ライフサイエンスコーパス: slow muscle

1 the role of RLC phosphorylation in heart and slow muscle.

2 as up-regulated and 27 down-regulated in the slow muscle.

3 n-regulated in the fast muscle compared with slow muscle.

4 eral somite surface and generate superficial slow muscle.

5 muscle, and a six-layer Z-band in mammalian slow muscle.

6 ted by motoneuron pools that normally supply slow muscles.

7 1c knockout increased Mef2 protein levels in slow muscles.

8 " preparations, rapid, rhythmic inputs drive slow muscles.

9 solated from rabbit psoas (fast) and soleus (slow) muscles.

10 ds, otic vesicles, photoreceptor cell layer, slow muscle and cloaca.

11 een reported in fast muscle, its function in slow muscle and the function of Smyd1a, in general, are

12 e double mutants exhibit a severe deficit in slow muscles and their precursor, adaxial cells, reveali

13 ate early, whereas motor neurons innervating slow muscles and those involved in eye movement and pelv

14 le fibre bundles isolated from the soleus (a slow muscle) and extensor digitorum longus (a fast muscl

15 hc1 is essential for myogenesis in embryonic slow muscles, and loss of Smyhc1 results in defective sa

16 d Hspa8 trimethylation and protein levels in slow muscles, and Mettl21c overexpression in myoblasts i

17 search and data presented here indicate that slow muscles are also driven by rhythmic neuronal inputs

18 y neuronal activity in preparations in which slow muscles are common, it may be necessary to determin

19 ell known invertebrate "model" preparations, slow muscles are driven by rapid, rhythmic inputs.

20 Slow muscles are often believed to function primarily in

21 This is particularly so in animals with many slow muscles, as is the case in insects-many of which ar

22 ild-type or mutant embryos, leads to ectopic slow muscle at the expense of fast.

23 minately on fast- or mixed-fibre muscle with slow muscle being much less studied.

24 ant fish lacking shh expression fail to form slow muscle but do form fast muscle.

25 ion pattern was observed for TmyoD1-alpha in slow muscle but the differences were not significant.

26 redominantly fast muscles than predominantly slow muscles, but are not expressed in muscle cells them

27 of miR-214 results in a reduction or loss of slow-muscle cell types.

28 Furthermore, we show that slow muscle cells are sufficient to pattern the medial t

29 at Hedgehog signal perception is required by slow muscle cells but not by fast muscle cells for fast

30 Zebrafish slow muscle cells develop from adaxial cells, a one-cell

31 k slow muscle cells, providing evidence that slow muscle cells regulate the pattern of trunk neural c

32 neural activity is transmitted to developing slow muscle cells, and synchronized activity spreads via

33 rmal in Hedgehog signaling mutants that lack slow muscle cells, providing evidence that slow muscle c

34 eates GJ channels specifically in developing slow muscle cells.

35 from notochord specify adaxial cells to form slow muscle cells.

36 factor, fail to accumulate in the soleus, a slow muscle, compared with fast muscles (e.g., white vas

37 D-1 expression induced a transition toward a slow muscle contractile protein phenotype, slower shorte

38 pike number, not spike frequency, determines slow muscle contraction amplitude.

39 omponents are interdependent, and control of slow muscle contraction is thus likely complex.

40 are frequently used by insects to translate slow muscle contractions into rapid-release recoil movem

41 del suggests that as cycle period decreases, slow muscle contractions show increasing intercontractio

42 fibres provides a metabolic advantage during slow muscle contractions, but this benefit disappeared a

43 fibers oriented in chevrons and two pairs of slow muscle "cords" along the length of the tail.

44 fast and approximately 100 nm in cardiac and slow muscles, corresponding to the number of alpha-actin

45 ies to accelerate muscle regeneration and to slow muscle degeneration in myositis, focusing primarily

46 Partial loss-of-function mutations cause slow muscle depolarization and feeble contraction.

47 Slow muscle derives from medial adaxial myoblasts that d

48 mediates bioelectric signaling required for slow muscle development and function.

49 ed for Myod to regulate fast-muscle, but not slow-muscle, development.

