ライフサイエンスコーパス: cardiac muscle

1 wo Gtl2-Dio3 miRNAs, miR-410 and miR-495, in cardiac muscle.

2 rom troponin C and the rate of relaxation in cardiac muscle.

3 t and protein carbonylation were measured in cardiac muscle.

4 role in matching energy supply and demand in cardiac muscle.

5 least four Hax-1 transcripts in healthy rat cardiac muscle.

6 , a 65-kDa protein expressed in skeletal and cardiac muscle.

7 ribed to SCN5A, which is highly expressed in cardiac muscle.

8 ost appendages and injured organs, including cardiac muscle.

9 active alternative strategy for regenerating cardiac muscle.

10 ular lipid accumulation in both skeletal and cardiac muscle.

11 eptors, and termination of calcium sparks in cardiac muscle.

12 generation and necrosis of both skeletal and cardiac muscle.

13 Nav1.5 drive electrogenesis in skeletal and cardiac muscle.

14 itor cells develop into strongly contractile cardiac muscle.

15 ence of force-pCa relations in demembranated cardiac muscle.

16 Here, we characterize this pathway in cardiac muscle.

17 Phospholemman oligomers exist in cardiac muscle.

18 , and restores function in both skeletal and cardiac muscle.

19 um sensitivity and contractile efficiency of cardiac muscle.

20 2 months in skeletal muscle, but shorter in cardiac muscle.

21 impacted muscle compliance in Fhl1 knock-out cardiac muscle.

22 uired for excitation-contraction coupling in cardiac muscle.

23 normal levels in skeletal muscle, and 15% in cardiac muscle.

24 ting contractility and Ca(2+) sensitivity of cardiac muscle.

25 ed the effect of HSSTnT on the regulation of cardiac muscle.

26 pression in vascular SM, skeletal muscle, or cardiac muscle.

27 onsequences were analyzed in porcine skinned cardiac muscle.

28 ), thereby regulating calcium homeostasis in cardiac muscle.

29 eloping and maintaining somatic/skeletal and cardiac muscle.

30 isoforms of this transporter in skeletal and cardiac muscle.

31 l for the function of excitable tissues like cardiac muscle.

32 r substrates Irs1 and Irs2 in mouse skeletal/cardiac muscle.

33 acterized by impairment of both skeletal and cardiac muscle.

34 gamma1 subunit is not expressed, however, in cardiac muscle.

35 d regeneration of various tissues, including cardiac muscle.

36 nefficient energy utilization by the mutated cardiac muscle.

37 rapeutic overexpression of SERCA isoforms in cardiac muscle.

38 itation-contraction coupling in skeletal and cardiac muscle.

39 egulation of Ca(V)1 channels in skeletal and cardiac muscle.

40 ntributes to force-Ca(2+) dynamics of intact cardiac muscle.

41 uces the Ca(2+)-activated maximal tension of cardiac muscle.

42 role in matching energy supply and demand in cardiac muscle.

43 It also has an anti-inflammatory role in cardiac muscle.

44 Pip peptide-AOs demonstrate high activity in cardiac muscle.

45 eas alphaCAA and alphaSKA are coexpressed in cardiac muscle.

46 the force and kinetics of twitches in living cardiac muscle.

47 s potential impact on the function of intact cardiac muscle.

48 highly expressed in human adult skeletal and cardiac muscle.

49 sensitivity in streptozotocin (STZ) diabetic cardiac muscles.

50 itation-contraction coupling of skeletal and cardiac muscles.

51 surements in ventricular myocytes and intact cardiac muscles.

52 plasmic reticulum (SR) lumen in skeletal and cardiac muscles.

53 pression in autophagy-deficient skeletal and cardiac muscles.

54 ntly expressed at sarcomeres in skeletal and cardiac muscles.

55 0% activation (Ca(50)) in intact and skinned cardiac muscles.

56 ondrion-associated membranes in skeletal and cardiac muscles.

57 xpression of dystrophin in both skeletal and cardiac muscles.

58 the structure and physiology of skeletal and cardiac muscles.

59 phin expression in skeletal, respiratory and cardiac muscles.

