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1 o the plasma membrane of muscle fiber cells (sarcolemma).
2 onsisting of sheet-like invaginations of the sarcolemma.
3 g ~500-600 nm underneath and parallel to the sarcolemma.
4 red for anchoring neuronal NOS (nNOS) to the sarcolemma.
5 dence of damage to both the myosepta and the sarcolemma.
6 inuous with, but do not directly contact the sarcolemma.
7 of LPI converges to hyperpolarization of the sarcolemma.
8 phin and Galgt2-modified alpha-DG around the sarcolemma.
9 to subpopulations in the T-space and M-space sarcolemma.
10 association of mitochondria with the injured sarcolemma.
11 particularly sheet-like invaginations of the sarcolemma.
12 porter CD36 from intracellular stores to the sarcolemma.
13 Type Ca(2+) channel distributions across the sarcolemma.
14 ric oxide synthase were also restored at the sarcolemma.
15 in cytoskeleton and reduced cortactin at the sarcolemma.
16 tory adhesion complexes at the extrasynaptic sarcolemma.
17 the capacity to autonomously localize to the sarcolemma.
18 stent with altered nAChR localization at the sarcolemma.
19 dystrophin, the DGC is disassembled from the sarcolemma.
20 oglycans were completely eliminated from the sarcolemma.
21 ns and other DAPs can be detected at the mdx sarcolemma.
22 strophin-glycoprotein complex (DGC) from the sarcolemma.
23 showed enhanced formation of caveolae on the sarcolemma.
24 ention at costameres but not delivery to the sarcolemma.
25 es was restricted to regions proximal to the sarcolemma.
26 nous and recombinant FKRP are present at the sarcolemma.
27 reduced conductance of chloride ions in the sarcolemma.
28 duced temporary dystrophin expression at the sarcolemma.
29 hich anchor the contractile apparatus to the sarcolemma.
30 at NCX1 is redistributed away from the outer sarcolemma.
31 kinases A and C in heart and skeletal muscle sarcolemma.
32 orylated by ecto 5'nucleotidase bound to the sarcolemma.
33 calized activation of assembly events at the sarcolemma.
34 axillin, and anchor myofibril Z-bands to the sarcolemma.
35 alpha- and beta1-syntrophin, and nNOS at the sarcolemma.
36 rks that couple peripheral myofibrils to the sarcolemma.
37 ectrin and disrupted the organization of the sarcolemma.
38 ed by alterations in the excitability of the sarcolemma.
39 rated into sarcomeres, with no effect on the sarcolemma.
40 on ICa in the t-tubules than at the surface sarcolemma.
41 ith the increase in KATP channel proteins in sarcolemma.
42 to the organization of both the myoplasm and sarcolemma.
43 and the dystrophin-based cytoskeleton at the sarcolemma.
44 1 isoform and the Na/Ca exchanger in cardiac sarcolemma.
45 /K-ATPase between the t-tubules and external sarcolemma.
46 characterized by the loss of nNOSmu from the sarcolemma.
47 at the protein is exclusively located on the sarcolemma.
48 es is 3-3.5-fold higher than in the external sarcolemma.
49 ucing the level of dystrophin protein at the sarcolemma.
50 ain and CT were exclusively localized at the sarcolemma.
51 tegrin attachment complexes to stabilize the sarcolemma.
52 e was sufficient to establish the DGC at the sarcolemma.
53 specially of lengthened muscle, disrupts the sarcolemma.
54 A6 associated with impaired resealing of the sarcolemma.
55 tein that also targets other proteins to the sarcolemma.
56 ndance of utrophin around the extra-synaptic sarcolemma.
57 sarcomere, the intercalated disc, and at the sarcolemma.
58 of depolarization or Ca(2+) flux across the sarcolemma.
59 vesicle fusion needed for repair of myofiber sarcolemma.
60 zing sarcomeric anchoring structures and the sarcolemma.
61 rin repeat protein 3 (Shank3) complex at the sarcolemma.
62 by confocal imaging after the removal of the sarcolemma.
63 apparatus with mitochondria, nuclei, and the sarcolemma.
64 and Ca(2)(+) selective Orai1 channels in the sarcolemma.
65 ns and neuronal nitric oxide synthase at the sarcolemma.
