ライフサイエンスコーパス: muscle protein

1 of lipid stores, and severe loss of skeletal muscle protein.

2 at accompany stress states favor the loss of muscle protein.

3 ic dystrophy does not eliminate an essential muscle protein.

4 cts the intense oxidative degradation of the muscle proteins.

5 y demonstrations linking FHC to mutations in muscle proteins.

6 ns, which form an important class of ABDs in muscle proteins.

7 known structures of similar ABDs from other muscle proteins.

8 tial for the accelerated degradation of most muscle proteins.

9 fiber-type switching, and the degradation of muscle proteins.

10 oteasome, which increases the degradation of muscle proteins.

11 nergistically to increase the degradation of muscle proteins.

12 he effects of disease-producing mutations in muscle proteins.

13 in is one of the least well understood major muscle proteins.

14 nfluencing both synthesis and degradation of muscle proteins.

15 ells induced SM actin, calponin1, and smooth muscle protein 22-alpha (SM22alpha) in a dose- and time-

16 nx2, increased expression of vascular smooth muscle protein 22-alpha, and restored aortic expression

17 nd vascular smooth muscle cells using smooth muscle protein 22-driven Cre recombinase (SMGRKO mice) a

18 e recombinase allele regulated by the smooth muscle protein-22 (SM22) promoter (Tsc1c/cSM22cre+/-) to

19 Mice with smooth muscle protein-22alpha promotor-driven deficiency of the

20 t of resistance-type exercise stimulates net muscle protein accretion during acute postexercise recov

21 Hindlimb weight, linear growth rate, muscle protein accretion rate and fractional synthetic r

22 ncy that develop to slow hindlimb growth and muscle protein accretion.

23 not impair the ability to acutely synthesize muscle protein after ingestion of a common protein-rich

24 importance of the degradation of individual muscle proteins after exercise in human skeletal muscle.

25 ptic membranes of muscles and binding to the muscle protein alpha-dystroglycan through its glycan cha

26 increasing physical activity can enhance the muscle protein anabolic effect of essential amino acid (

27 ability during hyperinsulinemia improves the muscle protein anabolic effect of insulin in older adult

28 le in stimulating translation initiation and muscle protein anabolism and is the focus of ongoing res

29 ke beyond 0.8 g x kg(-1) x d(-1) may enhance muscle protein anabolism and provide a means of reducing

30 hypothesized that aerobic exercise restores muscle protein anabolism in response to insulin by impro

31 Our objective was to measure muscle protein anabolism in response to Leu and its meta

32 Nutrient stimulation of muscle protein anabolism is blunted with aging and may c

33 ein diet may provide a stimulatory effect on muscle protein anabolism, favoring the retention of lean

34 sotopically label newly synthesized skeletal muscle proteins and DNA.

35 There were correlations between log K(pw) of muscle proteins and log K(ow) (R(2) = 0.83-0.86, SD: 0.3

36 and simultaneous identification of skeletal muscle proteins and peptides as well as other components

37 etic ablation of TWEAK decreases the loss of muscle proteins and spared fiber cross-sectional area, m

38 Loss of muscle proteins and the consequent weakness has importan

39 neration, including strong downregulation of muscle proteins and upregulation of oncogenes, developme

40 cell phenotype, as levels of critical smooth muscle proteins are gradually reduced in mutant mice.

41 Because breakdown did not change, net muscle protein balance became positive only in the EX gr

42 e administration results in a more favorable muscle protein balance in severely burned patients.

43 on to assess muscle protein synthesis (MPS), muscle protein breakdown (MPB), and muscle mass by using

44 HMB consumption also attenuated muscle protein breakdown (MPB; -57%) in an insulin-indep

45 that Ang II, via its type 1 receptor, causes muscle protein breakdown and apoptosis and inhibits sate

46 study was to develop a method for detecting muscle protein breakdown and assess the effectiveness of

47 Identified mediators of muscle protein breakdown include inflammation, metabolic

48 -1 and muscle ring finger 1 (MuRF1), mediate muscle protein breakdown through the ubiquitin proteasom

49 known to regulate proteasomal and lysosomal muscle protein breakdown was also evident.

50 From the perspective of muscle protein breakdown, muscle-specific E3-ligases (MA

51 Because IL-6 stimulates muscle protein breakdown, we conclude that CKD increases

52 ription can lead to enhanced proteolysis and muscle protein breakdown.