50 At later stages, Shh promotes slow muscle differentiation cell-autonomously.

51 at Shh acts to induce myoblasts committed to slow muscle differentiation from uncommitted presomitic

52 that tonic contraction may be a property of slow muscles driven by rapid, rhythmic input, and in the

53 d and differentiate into skeleton, fast, and slow muscles during somitogenesis.

54 e contractions, particularly in systems with slow muscle dynamics, as in the crab (Cancer borealis) s

55 betaA/T-rich -269/-258) that is required for slow muscle expression and which potentiates MOV respons

56 in zebrafish, we hypothesize that migrating slow muscle facilitates myotome boundary formation in ae

57 ing of sarcoplasmic reticulum Ca(2+) stores, slow muscle fatigue, and increase running endurance with

58 Slow muscle fiber development in smu mutant embryos is a

59 Overexpression of Shh does not rescue slow muscle fiber development in smu(-/-) embryos, where

60 le precursors: wild-type muscle cells rescue slow muscle fiber development in smu(-/-) embryos, where

61 tors from the earlier promotion of embryonic slow muscle fiber differentiation.

62 , slow MyHC 3 gene expression coincides with slow muscle fiber formation as distinguished by slow MyH

63 II histone deacetylases (HDACs) may decrease slow muscle fiber gene expression by repressing myogenic

64 key role of calcineurin in activation of the slow muscle fiber phenotype.

65 In zebrafish, Hedgehog is required for slow muscle fiber specification.

66 edgehog signaling has been shown to regulate slow muscle fiber type development.

67 through Slow-muscle-omitted is necessary for slow muscle fiber type development.

68 in vitro system indicates that formation of slow muscle fiber types is dependent on both myoblast li

69 The slow muscle fiber-restricted expression of slow MyHC 3 d

70 sient increase in satellite cell numbers and slowed muscle fiber growth, followed by a period of acce

71 mbryos have a 99% reduction in the number of slow muscle fibers and a complete loss of Engrailed-expr

72 aphragm of FgfrL1 knockout animals lacks any slow muscle fibers at E18.5 as indicated by the absence

73 Slow muscle fibers develop from adaxial cells and depend

74 te muscle regions, containing either fast or slow muscle fibers during early neuromuscular developmen

75 he expression profile properties in fast and slow muscle fibers had been investigated at the mRNA lev

76 a step decrease in tension in both fast and slow muscle fibers in rigor, indicating thermal expansio

77 reas mutant muscle cells cannot develop into slow muscle fibers in wild-type embryos.

78 Adaxial cells differentiate into slow muscle fibers of the adult fish.

79 ed of a heterogeneous population of fast and slow muscle fibers that are selectively innervated durin

80 omprised of anatomically segregated fast and slow muscle fibers that possess different metabolic and

81 to the contractile properties of the fast or slow muscle fibers that they innervate.

82 Thus, the medial to lateral migration of slow muscle fibers through the somite creates a morphoge

83 enough to allow the motoneurons innervating slow muscle fibers to be driven to their maximum force l

84 its, which exclusively innervate superficial slow muscle fibers via septal nerves.

85 s or to some property of the developing fast-slow muscle fibers was not determined.

86 ofibrillar protein assembly, particularly in slow muscle fibers, and decreased levels of the hedgehog

87 fferentiation and migration of adaxial cells/slow muscle fibers, as well as mutants with specific def

88 These mice exhibited an increase in slow muscle fibers, but no evidence for skeletal muscle

89 ns of their target containing either fast or slow muscle fibers, we backlabeled neurons from each of

90 s expression of a reporter gene in embryonic slow muscle fibers, while a distal element, located grea

91 sufficient for the development of embryonic slow muscle fibers-the earliest differentiating muscle f

92 yos causes all somitic cells to develop into slow muscle fibers.

93 ion and in atrophy especially in the case of slow muscle fibers.

94 -threshold MNs innervating fatigue resistant slow muscle fibers.

95 ically required for embryonic development of slow muscle fibers.

96 this regulation is not mediated by embryonic slow muscle fibers.

97 ct fates: fast, non-pioneer slow, or pioneer slow muscle fibers.