66 ATPase density; (t), t-system membrane; (s), sarcolemma].
67 ty of beta1-ARs in both surface and T-tubule sarcolemma (55+/-4%, n=7, P<0.001; and 45+/-10%, n=7, P<
69 Smooth muscle responds to IP3-generating (sarcolemma acting) neurotransmitters and hormones by rel
70 ely 45% reduction in Na(V)1.5 protein at the sarcolemma after FGF13 knockdown, whereas no changes in
73 ed by an increased abundance of GLUT4 at the sarcolemma and a lowering of plasma glucose levels, indi
74 g to syntrophin on the inside surface of the sarcolemma and by way of Grb2-Sos1-Rac1-PAK1-JNK ultimat
75 Dystrophin forms an essential link between sarcolemma and cytoskeleton, perturbation of which cause
78 volves fusion of intracellular vesicles with sarcolemma and fusion of the muscle progenitor cells res
79 ma-actin most predominantly localized to the sarcolemma and in a faint reticular lattice within norma
81 glucose transporters translocate between the sarcolemma and intracellular compartments to regulate su
83 trafficking of intracellular vesicles to the sarcolemma and is required for movement of dysferlin to
85 des novel changes in the organization of the sarcolemma and its association with nearby contractile s
86 ks arises from the structural arrangement of sarcolemma and j-SR membrane and thus from the differenc
88 rect monitoring of calcium influx across the sarcolemma and may allow detection of molecular alterati
89 t in mouse alpha-catulin is localized at the sarcolemma and neuromuscular junctions and interacts wit
92 complex with the alpha7beta1 integrin at the sarcolemma and Ptrh2 expression is decreased in alpha7 i
93 delivered rhBGN up-regulates utrophin at the sarcolemma and reduces muscle pathology in the mdx mouse
94 uses detachment of the basal lamina from the sarcolemma and renders muscle prone to contraction-induc
95 Early phase involves healing the injured sarcolemma and restricting the spread of damage to the i
96 ease of [Ca(2+)](i) in the space between the sarcolemma and sarcoplasmic reticulum (SR) and this lead
99 local depletion of GLUT4 storage vesicles at sarcolemma and t-tubules rather than inducing movement o
100 omised, and insulin receptor distribution in sarcolemma and T-tubules was unaffected by denervation o
101 ractions increase GLUT4 translocation to the sarcolemma and t-tubules with similar kinetics and do no
102 rom intracellular vesicle depots to both the sarcolemma and t-tubules with similar kinetics, although
107 ificant increase in the distance between the sarcolemma and the nearest myofibrils, from less than 10
111 re the cell membrane (comprising the surface sarcolemma and transverse-tubules), the intracellular ca
112 a-actin levels were increased 10-fold at the sarcolemma and within the cytoplasm of striated muscle c
113 ocytes (i.e., from the T-tubules and surface sarcolemma) and in detubulated myocytes (i.e., from the
114 d and enlarged mitochondria, deeply infolded sarcolemma, and frequent Z-line streaming regions, which
115 activation of C3G, movement of GLUT4 to the sarcolemma, and glucose uptake in response to insulin.
116 s correctly processed, is transported to the sarcolemma, and is fully functional in mouse muscle.
117 he extracellular matrix and the muscle fiber sarcolemma, and proper glycosylation is critical for its
118 Expressions of Mrp1 in heart homogenate, sarcolemma, and submitochondrial particles (SMP) were in
119 uring ischemia, FAT/CD36 moved away from the sarcolemma as GLUT4 moved toward the sarcolemma, associa
120 rom its endosomal storage compartment to the sarcolemma as the primary mechanism of excessive myocell
122 tment of intracellular pools of Kv1.5 to the sarcolemma, as the response was prevented by the SNARE p
123 association between costameric actin and the sarcolemma, assembles the dystrophin-glycoprotein comple
124 rom the sarcolemma as GLUT4 moved toward the sarcolemma, associated with a shift from fatty acid oxid
125 ng myofibers, Ozz-E3 regulates the levels of sarcolemma-associated beta-catenin by mediating its degr
128 y, despite the presence of dystrophin at the sarcolemma, beta-sarcoglycan-deficient skeletal muscle p
129 s I molecules not only were expressed at the sarcolemma but also could accumulate intracellularly in
131 presence of caveolae not only at the surface sarcolemma, but also on transverse-tubular membranes in
132 ac hypertrophic response at the level of the sarcolemma, but the pathways underpinning this effect ha
133 ssociates with the dystrophin complex at the sarcolemma by binding to the PDZ domain of alpha-syntrop
135 cle nNOSmu is predominantly localized at the sarcolemma by interaction with the dystrophin protein co
136 rm of nNOSmu (NOS-M) that is targeted to the sarcolemma by palmitoylation, even in the absence of the
137 e prevailing model, nNOS is recruited to the sarcolemma by syntrophin, and in DMD this localization i
140 dine receptors (RyRs) are not coupled to the sarcolemma; cardiac remodeling increases noncoupled RyRs
141 on and Na/K pump inactivation cause opposing sarcolemma changes that may affect diverse membrane proc