53 in synthesis with no apparent stimulation of muscle protein breakdown; furthermore, muscle of immobil

54 indicated that systemic inflammation induces muscle-protein breakdown and wasting via muscular nuclea

55 fic analysis and differentiation of skeletal muscle proteins by direct surface desorption.

56 ting suggests that the reversible binding to muscle proteins can be considered to be nonspecific bind

57 clude membrane and storage lipids, serum and muscle proteins, carbohydrates, algae, mussels, polydime

58 During the cleavage of muscle proteins, caspase-3 leaves behind a characteristi

59 on of dietary uptake, de novo synthesis, and muscle protein catabolism.

60 TLR4 muscle protein content correlated with the severity of i

61 terations more than loss of myosin and other muscle protein content.

62 malities in insulin/IGF-I signaling activate muscle protein degradation in the UPS and caspase-3, a p

63 lly in skeletal muscle (mXIAP) and evaluated muscle protein degradation induced by CKD.

64 ic conditions, it was found that accelerated muscle protein degradation is triggered by activation of

65 Under these conditions, activation of muscle protein degradation requires endogenous glucocort

66 en to mice with muscle-specific IR deletion, muscle protein degradation was accelerated.

67 n, at the level of PDC, and up-regulation of muscle protein degradation, in LPS-induced endotoxaemia.

68 function, and decreased muscle fibrosis and muscle protein degradation.

69 uence of the GR contributes to activation of muscle protein degradation.

70 ubiquitination pathway in the physiology of muscle protein degradation.

71 There was a 29% reduction in the muscle protein: DNA ratio, a 56% reduction in pyruvate d

72 evented the LPS-induced 40% reduction in the muscle protein:DNA ratio and decrease in Akt phosphoryla

73 The muscle protein Dok-7 is essential for activation of the

74 y affected due to oxidative modifications of muscle proteins during its processing.

75 Deficiency of the vital muscle protein dystrophin triggers Duchenne/Becker muscu

76 gene leading to the absence of the essential muscle protein dystrophin.

77 permits evaluation of turnover of plasma and muscle proteins (e.g. dynamic proteomics) in addition to

78 after exercise accompanied enhanced skeletal muscle protein expression of key lipogenic enzymes and a

79 ly, chronic binge alcohol increased skeletal muscle protein expression of protein-tyrosine phosphatas

80 was increased in the presence of denervated muscle protein extracts.

81 body protein synthesis per fat-free mass and muscle protein fractional synthesis rate (FSR) were lowe

82 to quantify whole-body protein breakdown and muscle protein fractional synthesis rate using liquid ch

83 To quantify skeletal muscle protein fractional synthesis rates, a flooding do

84 ay in the training period by measurements of muscle protein fractional synthetic rate and phosphoryla

85 Protein synthesis measured by the muscle protein fractional synthetic rate was depressed i

86 Muscle protein from sardine (Sardina pilchardus) and hor

87 Muscle proteins from sardine (Sardina pilchardus) and sm

88 eutral organic chemicals were measured using muscle proteins (from chicken, fish, and pig), collagen

89 Muscle protein functionality plays an important role in

90 teins, K(pw) values were often in the order: muscle proteins > collagen >/= gelatin.

91 eversible event in SMA and also suggest that muscle proteins have the potential to act as novel bioma

92 oding Muscle RING Finger 1 (MuRF1) maintains muscle protein homeostasis by tagging the sarcomere prot

93 Skeletal muscle protein homeostasis during HD also improved with

94 isphosphate, and studied how PTEN influences muscle protein in diabetic wild-type mice and in mice wi

95 st to address the requirement for a specific muscle protein in trichinellosis by using mice deficient

96 ges in protein unfolding in vivo in skeletal muscle proteins in ALS mice.

97 Ectopic Arf expression induced smooth muscle proteins in cultured pericyte-like cells, and Arf

98 in DM were deficient in a number of skeletal muscle proteins including titin.