98 postmitotic adaxial cells differentiate into slow muscle fibers.

99 sequence that restricts enhancer activity to slow muscle fibers.

100 hanisms specifying the identity of these new slow-muscle fibers are different from those specifying t

101 We show that in zebrafish new slow-muscle fibers are first added at the end of the seg

102 red for the specification of adaxial-derived slow-muscle fibers in the embryo [4, 5], we show that in

103 e, despite the complete absence of embryonic slow-muscle fibers to serve as a scaffold for addition o

104 erve as a scaffold for addition of these new slow-muscle fibers.

105 ng the identity of adaxial-derived embryonic slow-muscle fibers.

106 sion in soleus, which is largely composed of slow-muscle fibers.

107 Intriguingly, we also observed changes in slow muscle fibre arrangement; previously, Dok-7 has not

108 all the tension components in both fast and slow muscle fibre bundles.

109 E-F), suggesting exercise intensity impacted slow muscle fibre mechanics.

110 In both fast and slow muscle fibre preparations, the plateau tension of t

111 t that lifelong endurance exercise benefited slow muscle fibre size and function.

112 eatures of ANM such as atrophy of extrafusal slow muscle fibres and increased fatigability.

113 Slow muscle fibres form and commence normal migration in

114 eration of a first wave of early superficial slow muscle fibres in tail somites.

115 y, we demonstrated that having predominantly slow muscle fibres provides a metabolic advantage during

116 Lifelong endurance exercisers had slow muscle fibres that were larger, stronger, faster an

117 viscoelasticity (44 +/- 2 ms, n = 12) of the slow muscle fibres were significantly larger than those

118 either Myf5 or Myod is sufficient to promote slow muscle formation from adaxial cells.

119 scle fiber distribution, and regained normal slow muscle formation.

120 tion while increasing Hedgehog signaling and slow muscle formation.

121 a handle on the molecular mechanism driving slow muscle formation.

122 (Shh) secreted from the notochord can induce slow muscle from medial cells of the somite.

123 sent in total muscle homogenates of fast and slow muscles from wild-type (WT) littermates.

124 se morphological changes are associated with slow muscle function and a greater resistance to contrac

125 investigate whether TEAD-1 is a modulator of slow muscle gene expression in vivo, we developed transg

126 ox6 as a fast myofiber-enriched repressor of slow muscle gene expression in vivo.

127 data support a role for TEAD-1 in modulating slow muscle gene expression.

128 d of fast-muscle genes is inhibited, whereas slow-muscle gene expression appears normal.

129 ow muscle precursors and expression of other slow muscle genes were not affected and fast muscles app

130 emonstrate that col15a1b participates in the slow muscle genetic program as a direct target of Hedgeh

131 We propose a model in which slow muscles guide fast myocytes by funneling them close

132 melanogaster indirect flight muscle with the slow muscle hinge B (exon 15b) allows examination of the

133 Substitution of the slow muscle hinge B impaired flight ability, increased s

134 t muscle isovariant hinge A was switched for slow muscle hinge B in the MHC isoforms of indirect flig

135 t, this mechanism can be extrapolated to the slow muscle in the hearts of large mammals, including hu

136 number and spike frequency dependence in two slow muscles in the lobster stomatogastric system.

137 t expressed the transgene in fast but not in slow muscles, indicating that these regulatory elements

138 Inhibition of Hedgehog-induced slow muscle induction in aei/deltaD and deadly seven (de

139 The bovine slow muscle investigated here reveals a Z-band comprisin

140 In contrast, death of the slow muscle is controlled by the other cell types of the

141 t, when the fiber pattern of future fast and slow muscle is established.

142 n (des)/notch1a mutant embryos suggests that slow muscle is necessary for myotome boundary recovery i

143 IFI) both decreased Drosophila IFM power and slowed muscle kinetics.

144 uires Myod in order to induce both fast- and slow-muscle markers but requires Pbx only to induce fast

145 Because we have previously demonstrated that slow muscle migration triggers fast muscle cell elongati

146 , immunofluorescent staining of fast but not slow muscle myosin was markedly decreased in scube3 morp

147 signaling, stratified hyperplastic growth of slow muscle occurs at the correct time and place, despit

148 is expressed in the developing heart and in slow muscles of the developing limb.

