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1            Skeletal muscle biopsies revealed subsarcolemmal accumulation of mitochondria and/or cytoc
2                                   A peculiar subsarcolemmal accumulation of mitochondria pointing tow
3                       It is characterized by subsarcolemmal accumulations of myosin that have a hyali
4                           This suggests that subsarcolemmal actin filament networks may be associated
5 er microscopy revealed alpha-B crystallin in subsarcolemmal aggresomes.
6                                              Subsarcolemmal and central [Ca(2+)](i) transient amplitu
7 io-temporal summation of Ca(2+) release from subsarcolemmal and central sites.
8 ign separations of organelle subtypes (e.g., subsarcolemmal and interfibrillar skeletal muscle mitoch
9                                              Subsarcolemmal and intermyofibrillar mitochondria were i
10 itochondria, and preparation of fractions of subsarcolemmal and intermyofibrillar mitochondria.
11                                              Subsarcolemmal and intermyofibrillar mitochondrial fract
12                 In experiments with isolated subsarcolemmal and intermyofibrillar mitochondrial subpo
13 ) release during the DD produces a localized subsarcolemmal Ca(2+) increase that spreads in a wavelik
14 icient Ca2+ for normal triggering, even when subsarcolemmal Ca(2+) is lowered by EGTA.
15 d ryanodine receptor-derived diastolic local subsarcolemmal Ca(2+) release.
16                                    Localized subsarcolemmal Ca(2+) releases are generated by the sarc
17 nodine, beta-AR stimulation fails to amplify subsarcolemmal Ca(2+) releases, fails to augment the dia
18 eduction in Ca(2+) spark frequency (-49%), a subsarcolemmal Ca(2+) signal that evokes the BK transien
19 e amplitude of the local preaction potential subsarcolemmal Ca(2+) transient that, in turn, accelerat
20  interactions modulated by membrane voltage, subsarcolemmal Ca(2+), and protein kinase A and CaMKII-d
21 2+) release, provide information about local subsarcolemmal [Ca(2+)].
22                                Modulation of subsarcolemmal Ca2+ by the Na+-Ca2+ exchanger may be an
23 ring an action potential can account for the subsarcolemmal Ca2+ gradients in NB myocytes.
24                             In WT mice, high subsarcolemmal Ca2+ is not required for synchronous trig
25              These results suggest that high subsarcolemmal Ca2+ is required to ensure synchronous tr
26                                   Localized, subsarcolemmal Ca2+ release (LCR) via ryanodine receptor
27 dies using confocal microscopy indicate that subsarcolemmal Ca2+ release via ryanodine receptors occu
28                             Local, rhythmic, subsarcolemmal Ca2+ releases (LCRs) from the sarcoplasmi
29                                    While the subsarcolemmal Ca2+ response can be considered as stereo
30 ke process influences the time course of the subsarcolemmal Ca2+ signal that activates ICl(Ca).
31 of electrical excitation, spatially discrete subsarcolemmal Ca2+ signals were initiated.
32                                              Subsarcolemmal Ca2+ sparks had a slightly higher amplitu
33 st that low voltage-activated ICa,T triggers subsarcolemmal Ca2+ sparks, which in turn stimulate INa-
34             We hypothesize that the elevated subsarcolemmal Ca2+ that results from the absence of NCX
35  SANC models beat at a faster rate when this subsarcolemmal Ca2+ waveform measured under beta-AR stim
36                               Thus, reducing subsarcolemmal Ca2+ with EGTA in NCX KO mice reveals the
37                                 The discrete subsarcolemmal Ca2+-release sites, which responded in a
38 n which rapid influx of Ca2+ produces a high subsarcolemmal [Ca2+], favouring rapid Ca2+ removal by n
39                  Loading of the SR increased subsarcolemmal [Ca2+]i transient amplitude and subsequen
40 vate Ca2+-dependent eNOS/NOi production from subsarcolemmal caveolae sites.
41 genase, demonstrate abnormal accumulation of subsarcolemmal clumps of mitochondria in predominantly s
42  of Ca(2+) through I(CaL) and release from a subsarcolemmal compartment (L(0)).