99 eceptor recycling and mislocalization of key muscle proteins, including caveolin-3 and Fer1L5, a rela

100 esulting in elevated oxidization of skeletal muscle proteins, including the ryanodine receptor and ca

101 ce model we detected alterations in skeletal muscle proteins involved in BCAA metabolism but not in o

102 ence supporting a role for specific skeletal muscle proteins involved in intramyocellular lipids, mit

103 thesized that the expression of key skeletal muscle proteins involved in lipid droplet hydrolysis, DA

104 We found that the partitioning to muscle protein is typically weaker than that to lipids,

105 How expression of muscle proteins is coordinated to build the myofibril is

106 In cardiac myocytes, the muscle protein kinase A-anchoring protein beta (mAKAPbet

107 Muscle protein kinetic rates were measured using isotopi

108 normalization of hormonal influence improves muscle protein kinetics and ameliorates the loss of musc

109 an target of rapamycin (mTOR) signaling, and muscle protein kinetics in response to physiological loc

110 dy in this muscle injury model decreased the muscle protein levels of lymphotoxin alpha and Il17a by

111 els of the long isoform of TBC1D4, and lower muscle protein levels of the glucose transporter GLUT4,

112 ux through a number of different substrates (muscle proteins, lipids, glucose, DNA (satellite cells))

113 ificantly reduce muscle atrophy, and inhibit muscle protein loss and DNA loss, even when given after

114 hout acute hospital stay and had significant muscle protein loss as demonstrated by a negative muscle

115 TNF-alpha directly increased net muscle protein loss, which may contribute to cachexia an

116 ation blocks atrogin1/MAFbx upregulation and muscle protein loss.

117 on of metabolic acidosis, which can suppress muscle protein losses in patients with CKD who are or ar

118 could be a compensatory mechanism to prevent muscle protein losses.

119 neuronally derived ligand, and the following muscle proteins: LRP4, the receptor for Agrin; MuSK, a r

120 LP and E-UN offspring, but in L-UN offspring muscle protein mass remained significantly smaller even

121 umans.We aimed to compare the whole-body and muscle protein metabolic responses after the consumption

122 To assess muscle protein metabolic responses to varied protein int

123 estoring hormonal levels and/or influence on muscle protein metabolism in the stressed state.

124 Muscle protein metabolism is resistant to insulin's anab

125 Skeletal muscle protein metabolism is resistant to the anabolic a

126 Muscle protein metabolism was determined by stable isoto

127 okines, defects in IGF-1 signaling, abnormal muscle protein metabolism, and progressive muscle atroph

128 restores the effects of feeding on skeletal muscle protein metabolism.

129 ent study, we tested the hypothesis that the muscle protein myostatin is involved in mediating the pa

130 e protein loss as demonstrated by a negative muscle protein net balance (-0.05% +/- 0.007 nmol/100 mL

131 Females had a significant attenuated loss in muscle protein net balance (females: -0.028+/-0.001% vs.

132 This decrease is reflected in improved muscle protein net balance and preservation of lean body

133 ting in a significant increase (P < 0.05) in muscle protein net balance.

134 ic burn patients at 6 months postinjury, leg muscle protein net deposition is unresponsive to amino a

135 Caenorhabditis elegans homolog of the giant muscle protein obscurin, UNC-89, is required for normal

136 lored for the first time to analyze skeletal muscle proteins obtained from a mixture of standard prot

137 These data indicate that Fstl1 is a secreted muscle protein or myokine that can function to promote e

138 ive processes, and a concomitant increase in muscle protein oxidation.

139 ent through extensive qualitative changes in muscle protein pattern following ULLS, and these were re

140 markers and appearance of expression of non-muscle proteins ("proliferative phenotype").

141 d biomarker, autoantibodies against a 43-kDa muscle protein reported in 2011, has now been identified

142 Loss of skeletal muscle protein results from an imbalance between the rat

143 compared to those of squid (Dosidicus gigas) muscle proteins (SM).

144 ter and enhanced the degradation of specific muscle proteins such as CK and MyHCf.

145 ctin promoter and the expression of specific muscle proteins such as myosin heavy chain fast type and

146 creased mTOR/S6 kinase 1 phosphorylation and muscle protein synthesis (EX group: 49 +/- 11 to 89 +/-

147 rinsulinemia-induced increase in the rate of muscle protein synthesis (from 0.009 +/- 0.005%/h above

148 in degradation (cachexia), decreased rate of muscle protein synthesis (inactivity), or an alteration

149 mentation had no effect on the basal rate of muscle protein synthesis (mean +/- SEM: 0.051 +/- 0.005%

150 he potential role of supplemental leucine on muscle protein synthesis (MPS) and associated molecular

151 get of rapamycin on ribosome biogenesis, and muscle protein synthesis (MPS) and degradation.