60 In cardiac muscle, a subpopulation of phospholemman with a

61 t zebrafish and neonatal mice can regenerate cardiac muscle after injury, suggesting that latent rege

62 Zebrafish regenerate cardiac muscle after severe injuries through the activat

63 t in the mechanical properties of vertebrate cardiac muscle and essential to the flight muscles of mo

64 cardiac reprogramming factors generates new cardiac muscle and improved heart function after myocard

65 the authors reversed wasting of skeletal and cardiac muscle and increased life span by blocking ActRI

66 en shown to increase the power output of the cardiac muscle and is currently in clinical trials for t

67 yocarditis is an inflammatory disease of the cardiac muscle and is mainly caused by viral infections.

68 e peptides, most notably by phospholamban in cardiac muscle and sarcolipin in skeletal muscle.

69 g of Myocd exon 10a was a rare event in both cardiac muscle and SMC tissues.

70 ly shown that FKBP12 associates with RyR2 in cardiac muscle and that it modulates RyR2 function diffe

71 ) has enhanced capsid-associated tropism for cardiac muscle and the ability to cross the blood-brain

72 and -2 are highly expressed in skeletal and cardiac muscle and together with SUN (Sad1p/UNC84)-domai

73 DMD leads to degeneration of skeletal and cardiac muscles and to chronic inflammation.

74 ne that lead to degeneration of skeletal and cardiac muscles and to chronic inflammation.

75 s (IC50) estimated at 130, 19, and 9 microM (cardiac muscle) and 104, 13, and 5 microM (SkM SR).

76 increase of glucose uptake into skeletal and cardiac muscle, and a twofold increase in insulin signal

77 le in modulating mitochondrial metabolism in cardiac muscle, and Grx2 deficiency leads to pathology.

78 n when pre-established, in both skeletal and cardiac muscle, and improves skeletal muscle function.

79 (2+)-release channels (RyRs) of skeletal and cardiac muscle are essential for Ca(2+) release from the

80 Skeletal and cardiac muscles are remarkable biological machines that

81 lated differences in dystrophic skeletal and cardiac muscles as compared with their age-matched contr

82 all response to this stress may culminate in cardiac muscle atrophy.

83 ificant not only because LDA is prominent in cardiac muscle but also because it contributes to the Fr

84 tly modulating actin thin filament length in cardiac muscle by binding monomeric actin and limiting i

85 Most LMNA mutations affect skeletal and cardiac muscle by mechanisms that remain incompletely un

86 cardiomyopathies remains unclear, improving cardiac muscle Ca(2+) sensitivity through either pharmac

87 ile therapeutic strategy to restore diseased cardiac muscle Ca(2+) sensitivity.

88 The pH sensitivity of cardiac muscle can be reduced by replacing cardiac tropo

89 eart to work at a level much higher than the cardiac muscle can handle.

90 with heart failure, a condition with reduced cardiac muscle cBIN1, both of which support cBIN1 releas

91 ly, few methods can predict the state of the cardiac muscle cell and its metabolic conditions during

92 enrichment > 2) were identified, including 'cardiac muscle cell differentiation'.

93 rced expression of POPDC1(S201F) in a murine cardiac muscle cell line (HL-1) increased hyperpolarizat

94 Spontaneous Ca(2)(+) waves in cardiac muscle cells are thought to arise from the seque

95 the contractile strains produced by beating cardiac muscle cells can be optimized by substrate stiff

96 eton; their disruption within epithelial and cardiac muscle cells cause skin-blistering diseases and

97 about whether the epicardium is a source of cardiac muscle cells during heart development.

98 Cardiac muscle cells have an intrinsic ability to sense

99 lly results from a deficiency of specialized cardiac muscle cells known as cardiomyocytes, and a robu

100 e repair process, especially in skeletal and cardiac muscle cells, in which contraction-induced mecha

101 In cardiac muscle cells, spontaneous store overload-induced

102 sarcoplasmic reticulum (SR) in skeletal and cardiac muscle cells, where it is thought to bind to the

103 structural substates for SERCA expressed in cardiac muscle cells.

104 ) release through RyRs in neuronal cells and cardiac muscle cells.

105 lcNAcylation modulates DRP1 functionality in cardiac muscle cells.

106 sociation and underwent rapid endocytosis in cardiac muscle cells.

107 al differentiation of subtypes of neural and cardiac muscle cells.

108 te or inhibit contractility in demembranated cardiac muscle cells.

109 on of contractile genes in smooth muscle and cardiac muscle cells.

110 orm physical and functional connections with cardiac muscle cells.