142 ly expressed myr-PKBalpha was present in the sarcolemma, colocalized with NHE1 at the intercalated di
143 X) is the major Ca(2+) efflux pathway on the sarcolemma, counterbalancing Ca(2+) influx via L-type Ca
146 n is well tolerated in mdx mice and improves sarcolemma defects that underlie skeletal muscle and pul
147 single-voltage clamped smooth muscle cells, sarcolemma depolarization generated uniform increases in
148 pport a new mechanism whereby recruitment of sarcolemma-derived dysferlin creates an active zone of h
149 actin cytoskeleton decreased recruitment of sarcolemma-derived dysferlin to lesions in dysf-pHGFP fi
151 gy with reduced caveolin-3 expression at the sarcolemma developed coincident with the onset of weakne
152 -related persistence of mechanically induced sarcolemma disruptions causes myofiber damage and necros
153 in patients with pre-LVAD ryanodine receptor-sarcolemma distances >1 microm did not improve after mec
154 HF, leading to increased ryanodine receptor-sarcolemma distances (0.96+/-0.05 versus 0.64+/-0.1 micr
156 Hence, Ca(2+) influx across an unstable sarcolemma due to increased activity of a STIM1-Orai1 co
158 ion to fusing patch repair vesicles with the sarcolemma dysferlin is also involved in the release of
159 nges of PIP(2) concentrations in the cardiac sarcolemma, either locally or globally, is not well supp
163 ent mice have reduced capacity to repair the sarcolemma following laser-induced damage, exhibit delay
166 endocytosis of the insulin-responsive GLUT4, sarcolemma GLUT4 protein levels were increased in both t
168 ected in mitochondria in addition to that in sarcolemma; however, adduction with HNE inhibits Mrp1 ac
169 t-tubules (ie, in control cells) and surface sarcolemma (ie, in detubulated cells) of cardiac ventric
170 lycoprotein complex was also restored in the sarcolemma in both strains although at levels lower than
171 zation of CNTF receptors (CNTFRalpha) to the sarcolemma in C57BL/6, ob/ob and db/db was confirmed in
173 py showed that some of the structures at the sarcolemma in FSHD samples were misaligned with respect
174 bserved partial translocation of NOS1 to the sarcolemma in ischemic hearts, and a direct relationship
181 n, other DGC components were restored to the sarcolemma including alpha-sarcoglycan, alpha-/beta-dyst
184 annels do not distribute homogenously on the sarcolemma instead, they segregate into clusters of vari
190 ption of sarcomeric anchoring structures and sarcolemma integrity, observed at the onset of the muscl
191 the NBC isoforms NBCe1 and NBCn1 to lateral sarcolemma, intercalated discs and transverse tubules (t
192 association of mitochondria with the injured sarcolemma involves translocation of mitochondria to the
194 ence indicates that nNOS localization at the sarcolemma is not required to achieve NO-mediated reduct
195 orm, which is normally enhanced on the outer sarcolemma, is up-regulated 2.5-fold without change in s
198 or dystrophic disease, which stabilizes the sarcolemma leading to less myofiber degeneration and inc
199 imately 30 mum of local dysferlin-containing sarcolemma, leading to formation of stable dysferlin acc
200 observed that amylin oligomers attach to the sarcolemma, leading to myocyte Ca(2+) dysregulation, pat
202 of GLUT4 is altered, resulting in increased sarcolemma levels that can account for increased glucose
203 ore elastic response of the actin-dystrophin-sarcolemma linkage to muscle stretches, compared with ut
204 enic overexpression of utrophin causes broad sarcolemma localization of utrophin, restoration of lami
205 Caveolae, lipid-rich microdomains of the sarcolemma, localize and enrich cardiac-protective signa
206 lack of contraction-induced signalling from sarcolemma-localized nNOS, which decreases cGMP-mediated
207 pecific force production by muscle, and that sarcolemma-localized signalling by neuronal nitric oxide
209 tes for the first time that the electrogenic sarcolemma membrane cardiac NCX1 can act as a regulator
210 ow that increased Serpina3n promotes greater sarcolemma membrane integrity and stability in dystrophi
211 hin protein compromises the stability of the sarcolemma membrane surrounding each muscle cell fiber,
212 s that lead to structural instability of the sarcolemma membrane, myofiber degeneration/regeneration
214 e results in more functional integrin at the sarcolemma, more matrix laminin and decreased damage of
215 ay contribute to stability of sarcomeres and sarcolemma, myofibrillary assembly, and transcriptional
216 rcoglycan-sarcospan complex was noted at the sarcolemma, neuromuscular junction, myotendinous junctio
218 tive K+ (K(ATP)) channels are present in the sarcolemma of cardiac myocytes where they link membrane
222 levels were significantly upregulated at the sarcolemma of murine gamma-SG-null (gsg(-/-)) muscle but
223 ated protein 1 (Mrp1; Abcc1) is expressed in sarcolemma of murine heart, where it probably protects t
226 lasts, where dystrophin was expressed at the sarcolemma of myotubes after myogenic differentiation.