152 estigated the relationship between long-term muscle protein synthesis (MPS) and hypertrophic response

153 old) participated in a study that determined muscle protein synthesis (MPS) and leg protein breakdown

154 However, muscle protein synthesis (MPS) and mitochondrial biogene

155 Muscle protein synthesis (MPS) fluctuates widely over th

156 We previously showed that human muscle protein synthesis (MPS) increased during infusion

157 Muscle protein synthesis (MPS) is the driving force behi

158 akes, stimulates a greater acute response of muscle protein synthesis (MPS) to protein ingestion in r

159 sies were taken at 3 and 6 weeks to quantify muscle protein synthesis (MPS) via gas chromatography-py

160 Muscle protein synthesis (MPS) was measured using [1, 2-

161 to determine mitochondrial and myofibrillar muscle protein synthesis (MPS) when carbohydrate (CHO) o

162 lator of translation initiation and skeletal muscle protein synthesis (MPS), can protect skeletal mus

163 and ~6 wk after surgical resection to assess muscle protein synthesis (MPS), muscle protein breakdown

164 cle and, similarly to 3.42 g Leu, stimulated muscle protein synthesis (MPS; HMB +70% vs. Leu +110%).

165 Resistance exercise increases muscle protein synthesis acutely, and muscle mass with t

166 , which leads to the stimulation of skeletal muscle protein synthesis after ingestion of a meal that

167 synthesis rates and the ability to increase muscle protein synthesis after protein ingestion.

168 ry recruitment would improve the response of muscle protein synthesis and anabolism to insulin.

169 cirrhosis that results in impaired skeletal muscle protein synthesis and breakdown (proteostasis).

170 se training (RET) has a beneficial effect on muscle protein synthesis and can be augmented by protein

171 We evaluated the control of muscle protein synthesis and degradation in mouse models

172 debate concerning the relative importance of muscle protein synthesis and degradation to muscle mass

173 esults from an imbalance between the rate of muscle protein synthesis and degradation.

174 the habitual intake is associated with lower muscle protein synthesis and higher proteolysis rates, w

175 he habitual intake is associated with higher muscle protein synthesis and lower proteolysis rates.

176 We measured muscle protein synthesis and mTOR-associated upstream an

177 Muscle protein synthesis and mTORC1 signalling are concu

178 esistance exercise is a potent stimulator of muscle protein synthesis and muscle cell growth, with th

179 otential site for the regulation of skeletal muscle protein synthesis and muscle mass, it does not ap

180 Muscle protein synthesis and net balance (nmol . min(-1)

181 controversy over the effects of older age on muscle protein synthesis and proteolysis rates.

182 The rate of muscle protein synthesis and the phosphorylation of key

183 Signaling pathways that regulate muscle protein synthesis at the translational level are

184 AMPK activation decreases muscle protein synthesis by inhibiting mTOR signalling t

185 he TOR pathway plays a key role in promoting muscle protein synthesis by inhibition of eIF4EBPs (euka

186 the cellular mechanism for the inhibition of muscle protein synthesis during an acute bout of resista

187 s of dietary protein on body composition and muscle protein synthesis during energy deficit (ED).

188 on, phenylalanine delivery, net balance, and muscle protein synthesis during the consumption of EAA+s

189 form essential amino acids acutely stimulate muscle protein synthesis in both the young and the elder

190 ma amino acid concentrations and to quantify muscle protein synthesis in healthy young (41 +/- 8 y ol

191 TORC1 signalling is essential for regulating muscle protein synthesis in humans, we treated subjects

192 ating the contraction-induced stimulation of muscle protein synthesis in humans, while dual activatio

193 Omega-3 fatty acids stimulate muscle protein synthesis in older adults and may be usef

194 -3 fatty acid supplementation on the rate of muscle protein synthesis in older adults.

195 ake distribution across meals increased 24-h muscle protein synthesis in young adults compared with a

196 However, by 1-2 h post-exercise, muscle protein synthesis increased in association with a

197 Muscle protein synthesis increased only in the young dur

198 ent studies show that during energy deficit, muscle protein synthesis is down-regulated with concomit

199 Muscle protein synthesis is increased after exercise, bu

200 otein kinetics does not significantly reduce muscle protein synthesis or increase proteolysis.