111 Ca2+]i, regulate the contractile function of cardiac muscle cells.

112 l role in excitation-contraction coupling in cardiac muscle cells.

113 in with a role in the repair of skeletal and cardiac muscle cells.

114 t failure (HF), energy metabolism pathway in cardiac muscle changes from fatty acid beta-oxidation to

115 For cardiac-muscle channels (NaV1.5), reported effects from

116 t activation (LDA) is a prominent feature of cardiac muscle characterized by decreases in the Ca(2+)

117 Similarly, cardiac muscle (CM)-specific Plin5 overexpression (CM-Pl

118 osin light chain kinase is expressed only in cardiac muscle (cMLCK), similar to the tissue-specific e

119 y muscles was also restored in CRISPR-edited cardiac muscles compared with untreated controls.

120 The cardiac muscle comprises dynamically interacting compone

121 nflammation (miR-21, miR-146a), skeletal and cardiac muscle contractility (miR-21, miR-133a), and hyp

122 ypothesized that PI(3,5)P2 may also modulate cardiac muscle contractility by altering intracellular C

123 innovative therapeutic approaches to enhance cardiac muscle contractility.

124 into the modulatory role of this protein in cardiac muscle contractility.

125 nd explain the importance of alpha2beta2 for cardiac muscle contractility.

126 ,K-ATPase alpha2 subunit plays a key role in cardiac muscle contraction by regulating intracellular C

127 Myocardial depolarization leading to cardiac muscle contraction is reflected by the amplitude

128 ding myosin, the molecular motor that powers cardiac muscle contraction, and its accessory protein, c

129 to its central role as the Ca(2+) sensor for cardiac muscle contraction, troponin C (TnC) stands out

130 rk for understanding cMyBP-C's modulation of cardiac muscle contraction.

131 ed muscle thick filaments and a modulator of cardiac muscle contraction.

132 n cardiomyocytes and determines the force of cardiac muscle contraction.

133 actin and myosin that allows fine tuning of cardiac muscle contraction.

134 role in the activation of calcium-dependent cardiac muscle contraction.

135 r Mlc2 (Mlc2v) phosphorylation in regulating cardiac muscle contraction.

136 roteins play a key role in the regulation of cardiac muscle contraction.

137 that interacts with troponin I and initiates cardiac muscle contraction.

138 is a key molecule in the regulation of human cardiac muscle contraction.

139 ation of utilizing exclusively ssTnT in toad cardiac muscle corresponded to a fitness value from impr

140 urologic function as well as in skeletal and cardiac muscle defects.

141 flammation substantially affect skeletal and cardiac muscle degeneration in Duchenne muscular dystrop

142 aging of Drosophila skeletal muscle, but not cardiac muscle, despite the strong evolutionary conserva

143 The deletion of VEGF in cardiac muscle did not affect cardiac output.

144 aveolae in endothelial cells of the lung and cardiac muscle disassemble in response to acute increase

145 in (DES) mutations cause severe skeletal and cardiac muscle disease with heterogeneous phenotypes.

146 of RLC phosphorylation and its importance in cardiac muscle disease.

147 iac function, and mutations in cMyBP-C cause cardiac muscle disease.

148 DES mutations cause severe skeletal and cardiac muscle diseases with heterogeneous phenotypes.

149 In Trpm4(-/-) mice, cardiac muscle displays an increased beta-adrenergic ino

150 s and is caused by the lack of oxygen within cardiac muscles due to an imbalance between oxygen suppl

151 ut the contractile properties of human fetal cardiac muscle during development.

152 In cardiac muscle, dysferlin is located at the intercalated

153 itric-oxide-signaling cascade that increases cardiac muscle elasticity.

154 -like fiber orientation in both skeletal and cardiac muscle, enabling scale up of tissue constructs t

155 cited by exercise in the autophagy deficient cardiac muscle enhances whole-body metabolism, at least

156 tors, ion channels critical for skeletal and cardiac muscle excitation-contraction coupling and synap

157 Upon activation, contraction of cardiac muscle expels blood into the circulation.

158 in Escherichia coli confirmed that the toad cardiac muscle expresses solely ssTnT, predominantly the

159 sufficient ability to replenish the damaged cardiac muscles, extensive research has been devoted tow

160 Cardiac muscle fiber mechanic studies demonstrate cross-

161 s a noted restoration in the architecture of cardiac muscle fibers and a reduction in the extent of f

162 tergent-skinned guinea pig (Cavia porcellus) cardiac muscle fibers in the absence and presence of 0.3

163 RfsT1-RcT2- and RcT1-RfsT2-reconstituted rat cardiac muscle fibers were captured by fitting the recru

164 conformational behavior of N-cTnC in skinned cardiac muscle fibers.

