ライフサイエンスコーパス: subsarcolemmal

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 itochondria, and preparation of fractions of subsarcolemmal and intermyofibrillar mitochondria.

10 Subsarcolemmal and intermyofibrillar mitochondrial fract

11 In experiments with isolated subsarcolemmal and intermyofibrillar mitochondrial subpo

12 ) release during the DD produces a localized subsarcolemmal Ca(2+) increase that spreads in a wavelik

13 icient Ca2+ for normal triggering, even when subsarcolemmal Ca(2+) is lowered by EGTA.

14 d ryanodine receptor-derived diastolic local subsarcolemmal Ca(2+) release.

15 Localized subsarcolemmal Ca(2+) releases are generated by the sarc

16 nodine, beta-AR stimulation fails to amplify subsarcolemmal Ca(2+) releases, fails to augment the dia

17 eduction in Ca(2+) spark frequency (-49%), a subsarcolemmal Ca(2+) signal that evokes the BK transien

18 e amplitude of the local preaction potential subsarcolemmal Ca(2+) transient that, in turn, accelerat

19 interactions modulated by membrane voltage, subsarcolemmal Ca(2+), and protein kinase A and CaMKII-d

20 2+) release, provide information about local subsarcolemmal [Ca(2+)].

21 Modulation of subsarcolemmal Ca2+ by the Na+-Ca2+ exchanger may be an

22 ring an action potential can account for the subsarcolemmal Ca2+ gradients in NB myocytes.

23 In WT mice, high subsarcolemmal Ca2+ is not required for synchronous trig

24 These results suggest that high subsarcolemmal Ca2+ is required to ensure synchronous tr

25 Localized, subsarcolemmal Ca2+ release (LCR) via ryanodine receptor

26 dies using confocal microscopy indicate that subsarcolemmal Ca2+ release via ryanodine receptors occu

27 Local, rhythmic, subsarcolemmal Ca2+ releases (LCRs) from the sarcoplasmi

28 While the subsarcolemmal Ca2+ response can be considered as stereo

29 ke process influences the time course of the subsarcolemmal Ca2+ signal that activates ICl(Ca).

30 of electrical excitation, spatially discrete subsarcolemmal Ca2+ signals were initiated.

31 Subsarcolemmal Ca2+ sparks had a slightly higher amplitu

32 st that low voltage-activated ICa,T triggers subsarcolemmal Ca2+ sparks, which in turn stimulate INa-

33 We hypothesize that the elevated subsarcolemmal Ca2+ that results from the absence of NCX

34 SANC models beat at a faster rate when this subsarcolemmal Ca2+ waveform measured under beta-AR stim

35 Thus, reducing subsarcolemmal Ca2+ with EGTA in NCX KO mice reveals the

36 The discrete subsarcolemmal Ca2+-release sites, which responded in a

37 n which rapid influx of Ca2+ produces a high subsarcolemmal [Ca2+], favouring rapid Ca2+ removal by n

38 Loading of the SR increased subsarcolemmal [Ca2+]i transient amplitude and subsequen

39 vate Ca2+-dependent eNOS/NOi production from subsarcolemmal caveolae sites.

40 genase, demonstrate abnormal accumulation of subsarcolemmal clumps of mitochondria in predominantly s

41 of Ca(2+) through I(CaL) and release from a subsarcolemmal compartment (L(0)).

42 lowing novel features: 1), the addition of a subsarcolemmal compartment to the other two commonly for

43 the sarcolemma and forms a link between the subsarcolemmal cytoskeleton and the extracellular matrix

44 suggest the link between dystrophin and the subsarcolemmal cytoskeleton involves more than a simple

45 hanical role in skeletal muscle, linking the subsarcolemmal cytoskeleton with the extracellular matri

46 o actin and possibly other components of the subsarcolemmal cytoskeleton, while the carboxy terminus

47 The role of the SR in contributing to subsarcolemmal cytosolic microdomains in uterus is evalu

48 mp subunit glutathionylation, not restricted subsarcolemmal diffusion of Na(+).

49 course of the consequent Ca2+ signal in the subsarcolemmal domain containing Ca(2+)-activated chlori

50 hosphate receptor-mediated Ca(2+) release in subsarcolemmal domains of atrial myocytes.

51 fibrillar mitochondrial subpopulations, only subsarcolemmal exhibited NAD(+)-dependent lactate oxidat

52 al myopathy characterized by the presence of subsarcolemmal inclusions of myosin in the majority of t

53 a2+ signal propagated more reliably from the subsarcolemmal initiation sites into the centre of the c

54 lly specific recruitment of Ca(2+) sparks by subsarcolemmal InsP(3)Rs.

55 usly beating pacemaker cells, an increase in subsarcolemmal intracellular Ca2+ concentration occurred

56 anism indicates a pivotal role for ICa,T and subsarcolemmal intracellular Ca2+ release in normal atri

57 ich lack transverse tubules and contain both subsarcolemmal junctional (j-SR) and central nonjunction

58 II ryanodine receptors (RyRs) revealed both subsarcolemmal 'junctional' RyRs, and also 'non-junction

59 eous SANC firing was critically dependent on subsarcolemmal LCRs, ie, PDE inhibition increased LCR am

60 in the context of the yellow autofluorescent subsarcolemmal lipofuscin granules.

