ライフサイエンスコーパス: sarcolemmal

1 and activates PKD that remains predominantly sarcolemmal.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

30 Sarcolemmal ATP-sensitive potassium channels (KATP chann

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

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

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

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

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

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

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

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

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

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

41 (2+) leak causes an enlarged basal influx of sarcolemmal Ca(2+) that results in chronically elevated

42 tion involves rapid, dynamic augmentation of sarcolemmal Ca(V) 1.2 channel abundance after ISO applic

43 l concept that a pre-synthesized pool of sub-sarcolemmal Ca(V) 1.2 channel-containing vesicles/endoso

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

45 Trans-sarcolemmal Ca2+ entries were measured fluorometrically

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

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

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

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

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

51 uptake which was balanced by enhanced trans-sarcolemmal calcium fluxes (calcium current and sodium/c

52 ssed SR Ca(2+) sequestration, enhanced trans-sarcolemmal calcium fluxes, and AF, establishing a mecha

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

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

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

56 Nonspecific sarcolemmal cation channels are critical for the pathoge

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

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

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

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

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

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

63 Sarcolemmal CD36 facilitates myocardial fatty acid (FA)

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

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

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

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

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

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

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

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

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

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

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

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

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

77 The fibrosis-entrapped cardiomyocytes showed sarcolemmal damage and connexin 43 redistribution/intern

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

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

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

81 e we show that Thbs3 antithetically promotes sarcolemmal destabilization by reducing integrin functio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 er cachexia, including muscle fiber atrophy, sarcolemmal fragility, and impaired muscle regeneration.

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 Increases in sarcolemmal immunolabelling for utrophin and beta-dystro

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

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

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

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

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

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

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

123 dystrophin at costameres, and maintenance of sarcolemmal integrity.

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

125 cantly reduced cardiac fibrosis and improved sarcolemmal integrity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 ents that revealed a significantly increased sarcolemmal lateral stiffness.

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

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

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

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

167 Sarcolemmal localization of gamma-SG was achieved regard

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

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

170 R10-12 showed both cytosolic and sarcolemmal localization.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 y associated with intracellular vesicles and sarcolemmal membrane.

193 nced vesicle trafficking to and budding from sarcolemmal membrane.

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

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

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

197 cilitate stabilization and repair of damaged sarcolemmal membranes following myocardial injury.

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

199 no acid transporter activity were similar in sarcolemmal membranes isolated from control and IUGR hin

200 tivity and Na(+) K(+) -ATPase activity using sarcolemmal membranes isolated from hindlimb muscle of c

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

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

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

204 d as determined by radioligand binding in LV sarcolemmal membranes.

205 with abnormalities of intercalated discs and sarcolemmal membranes.

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

207 Recovery of sarcolemmal microstructure correlated with functional be

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

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

210 (SV2), encoded by the SVIL gene, is a large sarcolemmal myosin II- and F-actin-binding protein.

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

212 We speculate that reduced muscle sarcolemmal Na(+) K(+) -ATPase activity and lower ATP co

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 Sarcolemmal nNOS staining was decreased in patient biops

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

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

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

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

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

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

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

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

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

239 inflammatory cell infiltration and increased sarcolemmal permeability.

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

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

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

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

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

245 data, we suggest a new model in which a sub-sarcolemmal pool of pre-synthesized Ca(V) 1.2 channels r

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

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

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

249 The sarcolemmal protein phospholemman (PLM) was found associ

250 Dystrophin is a large sub-sarcolemmal protein.

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

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

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

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

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

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

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

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

259 bodies from these same serum samples rescues sarcolemmal repair capacity.

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

261 ve transfer mouse model of IIM, we show that sarcolemmal repair is significantly compromised in dista

262 A compromised sarcolemmal repair process could promote an aberrant exp

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

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

265 ted levels of TRIM72 autoantibodies suppress sarcolemmal resealing in healthy skeletal muscle, and de

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

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

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

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

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

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

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

273 This results in improved sarcolemmal stability and prevents dystrophic pathology

274 ct striated muscle from disease by enhancing sarcolemmal stability through increased integrin and dys

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

276 predisposing effects of Thbs3 by augmenting sarcolemmal stability.

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

278 expression improves dystrophic pathology and sarcolemmal stability.

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

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

281 howed improved contractility and reversal of sarcolemmal structure.

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

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

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

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

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

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

288 hese proteins is nonuniform between the bulk sarcolemmal surface and membrane invaginations known as

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

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

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

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

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

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

295 nuclear activation of PKD, without preceding sarcolemmal translocation.

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

297 The sarcolemmal voltage gated sodium channel Na(V)1.4 conduc

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

299 tein complex, leading to contraction-induced sarcolemmal weakening, muscle tearing, fibrotic infiltra

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