43 lowing novel features: 1), the addition of a subsarcolemmal compartment to the other two commonly for
44  the sarcolemma and forms a link between the subsarcolemmal cytoskeleton and the extracellular matrix
45  suggest the link between dystrophin and the subsarcolemmal cytoskeleton involves more than a simple
46 hanical role in skeletal muscle, linking the subsarcolemmal cytoskeleton with the extracellular matri
47 o actin and possibly other components of the subsarcolemmal cytoskeleton, while the carboxy terminus
48        The role of the SR in contributing to subsarcolemmal cytosolic microdomains in uterus is evalu
49 mp subunit glutathionylation, not restricted subsarcolemmal diffusion of Na(+).
50  course of the consequent Ca2+ signal in the subsarcolemmal domain containing Ca(2+)-activated chlori
51 hosphate receptor-mediated Ca(2+) release in subsarcolemmal domains of atrial myocytes.
52 fibrillar mitochondrial subpopulations, only subsarcolemmal exhibited NAD(+)-dependent lactate oxidat
53 al myopathy characterized by the presence of subsarcolemmal inclusions of myosin in the majority of t
54 a2+ signal propagated more reliably from the subsarcolemmal initiation sites into the centre of the c
55 lly specific recruitment of Ca(2+) sparks by subsarcolemmal InsP(3)Rs.
56 usly beating pacemaker cells, an increase in subsarcolemmal intracellular Ca2+ concentration occurred
57 anism indicates a pivotal role for ICa,T and subsarcolemmal intracellular Ca2+ release in normal atri
58 ich lack transverse tubules and contain both subsarcolemmal junctional (j-SR) and central nonjunction
59  II ryanodine receptors (RyRs) revealed both subsarcolemmal 'junctional' RyRs, and also 'non-junction
60 eous SANC firing was critically dependent on subsarcolemmal LCRs, ie, PDE inhibition increased LCR am
61 in the context of the yellow autofluorescent subsarcolemmal lipofuscin granules.
62                        Spontaneous, rhythmic subsarcolemmal local Ca(2+) releases driven by cAMP-medi
63 hypertrophic cardiomyopathy characterized by subsarcolemmal MHC accumulation, myofiber fragmentation,
64 nic utrophin overexpression does not correct subsarcolemmal microtubule lattice disorganization, loss
65  vivo correlates with disorganization of the subsarcolemmal microtubule lattice, increased detyrosina
66 ons of mitochondria exist in the myocardium: subsarcolemmal mitochondria (SSM) and interfibrillar mit
67          Dystrophin was required to maintain subsarcolemmal mitochondria (SSM) pool density, implicat
68  periodic crests, relying on the presence of subsarcolemmal mitochondria (SSM) with unknown role.
69 ylation, and O(2) affinity (lower P(50) ) of subsarcolemmal mitochondria compared to low-altitude mic
70  findings suggest that functional changes in subsarcolemmal mitochondria contribute to improving aero
71               Rotenone treatment of isolated subsarcolemmal mitochondria decreased the production of
72 r in type 2 diabetic and obese subjects, but subsarcolemmal mitochondria electron transport chain act
73       Because of the potential importance of subsarcolemmal mitochondria for signal transduction and
74 the orderly pattern of intermyofibrillar and subsarcolemmal mitochondria in denervated muscle.
75 itochondria; we further found that subjacent subsarcolemmal mitochondria preferentially host the mito
76                                              Subsarcolemmal mitochondria sustain progressive damage d
77                               A reduction in subsarcolemmal mitochondria was confirmed by transmissio
78 , including those under the plasma membrane, subsarcolemmal mitochondria, and those between the myofi
79 chondria, IFM) or beneath the cell membrane (subsarcolemmal mitochondria, SSM), with several structur
80 ubstantial increase in the number/density of subsarcolemmal mitochondria.
81 med by sodium channel clusters and subjacent subsarcolemmal mitochondria.
82 l densities fell by 21%, with loss of 73% of subsarcolemmal mitochondria.
83 s and higher densities of interfibrillar and subsarcolemmal mitochondria.