61 Spontaneous, rhythmic subsarcolemmal local Ca(2+) releases driven by cAMP-medi

62 hypertrophic cardiomyopathy characterized by subsarcolemmal MHC accumulation, myofiber fragmentation,

63 nic utrophin overexpression does not correct subsarcolemmal microtubule lattice disorganization, loss

64 vivo correlates with disorganization of the subsarcolemmal microtubule lattice, increased detyrosina

65 ons of mitochondria exist in the myocardium: subsarcolemmal mitochondria (SSM) and interfibrillar mit

66 Dystrophin was required to maintain subsarcolemmal mitochondria (SSM) pool density, implicat

67 Rotenone treatment of isolated subsarcolemmal mitochondria decreased the production of

68 r in type 2 diabetic and obese subjects, but subsarcolemmal mitochondria electron transport chain act

69 Because of the potential importance of subsarcolemmal mitochondria for signal transduction and

70 the orderly pattern of intermyofibrillar and subsarcolemmal mitochondria in denervated muscle.

71 Subsarcolemmal mitochondria sustain progressive damage d

72 A reduction in subsarcolemmal mitochondria was confirmed by transmissio

73 , including those under the plasma membrane, subsarcolemmal mitochondria, and those between the myofi

74 l densities fell by 21%, with loss of 73% of subsarcolemmal mitochondria.

75 s and higher densities of interfibrillar and subsarcolemmal mitochondria.

76 tion could not be reconciled with restricted subsarcolemmal Na(+) diffusion.

77 The source of the increase in subsarcolemmal [Na+] requires further investigation.

78 Initial I(pump) sag might be explained by subsarcolemmal [Na](i) ([Na](SL)) depletion produced by

79 The observed early loss of subsarcolemmal neuronal nitric oxide synthase activity,

80 ed in bulk cytoplasm (although this could be subsarcolemmal only).

81 In atrial cells Ca2+ release started at subsarcolemmal peripheral regions and subsequently sprea

82 ealed subcellular structures consistent with subsarcolemmal, perivascular, intersarcomeric, and paran

83 density falls, with a particular loss of the subsarcolemmal population.

84 Muscle biopsy from the proband showed subsarcolemmal proliferation of mitochondria and decreas

85 nnel and protein kinase Calpha at only a few subsarcolemmal regions in resistance arteries.

86 Subsarcolemmal release fused to build a peripheral ring

87 Increases started at distinct subsarcolemmal release sites spaced approximately 2 micr

88 nally increased NOi by recruiting additional subsarcolemmal release sites.

89 2+, the response was largely restricted to a subsarcolemmal 'ring', while the central bulk of the cel

90 placed nuclei resembling fetal myotubes, and subsarcolemmal ringed and central dense areas highlighte

91 ulation is critically dependent on localized subsarcolemmal ryanodine receptor (RyR) Ca(2+) releases

92 P-mediated, protein kinase A-dependent local subsarcolemmal ryanodine receptor Ca(2+) releases (LCRs)

93 Stochastic but roughly periodic LCRs (Local subsarcolemmal ryanodine receptor-mediated Ca(2+) Releas

94 y showed that PE stimulated NOi release from subsarcolemmal sites and this was prevented by 2 mm meth

95 led that ACh exposure increased NOi at local subsarcolemmal sites, and ACh withdrawal additionally in

96 cytes, ACh stimulates NOi release from local subsarcolemmal sites.

97 to compare fluo-3 [Ca2+]i transients in the subsarcolemmal space and cell center of field-stimulated

98 s a dense two-dimensional network within the subsarcolemmal space around the fiber, running ~500-600

99 Ca2+]i occurred sooner and was higher in the subsarcolemmal space compared with the cell center in NB

100 SDTs arise from RyR stores localized to the subsarcolemmal space during myofibrillogenesis.

101 ate the time course of local [Ca(2+)] in the subsarcolemmal space near Ca(2+) channels produced by SR

102 sparks, occurred at higher frequency in the subsarcolemmal space than in more central regions of the

103 h low SR Ca2+ load [Ca2+]i transients in the subsarcolemmal space were small and no Ca2+ release in t

104 evealed that the latter were arranged in the subsarcolemmal space where they largely co-localised wit

105 The existence of a subsarcolemmal space with restricted diffusion for Na(+)

106 in membrane potential, and propagate in the subsarcolemmal space.

107 xplained by a slower removal of Na+ from the subsarcolemmal space.

108 with similar profiles at the cell center and subsarcolemmal space.

109 Both types of events are initiated only at subsarcolemmal SR Ca2+ release sites suggesting that in

110 PE also increased local, subsarcolemmal SR Ca2+ release via IP3-dependent signall

111 spontaneous Ca2+ sparks from j-SR and nj-SR, subsarcolemmal (SS) Ca2+ sparks from the j-SR were 3-4 t

112 In contrast, there was no change in subsarcolemmal (SS) Mito(VD).

113 (CICR) from the junctional-SR (j-SR, in the subsarcolemmal (SS) space) and non-junctional-SR (nj-SR,

114 nd had more than twofold greater IMCL in the subsarcolemmal (SSL) region.

115 e-dependent bivariate probability density of subsarcolemmal subspace and junctional sarcoplasmic reti

116 ng the time-dependent probability density of subsarcolemmal subspace and junctional sarcoplasmic reti

117 A subsarcolemmal tubular system network (SSTN) has been de