228 uvate, and other monocarboxylates across the sarcolemma of skeletal and cardiac myocytes occurs via p
230 ave focused on its role in the repair of the sarcolemma of skeletal muscle, but dysferlin's associati
232 signals modulate ion channel activity in the sarcolemma of SMCs, resulting in altered intracellular c
240 ere stationary in their original position at sarcolemma or t-tubules and were locally depleted of GLU
241 cles induces atrophy, preceded by changes in sarcolemma permeability of causes not yet completely und
245 motic shock of most tubules from the surface sarcolemma prevents AP propagation not only in the disco
246 ores with a delay in t-tubules compared with sarcolemma, probably reflecting delayed disappearance of
247 onal nitric oxide synthase (nNOSmu) from the sarcolemma, producing functional ischemia when the muscl
248 ouse models of nNOS mislocalization from the sarcolemma, prolonged inactivity was only relieved by ph
251 Since SSPN-mediated stabilization of the sarcolemma represents a promising therapeutic strategy i
254 ression of alpha(7)-integrin, stabilized the sarcolemma, restored serum creatine kinase to wild-type
255 Quantitative analysis of data at the surface sarcolemma showed that 4.8% of RyR labeling colocalized
256 it is unknown whether concomitant injury to sarcolemma (SL)-associated NOS isoforms may contribute t
257 occurs because there are so few GLUTs on the sarcolemma surface in the basal state and that they are
258 - and LTCCs are in different portions of the sarcolemma (surface membrane versus T-tubules) and that
260 e and corresponding T-tubular portion of the sarcolemma, the other (M-space) encompassing the rest of
261 functional ion channels on the cardiomyocyte sarcolemma, thereby allowing characterization of ion cha
262 epresent only approximately 32% of the total sarcolemma, they contribute approximately 60% to the tot
263 enne muscular dystrophy--anchors nNOS to the sarcolemma through a direct interaction with dystrophin
264 nction is ensured by its localization at the sarcolemma through an interaction of its PDZ domain with
265 activity that could augment weakening of the sarcolemma through greater degradation of cellular attac
266 keletal muscle basal lamina is linked to the sarcolemma through transmembrane receptors, including in
267 induced swelling associated with a defective sarcolemma, thus reducing myofiber necrosis in two disti
268 nsient outward currents) by depolarizing the sarcolemma to -20 mV and again ryanodine was effective i
269 regulate fusion of repair vesicles with the sarcolemma to facilitate membrane repair, but the dysfer
270 matrix laminin binding on the outside of the sarcolemma to Grb2 binding to syntrophin on the inside s
271 from hypofunction of Kir2.6 predisposes the sarcolemma to hypokalemia-induced paradoxical depolariza
272 e (FAT/CD36) would translocate away from the sarcolemma to limit fatty acid uptake when fatty acid ox
273 s linking the absence of dystrophin from the sarcolemma to myofiber necrosis are not fully known.
275 e show that PKA activity is shifted from the sarcolemma to the myofilaments in hypertrophic failing r
276 aM binding attenuates GRK5 movement from the sarcolemma to the nucleus and, importantly, overexpressi
277 macrophages, is rapidly sorted from adjacent sarcolemma to the repair patch in a Dysferlin (Dysf) dep
278 is driven by the influx of Ca(2+) across the sarcolemma triggering Ca(2+) release from the sarcoplasm
279 but may constitutively contribute to cardiac sarcolemma turnover in dependence on metabolic stress.
280 tive importance of the loss of nNOS from the sarcolemma versus the importance of loss of total nNOS f
281 Thus, transmission of neural signals to the sarcolemma was effective and the reduction in force must
286 microscopy studies, where large gaps between sarcolemmas were visualized, although normal sarcomeric
287 els of utrophin to therapeutic levels at the sarcolemma, where attachment to laminin is restored.
288 r, the green fusion protein localized on the sarcolemma, where it assembled the dystrophin-glycoprote
290 e, dysferlin is located predominantly at the sarcolemma, where it plays a role in membrane fusion and
291 s (T-tubules) to the non-native crest of the sarcolemma, where their open probability was dramaticall
292 gher PKA activity in the cytosol than at the sarcolemma, whereas isoproterenol triggered faster sarco
293 equally in T-tubules and crest areas of the sarcolemma, whereas, in ventricular myocytes, LTCCs prim
294 strophin glycoprotein complex (DGC) from the sarcolemma which contributes to the dystrophic phenotype
295 d transporters when they are inserted in the sarcolemma, while a lack of PIP(2) on internal membranes
298 otentials (APs) at multiple sites within the sarcolemma with submillisecond temporal and submicromete
299 UT4-containing domains before they reach the sarcolemma, with the consequent movement of the insulin
300 ically links the costameric cytoskeleton and sarcolemma, yet dystrophin-deficient muscle exhibits abn
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