84 ubpopulation in close proximity to subjacent subsarcolemmal mitochondria; we further found that subja
85 tion could not be reconciled with restricted subsarcolemmal Na(+) diffusion.
86                The source of the increase in subsarcolemmal [Na+] requires further investigation.
87    Initial I(pump) sag might be explained by subsarcolemmal [Na](i) ([Na](SL)) depletion produced by
88                   The observed early loss of subsarcolemmal neuronal nitric oxide synthase activity,
89 ed in bulk cytoplasm (although this could be subsarcolemmal only).
90      In atrial cells Ca2+ release started at subsarcolemmal peripheral regions and subsequently sprea
91 ealed subcellular structures consistent with subsarcolemmal, perivascular, intersarcomeric, and paran
92 density falls, with a particular loss of the subsarcolemmal population.
93        Muscle biopsy from the proband showed subsarcolemmal proliferation of mitochondria and decreas
94 nnel and protein kinase Calpha at only a few subsarcolemmal regions in resistance arteries.
95                                              Subsarcolemmal release fused to build a peripheral ring
96                Increases started at distinct subsarcolemmal release sites spaced approximately 2 micr
97 nally increased NOi by recruiting additional subsarcolemmal release sites.
98 2+, the response was largely restricted to a subsarcolemmal 'ring', while the central bulk of the cel
99 placed nuclei resembling fetal myotubes, and subsarcolemmal ringed and central dense areas highlighte
100 ulation is critically dependent on localized subsarcolemmal ryanodine receptor (RyR) Ca(2+) releases
101 P-mediated, protein kinase A-dependent local subsarcolemmal ryanodine receptor Ca(2+) releases (LCRs)
102  Stochastic but roughly periodic LCRs (Local subsarcolemmal ryanodine receptor-mediated Ca(2+) Releas
103 y showed that PE stimulated NOi release from subsarcolemmal sites and this was prevented by 2 mm meth
104 led that ACh exposure increased NOi at local subsarcolemmal sites, and ACh withdrawal additionally in
105 cytes, ACh stimulates NOi release from local subsarcolemmal sites.
106  to compare fluo-3 [Ca2+]i transients in the subsarcolemmal space and cell center of field-stimulated
107 s a dense two-dimensional network within the subsarcolemmal space around the fiber, running ~500-600
108 Ca2+]i occurred sooner and was higher in the subsarcolemmal space compared with the cell center in NB
109  SDTs arise from RyR stores localized to the subsarcolemmal space during myofibrillogenesis.
110 ate the time course of local [Ca(2+)] in the subsarcolemmal space near Ca(2+) channels produced by SR
111  sparks, occurred at higher frequency in the subsarcolemmal space than in more central regions of the
112 h low SR Ca2+ load [Ca2+]i transients in the subsarcolemmal space were small and no Ca2+ release in t
113 evealed that the latter were arranged in the subsarcolemmal space where they largely co-localised wit
114                           The existence of a subsarcolemmal space with restricted diffusion for Na(+)
115 with similar profiles at the cell center and subsarcolemmal space.
116  in membrane potential, and propagate in the subsarcolemmal space.
117 xplained by a slower removal of Na+ from the subsarcolemmal space.
118   Both types of events are initiated only at subsarcolemmal SR Ca2+ release sites suggesting that in
119                     PE also increased local, subsarcolemmal SR Ca2+ release via IP3-dependent signall
120 spontaneous Ca2+ sparks from j-SR and nj-SR, subsarcolemmal (SS) Ca2+ sparks from the j-SR were 3-4 t
121          In contrast, there was no change in subsarcolemmal (SS) Mito(VD).
122  (CICR) from the junctional-SR (j-SR, in the subsarcolemmal (SS) space) and non-junctional-SR (nj-SR,
123 nd had more than twofold greater IMCL in the subsarcolemmal (SSL) region.
124 e-dependent bivariate probability density of subsarcolemmal subspace and junctional sarcoplasmic reti
125 ng the time-dependent probability density of subsarcolemmal subspace and junctional sarcoplasmic reti
126                                            A subsarcolemmal tubular system network (SSTN) has been de

 
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