165 It can be observed in both skeletal and cardiac muscle fibers.

166 Detergent-skinned cardiac muscle fibre bundles were used to study how the

167 Cardiac muscle fibres from these mice contained approxim

168 licated a wide range of molecular targets in cardiac muscle for the major green tea catechin, (-)-epi

169 lation plays an important role in modulating cardiac muscle function and accelerating contraction.

170 vs. cardiac isoforms of either TnI or MHC on cardiac muscle function and contractile dynamics.

171 Myocardial mass is a key determinant of cardiac muscle function and hypertrophy.

172 n to be implicated in lung, reproductive and cardiac muscle function and in the cause of cancer.

173 ng mechanisms underlying titin regulation in cardiac muscle function is of critical importance given

174 Skeletal and cardiac muscle function, inflammation, regeneration, his

175 Ca storage organelle, is critical for proper cardiac muscle function.

176 ction pathways are critical for skeletal and cardiac muscle function.

177 ell (SC) exhaustion and loss of skeletal and cardiac muscle function.

178 disease-related changes in cTnT isoforms on cardiac muscle function.

179 ing protein, are critical to maintain proper cardiac muscle function; however, the connection between

180 se of Ca from intracellular stores is key to cardiac muscle function; however, the molecular control

181 multiple cellular lineages, but its role in cardiac muscle has remained unclear.

182 Force and power in cardiac muscle have a known dependence on phosphorylatio

183 The contractile properties of human fetal cardiac muscle have not been previously studied.

184 he original GDF11 hypothesis in skeletal and cardiac muscle have not been validated by several indepe

185 h, the cellular origins of newly regenerated cardiac muscle have remained unclear.

186 muscle type than species: slow skeletal and cardiac muscles have wider Z-bands than fast skeletal mu

187 dystrophin protein in skeletal myofibers and cardiac muscle, improvement of muscle biochemistry, and

188 gene cmlc2 before injury, each labelled most cardiac muscle in the ensuing regenerate.

189 stained myosin filaments isolated from human cardiac muscle in the normal (undiseased) relaxed state.

190 ed subtomogram averaging of tomograms of rat cardiac muscle in which subtomograms are extracted and c

191 the importance of treating both skeletal and cardiac muscles in DMD therapy.

192 undamental force-generating machinery of the cardiac muscle, including beta-cardiac myosin.

193 KA, which phosphorylates multiple targets in cardiac muscle, including the cardiac ryanodine receptor

194 has revealed severe myofibrillar defects in cardiac muscle indicating a requirement for Mef2A in cyt

195 le disease mechanisms affecting skeletal and cardiac muscles, inflammatory cells, brain, and bone.

196 However, cardiac muscle is also a subtype of striated muscle and

197 osphorylation of these sites in skeletal and cardiac muscle is directly involved in calcium channel r

198 on of similar macromolecular organization in cardiac muscle is missing.

199 phosphorylated RLC region of myosin heads in cardiac muscle is primarily determined by an interaction

200 region of the myosin heads on activation of cardiac muscle is small; the RLC regions of most heads r

201 Contraction of skeletal and cardiac muscles is regulated by Ca(2+) binding to tropon

202 take in many tissues, including skeletal and cardiac muscle, is not sufficient to silence target mess

203 tions cause a severe phenotype especially in cardiac muscle leading to cardiomyopathy that can be let

204 In the heart, calcification of cardiac muscle leads to conduction system disturbances a

205 negative regulator of postnatal skeletal and cardiac muscle mass and modulates metabolic processes.

