart failure show plasticity w

284 howed improved contractility and reversal of sarcolemmal structure.

285 es have highlighted various cytoskeletal and sarcolemmal structures in cardiac myocytes as the likely

286 f the t-system and dissociation of RyRs from sarcolemmal structures in lateral cells.

287 Simultaneous measurement of Ca2+ sparks and sarcolemmal structures showed that cells without TATS ha

288 PLM (FXYD1) is the primary sarcolemmal substrate for PKC and PKA in the heart.

289 Phospholemman (PLM), the principal sarcolemmal substrate for protein kinases A and C in the

290 spholemman (PLM), the principal quantitative sarcolemmal substrate for protein kinases A and C in the

291 ndicated that they occupy ~16 and ~5% of the sarcolemmal surface in myofibers and cardiocytes, respec

292 dystrophin deletion constructs, we show that sarcolemmal targeting of nNOS was dependent on the spect

293 e mainly in patients whose mutations disrupt sarcolemmal targeting of nNOSmu, with the vasoconstricto

294 peats 16 and 17 as a novel scaffold for nNOS sarcolemmal targeting.

295 and the adaptor protein alpha-syntrophin for sarcolemmal targeting.

296 and ceramides or suppress muscle PKCepsilon sarcolemmal translocation in db/db mice.

297 nuclear activation of PKD, without preceding sarcolemmal translocation.

298 ATPase activity in sarcolemmal vesicles also showed a lower Km(Na) in PLM-K

299 c myocytes increases the open probability of sarcolemmal voltage-sensitive Ca2+ channels and flux of

300 bution of the annexins and the efficiency of sarcolemmal wound-healing are significantly disrupted in