201 orn oil supplementation had no effect on the muscle protein synthesis rate and the extent of anabolic

202 During amino acid infusion, leg muscle protein synthesis rate significantly increased (P

203 ein synthesis rates or increase postprandial muscle protein synthesis rates after ingestion of 25 g p

204 ein synthesis rates or increase postprandial muscle protein synthesis rates after ingestion of 25 g p

205 ared with HIGH PRO on basal and postprandial muscle protein synthesis rates after the ingestion of 25

206 ared with HIGH PRO on basal and postprandial muscle protein synthesis rates after the ingestion of 25

207 ss maintenance is largely regulated by basal muscle protein synthesis rates and the ability to increa

208 s and blood samples were collected to assess muscle protein synthesis rates as well as dietary protei

209 Skeletal muscle protein synthesis rates did not differ between tr

210 Excess body fat diminishes muscle protein synthesis rates in response to hyperinsul

211 validated a strategy for monitoring skeletal muscle protein synthesis rates in rodents and humans ove

212 Muscle protein synthesis rates increased from 0.031% +/-

213 Muscle protein synthesis rates increased from 0.031% +/-

214 Slower hindlimb linear growth and muscle protein synthesis rates match reduced hindlimb bl

215 in the circulation and does not lower basal muscle protein synthesis rates or increase postprandial

216 in the circulation and does not lower basal muscle protein synthesis rates or increase postprandial

217 emonstrate slower hindlimb linear growth and muscle protein synthesis rates that match the reduced hi

218 tors other than protein intake explain lower muscle protein synthesis rates with advanced age.

219 this does not result in greater postprandial muscle protein synthesis rates.

220 l as whole-body protein balance and skeletal muscle protein synthesis rates.

221 ein after exercise did not increase skeletal muscle protein synthesis rates.

222 r resistance exercise increases postexercise muscle protein synthesis rates.

223 protein-dense foods to augment postexercise muscle protein synthesis rates.

224 Insulin and IGF-1 enhance muscle protein synthesis through their receptors, but th

225 e of immobilized legs is unable to stimulate muscle protein synthesis to the same extent as that of n

226 that a sex difference exists in the rate of muscle protein synthesis under postabsorptive conditions

227 ute and potent stimulation of human skeletal muscle protein synthesis via enhanced translation initia

228 s of other amino acids and as a modulator of muscle protein synthesis via the insulin-signaling pathw

229 Muscle protein synthesis was determined by stable isotop

230 efore refeeding, and 2, 7 and 21 days later, muscle protein synthesis was measured in vivo.

231 position and postabsorptive and postprandial muscle protein synthesis were assessed during WM (d 9-10

232 by their capacity to upregulate postprandial muscle protein synthesis when refed (P < 0.001), a diffe

233 Immobility per se causes a decrease in muscle protein synthesis with no apparent stimulation of

234 kt/mTORC1 signaling by Western blotting; and muscle protein synthesis, amino acid, and glucose kineti

235 tenuates intracellular proteolysis, restores muscle protein synthesis, and mitigates skeletal muscle

236 In addition, muscle protein synthesis, breakdown rates, and respectiv

237 In contrast, muscle protein synthesis, DNA, and phospholipid synthesi

238 on profile, organ function, hypermetabolism, muscle protein synthesis, incidence of wound infection s

239 DNA transcription has been proposed to limit muscle protein synthesis, making ribosome biogenesis cen

240 Ingestion of EAC significantly increased muscle protein synthesis, modestly reduced AMPK phosphor

241 nsitive mTOR in the RE-induced activation of muscle protein synthesis, ribosome biogenesis, PGC-1alph

242 enhances nitrogen retention and up-regulates muscle protein synthesis, which in turn may promote posi

243 moderately high-protein meals improves 24-h muscle protein synthesis.

244 reduced (by approximately 40%) efficiency of muscle protein synthesis.

245 uired for full stimulation of human skeletal muscle protein synthesis.

246 duced increase ( approximately 40%) in human muscle protein synthesis.

247 vents in humans, particularly in relation to muscle protein synthesis.