149 pathway mutants, chameleon (con(tf18b)) and slow muscle omitted (smu(b641)) exhibit a striking parti

150 ignaling in zebrafish, we have characterized slow muscle omitted (smu) mutants.

151 also examined the eye phenotype of zebrafish slow muscle-omitted (smu) mutants, which lack a function

152 report here that mutations in the zebrafish slow-muscle-omitted (smu) gene disrupt many developmenta

153 Therefore, Hedgehog signaling through Slow-muscle-omitted is necessary for slow muscle fiber t

154 Aplysia has long been studied as a typical "slow" muscle, one that would be assumed to respond only

155 bers derived from myoblasts of both fast and slow muscle origin in cocultures, and slow MyHC gene exp

156 and muscle fibers derived from myoblasts of slow muscle origin.

157 What determines slow muscle output is less well understood.

158 Thus, both of these parameters can determine slow muscle output.

159 Endurance training induces a partial fast-to-slow muscle phenotype transformation and mitochondrial b

160 cells strongly resembles that of the primary slow muscle pioneer cells of the zebrafish.

161 dgehog signal first induces the formation of slow muscle precursor cells, and subsequent Hedgehog and

162 inducing expression of cdkn1c (p57(Kip2)) in slow muscle precursor cells, but neither Hh nor Cdkn1c i

163 s now been shown to be required in embryonic slow muscle precursor cells.

164 essed and deposited in the motor path ECM by slow muscle precursors also called adaxial cells.

165 However, the formation of slow muscle precursors and expression of other slow musc

166 show that the synthesis of collagen XV-B by slow muscle precursors and its deposition in the common

167 Our results demonstrate that slow muscle precursors form independently of Hedgehog si

168 In contrast, pioneer and non-pioneer slow muscle precursors share a common lineage from the o

169 rotein kinase A in zebrafish embryos induces slow muscle precursors throughout the somite but muscle

170 rsors, whereas its expression in the adaxial slow muscle precursors was largely unaffected.

171 ed by Hedgehog (Hh) signaling in prospective slow muscle precursors, and its activity alone is suffic

172 surgical removal of adaxial cells, which are slow muscle precursors, results in abnormal patterning o

173 p-injected zebrafish embryos, we unravel the slow muscle progenitors (SMP) pseudotemporal trajectory

174 er, we observed a close coordination between slow muscle rearrangements and fast myocyte fusion.

175 ound that motor axons projecting to fast and slow muscle regions sorted into separate but adjacent fa

176 a chick muscle containing distinct fast and slow muscle regions, was remarkably similar to normal wh

177 effects of non-linear contractile responses, slow muscle relaxation, and neuromodulation.

178 In addition to weakness, NEM6 patients have slow muscle relaxation, compromising contractility and d

179 Patients with myotonia congenita suffer from slowed muscle relaxation caused by hyperexcitability.

180 ith SmyD1a and SmyD1b expression in fast and slow muscles, respectively.

181 , we delineated a 15-bp region necessary for slow muscle specificity.

182 We conclude that slow-muscle-stratified hyperplasia begins after the segm

183 In contrast to the situation in slow muscles such as the soleus, the calcium concentrati

184 We describe three slow muscles that responded to low-frequency modulation

185 ivity is essential for proper development of slow muscle, the photoreceptor cell layer, branchial arc

186 The response of slow muscles to such inputs is little understood.

187 In addition, slow muscle twitch, tetanus tension, and susceptibility

188 m type IIB to IIX, concomitant with elevated slow muscle-type gene expression.

189 as in Drosophila embryonic muscle and other slow muscle types, a step associated with MgADP release

190 The impairments affect both fast and slow muscle types.

191 ibers formed from myoblasts derived from the slow muscle were cocultured with neural tube, the muscle

192 lite cells from either predominantly fast or slow muscles were indistinguishable from each other.

193 e two sets of alpha-actinin links, mammalian slow muscle Z-bands have six.