206 Thus, RLC phosphorylation in cardiac muscle may be regulated by two different protein

207 nction in cardiomyocytes and suggest that in cardiac muscle, MCL-1 also facilitates normal mitochondr

208 ory light chain (RLC) phosphorylation alters cardiac muscle mechanics is important because it is ofte

209 Thus, mtCU "hot spots" can be formed at the cardiac muscle mitochondria-SR associations via localiza

210 In cardiac muscle, mitochondrial ATP synthesis is driven by

211 chain (RLC) phosphorylation in skeletal and cardiac muscles modulates Ca(2+)-dependent troponin regu

212 In this review, we focus on mutations in the cardiac muscle molecular motor, myosin, and its associat

213 ng the dominant splice variants expressed in cardiac muscle (Myocd_v1 and v2) versus SMC-rich tissues

214 tension and the time course of relaxation in cardiac muscle myofibrils.

215 omecamtiv mecarbil (OM) specifically targets cardiac muscle myosin and is known to enhance cardiac mu

216 atomical location affected: skeletal muscle, cardiac muscle, neuromuscular junction, peripheral nerve

217 he marked increase in ATGL protein levels in cardiac muscle of CGI-58KOM mice was unable to compensat

218 e exercise induces autophagy in skeletal and cardiac muscle of fed mice.

219 e the migration of gammadelta T cells to the cardiac muscle of mdx mice and to characterize their phe

220 Here we report an exception that the cardiac muscle of toad (Bufo) expresses exclusively slow

221 aling, reduced Cthrc1 levels in skeletal and cardiac muscles of mice, representing DMD, CMD, and dysf

222 repeat containing 1 (Cthrc1) in skeletal and cardiac muscles of mice, representing Duchenne and conge

223 MR) techniques, we compared the skeletal and cardiac muscles of two different dystrophic mouse models

224 Injury to the cardiac muscle often leads to heart failure due to the l

225 human-induced pluripotent stem cell-derived cardiac muscle patch (hCMP), which was subsequently eval

226 ardiac muscle myosin and is known to enhance cardiac muscle performance, yet its impact on human card

227 inhibitor (sildenafil) improves skeletal and cardiac muscle performance.

228 urdles such as extremely low efficacy in the cardiac muscle, poor cellular uptake and relatively rapi

229 on of cryoablation lesions in blood-perfused cardiac muscle preparations and revealed similarities an

230 m the sarcoplasmic reticulum of skeletal and cardiac muscle preparations, its mechanism of action has

231 2+) sensitivity of contraction and ATPase in cardiac muscle preparations.

232 ird clonal population of common skeletal and cardiac muscle progenitor cells within cardiopharyngeal

233 c is essential to activate both skeletal and cardiac muscle programs.

234 ve than Myocd_v3 and Myocd_v4 in stimulating cardiac muscle promoters and Myocd_v1's activity was aug

235 trast, zebrafish efficiently regenerate lost cardiac muscle, providing a model for understanding how

236 nese quail myoglobin was isolated from quail cardiac muscles, purified using ammonium sulphate precip

237 In addition to its known effects on cardiac muscle, recent in vitro and in vivo evidence hig

238 iPs engrafted and repaired both skeletal and cardiac muscle, reducing functional defects.

239 r results indicate that electrically coupled cardiac muscle regenerates after resection injury, prima

240 Yet, there is little or no significant cardiac muscle regeneration after an injury such as acut

241 (ECM) directs cell activities essential for cardiac muscle regeneration.

242 ntricular apex and contribute prominently to cardiac muscle regeneration.

243 ic cardiomyopathy, characterized by impaired cardiac muscle relaxation and force development.

244 The rate-limiting step of cardiac muscle relaxation has been proposed to reside in

245 for example, myosin light chain-2 [MLC2]) in cardiac muscle remain poorly understood.

246 s capable of recovering or replacing damaged cardiac muscle require physiologically relevant environm

247 els that are highly enriched in skeletal and cardiac muscle, respectively, where they play an essenti

248 ~50% decrease in capillaries in skeletal and cardiac muscle, respectively.

249 ype I (RyR1) and II (RyR2) from skeletal and cardiac muscle, respectively.

250 Cardiac muscle restitution, or true regeneration, is an

251 Similarly, inactivation of Lig3 in cardiac muscle resulted in mitochondrial dysfunction and

252 ctural and metabolic changes in skeletal and cardiac muscles resulting in greater endurance capacity.

253 se A (PKA) phosphorylates class IIa HDACs in cardiac muscle, resulting in HDAC nuclear accumulation,

254 skeletal muscle, and L-type Ca(2+) entry in cardiac muscle, revealing a mechanism by which TCS weake

255 dentical to the 2460-2495 segment within the cardiac muscle RyR isoform (RyR2) central domain.