248 underpinned by chronic deficits in long-term muscle protein synthesis.

249 t only partially inhibited the activation of muscle protein synthesis.

250 of acutely increasing lipid availability on muscle protein synthesis.

251 acid involved in the regulation of skeletal muscle protein synthesis.

252 P)-containing meals may overcome the blunted muscle protein synthetic response to food intake in the

253 rotein intake (HIGH PRO) on the postprandial muscle protein synthetic response.

254 However, muscle protein synthetic responses after the ingestion o

255 so known as connectin) is an intrasarcomeric muscle protein that functions as a molecular spring and

256 inally, we identified mutations in genes for muscle proteins that affect axon pathways by distorting

257 question, we biochemically isolated skeletal muscle proteins that associate with Gadd45a as it induce

258 could be used to induce aggregation of fish muscle proteins, thereby improving gelling property of f

259 reas of protein mechanics: elasticity of the muscle protein titin and the extracellular matrix protei

260 This review uses the giant muscle protein titin as an example to showcase the capab

261 , and lysine-rich (PEVK) domain of the giant muscle protein titin is thought to be an intrinsically u

262 of one of the immunoglobulin domains of the muscle protein titin using molecular dynamics simulation

263 s those encoding olfactory receptors and the muscle protein titin), suggesting extensive false-positi

264 For the mechanostable muscle protein titin, a highly ductile model reconciles

265 and A168-A169, from the A-band of the giant muscle protein titin, reveal that they form tightly asso

266 Inspired by skeletal muscle protein titin, we have synthesized a biomimetic m

267 ce of extensive myopathy or a decline in the muscle protein to DNA ratio.

268 ion, metabolic pathways, or the breakdown of muscle proteins to amino acids used in gluconeogenesis o

269 c exercise restores the anabolic response of muscle proteins to insulin by improving endothelial func

270 tease that disrupts the complex structure of muscle proteins to provide substrates for the UPS.

271 s protein mass by appropriate stimulation of muscle protein turnover and inhibition of protein breakd

272 balance on the regulation of human skeletal muscle protein turnover are not well described.

273 function with age, the effect of obesity on muscle protein turnover in older adults remains unknown.

274 the effect of tumor burden and resection on muscle protein turnover in patients with nonmetastatic c

275 Accurate measurement of muscle protein turnover is critical for understanding th

276 muscle microvascular blood volume (MBV) and muscle protein turnover under post-absorptive and fed st

277 p between energy status, protein intake, and muscle protein turnover, and explores future research di

278 ct of critical illness on muscle morphology, muscle protein turnover, and the associated muscle-signa

279 R signaling is critical to the regulation of muscle protein turnover, and this regulation depends on

280 action and stretch have different effects on muscle protein turnover, but little is known about the m

281 To examine whether PTEN affects muscle protein turnover, we studied primary myotubes cul

282 used by ill-defined catabolic alterations in muscle protein turnover.

283 s ubiquitin E3 ligases in ubiquitin-mediated muscle protein turnover.

284 or its close homolog, PGC-1beta, influences muscle protein turnover.

285 cer-induced alterations in the regulation of muscle protein turnover.

286 anscription factors is essential to initiate muscle protein ubiquitination and degradation during atr

287 Muscle protein ubiquitylation was also 45% lower (P<0.05

288 ontaining protein 2 gene, SORBS2, a skeletal muscle protein using a modification of the chromosome co

289 Muscle protein was subjected to mass spectrometry-based

290 Muscle protein wasting in cancer cachexia is a critical

291 cts that can suppress appetite and stimulate muscle protein wasting.

292 r distribution coefficients (log DBSAw), and muscle protein-water distribution coefficients (log Dmpw

293 stable peptide markers unique to species and muscle protein were identified following data-dependent

294 Parameters for glycation of muscle protein were optimised using the bidimensional hi

295 on of deuterium oxide into newly synthesized muscle proteins were determined by mass spectrometry.

296 In this study, we found that muscle proteins were highly modified by S-nitrosylation,

297 The most abundant skeletal muscle proteins were identified and correctly classified

298 nces in K(pw) between chicken, fish, and pig muscle proteins were small.

299 that some chemicals may sorb irreversibly to muscle proteins, which needs further research.

300 Mutations in nebulin, a giant muscle protein with 185 actin-binding nebulin repeats, a