256 While exclusion of exon 2a was common in all cardiac muscle samples, exon skipping of Myocd exon 10a

257 In cardiac muscle, SERCA is regulated by phospholamban (PLB

258 ovascular system (such as endothelial cells, cardiac muscle, smooth muscle, inflammatory cells, and f

259 everal tissues; yet the role of skeletal and cardiac muscle-specific autophagy on the benefits of exe

260 lar system and present evidence supporting a cardiac muscle-specific effect of n-6 PUFAs.

261 Skeletal- and cardiac-muscle-specific SRF knockouts resulted in signif

262 single cardiac myofibrils and multicellular cardiac muscle strips of three HCM patients with the R40

263 Understanding the time course of human fetal cardiac muscle structure and contractile maturation can

264 signaling and beta-adrenergic regulation in cardiac muscle, suggesting a potential target for the tr

265 n, ventricular wall thickness, angiogenesis, cardiac muscle survival, and reducing fibrosis and infla

266 Here, using the cardiac muscle system, we demonstrate that nuclear recep

267 h (-)-epicatechin treatment for hindlimb and cardiac muscles than exercise alone.

268 In mammalian skeletal and cardiac muscle, the Tm is expressed from two separate ge

269 ined troponin organization on native relaxed cardiac muscle thin filaments by applying single particl

270 whereas MV is mainly expressed in smooth and cardiac muscle tissue.

271 In striated muscle, including involuntary cardiac muscle, Tm regulates muscle contraction by coupl

272 sfunction and blunted lusitropic response of cardiac muscle to beta-adrenergic stimulation indicate a

273 ction and blunted the inotropic responses of cardiac muscle to beta-adrenergic stimuli without abolis

274 brillin 1 in the physiological adaptation of cardiac muscle to elevated workload.

275 dystrophin protein expression in dystrophic cardiac muscles to a level approaching 40%.

276 ately in the thick and thin filaments of rat cardiac muscle, to elucidate that mechanism.

277 almost twofold higher for smooth compared to cardiac muscle tropomyosin.

278 in this allosteric/cooperative mechanism is cardiac muscle troponin T (cTnT), the central region (CR

279 anisms produced early defects in the rate of cardiac muscle twitch relaxation and ventricular torsion

280 Our analyses suggest that CIA is present in cardiac muscle under normal conditions and that its modu

281 Ca(2+) release that has been reported in the cardiac muscle under stress conditions.

282 ation and relaxation kinetics of human fetal cardiac muscle under well-controlled conditions.

283 ce deficient for the Klf4 gene in smooth and cardiac muscle using the SM22alpha promoter (SM22alpha-C

284 ully isolated thick filaments from zebrafish cardiac muscle, using a procedure similar to those for m

285 esistance in chow-fed mice with skeletal and cardiac muscle VEGF deletion (mVEGF(-/-)) and wild-type

286 However, neither extraocular nor cardiac muscle was affected in double-knockout animals.

287 mice, glycogen accumulation in skeletal and cardiac muscles was not affected, but glycogen content i

288 dystrophin loss that results in skeletal and cardiac muscle weakening and early death.

289 Defects in cardiac muscle were marked by reduced heart rate and in

290 essed as the greatest in skeletal muscle and cardiac muscle where it localized to the nucleus.

291 nt a model of Ca-regulated thin filaments in cardiac muscle where tropomyosin is treated as a continu

292 SPEG is present in cardiac muscle, where it plays a critical role; therefor

293 e in other muscle systems, such as mammalian cardiac muscle, where stretch activation is thought to a

294 applied load, in qualitative agreement with cardiac muscle, which contracts with a velocity inversel

295 ase in glycogen accumulation in skeletal and cardiac muscles, which in some cases is associated with

296 ic KKAy mice by increasing glucose uptake in cardiac muscle, white adipose tissue, and brown adipose

297 racterized MLCK, MLCK4, is also expressed in cardiac muscle with high catalytic domain sequence simil

298 exhibit abundant expression in skeletal and cardiac muscle with very low levels in SMC-containing ti

299 ression in all skeletal muscles and </=5% in cardiac muscle, with improvement in muscle function and

300 OBEC2 mRNA was most abundant in skeletal and cardiac muscle, with relatively low expression in the go