ライフサイエンスコーパス: glycogen

1 atic activity and accumulated high levels of glycogen.

2 mors; this was the result of accumulation of glycogen.

3 CPAP is primarily related to the presence of glycogen.

4 hancing muscle glucose uptake and storage as glycogen.

5 n, which is known to rapidly deplete hepatic glycogen.

6 plete and incomplete oxidation, and cellular glycogen.

7 crofilaraemic blood showed reduced levels of glycogen (-37.9%) and lipids (-49.7%) compared to contro

8 In agreement with the changes of glycogenes, 60 out of 63 N-glycans that were identified

9 Glycogen, a branched glucose polymer, helps regulate glu

10 Malstructured glycogen accumulates over time in Lafora disease (LD) an

11 on-resistant abnormally structured insoluble glycogen accumulates.

12 CCCs are distinguished by aberrant lipid and glycogen accumulation and are refractory to a broad rang

13 rt glucose-6-phosphate to glucose leading to glycogen accumulation and hepatosteatosis.

14 inhibited glycogen breakdown, which promoted glycogen accumulation and the secretion of inflammatory

15 These results suggest that glycogen accumulation associated with a clear-cell pheno

16 readily be detected in very young mice where glycogen accumulation has just begun.

17 ER), mitochondria size, foamy cytoplasm, and glycogen accumulation in the liver of the periodontitis

18 Inhibiting glycogen accumulation may provide a treatment for cancer

19 lating evidence suggests that suppression of glycogen accumulation represents a potential therapeutic

20 ed for cytochrome P450 (CYP3A4) zonation and glycogen accumulation through PAS staining.

21 Glycogen accumulation was halted at the 4-month level, w

22 d dedifferentiation, hallmarked by myolysis, glycogen accumulation, and alteration of structural prot

23 aired trophoblast differentiation, increased glycogen accumulation, and decreased angiogenesis in the

24 ression of this kinase in the liver leads to glycogen accumulation, decreased glycemia, and hampered

25 dial hepatic and intra-myocellular lipid and glycogen accumulation, employing magnetic resonance spec

26 ygen (ROS) production, increased cytoplasmic glycogen accumulation, mitochondrial dysfunction and dis

27 g GS activity in GSDs associated with excess glycogen accumulation.

28 duced AKTIP abundance and insulin-stimulated glycogen accumulation.

29 tic glucose production and increased hepatic glycogen accumulation.

30 gpn abolished gsn mRNA rhythms and rhythmic glycogen accumulation.

31 r hallmark of LD is the presence of abnormal glycogen aggregates in neurons and other tissues.

32 h high levels of CfrA present high levels of glycogen and a decrease in photosynthetic pigments and p

33 elates with the disease-pathogenic insoluble glycogen and can readily be detected in very young mice

34 kin) mice identified alterations in glucose, glycogen and fat metabolism pathways.

35 Glycogen and glucose transporter GLUT4 are decreased.

36 keletal muscle of LFABP(-/-) mice had higher glycogen and intramuscular triglyceride levels as well a

37 alysis confirmed that Gys1 knockout inhibits glycogen and LB accumulation.

38 chiff-diastase staining were used to analyze glycogen and LB accumulation.

39 down of all three candidate genes suppressed glycogen and lipid biosyntheses resulting in inhibition

40 y due in part to a corresponding decrease in glycogen and lipid levels over time in mosquitoes fed on

41 ity may be due to the effect of infection on glycogen and lipid reserves.

42 atomegaly because of further accumulation of glycogen and lipids as a result of reduced glycolysis an

43 the nanohaloarchaeon's ability to hydrolyze glycogen and starch to glucose enabled growth of Halomic

44 viscoadaptation" uses regulated synthesis of glycogen and trehalose to vary the viscosity of the cyto

45 y generated by the oxidation of the maternal glycogen and triacylglycerol (TAG) stores (Figure 1).

46 th GSD 1a exhibit severe hepatomegaly due to glycogen and triglyceride (TG) accumulation in the liver

47 Hepatic glycogen and triglyceride concentrations were measured a

48 hat fenofibrate can rapidly decrease hepatic glycogen and triglyceride levels and renal triglyceride

49 SD Ia, there is over-accumulation of hepatic glycogen and triglycerides that can lead to steatohepati

50 ificity, using the magnetic coupling between glycogen and water protons through the nuclear Overhause

51 The correlation between glycogenes and glycans revealed the importance of sialyl

52 mount of CfrA determines the accumulation of glycogen, and affects the synthesis of protein and photo

53 iated with the metabolism of lipids, glucose/glycogen, and heme.

54 associated with hepatic accumulation of G6P, glycogen, and lipids, whereas the expression of glycolyt

55 The overaccumulation of glycogen appears as a hallmark in various glycogen stora

56 tification methods for soluble and insoluble glycogen are critical to research, including therapeutic

57 tudy furnishes a deeper understanding of how glycogen biosynthesis is regulated in bacteria and the m

58 topic labeling of protein-bound amino acids, glycogen-bound glucose, and RNA-bound ribose.

59 , the autosomal recessive condition known as Glycogen Branching Enzyme Deficiency (GBED) is the resul

60 asts (CAFs) secrete cytokines that stimulate glycogen breakdown in ovarian cancer cells.

61 CAF-induced glycogen breakdown increases glycolysis and ATP generati

62 entified hypoxic cancer cells with inhibited glycogen breakdown, which promoted glycogen accumulation

63 e, the enzyme catalyzing the initial step of glycogen breakdown.

64 and allows CNO-dependent cAMP signaling and glycogen breakdown.

65 omes (type1) and inclusions with deposits of glycogen but without any kind of organelles and delimiti

66 Epithelial cells primarily store energy as glycogen, but until recently it has not been reported as

67 twice per day training protocol where muscle glycogen concentration is maintained within 200-350 mmol

68 In conditions where glycogen concentration is maintained within 200-350 mmol

69 triction may be regulated by absolute muscle glycogen concentration, the acute within-day fluctuation

70 glycoNOE) signal is correlated linearly with glycogen concentration, while pH and temperature have li

71 Bezafibrate decreased liver triglyceride and glycogen concentrations and partially reversed the autop

72 Notably, glycogen content and activity of the ROS/AMPK/EP300/beta

73 ADRbeta2, insulin receptor, glycogen content and citrate synthase activity were simi

74 lude that CO-EtOAc effectively increases the glycogen content and glucose uptake by stimulating the m

75 red glycogen metabolism and elevated hepatic glycogen content during unfed state.

76 The glycogen content in in situ stimulated rat muscles fatig

77 Glycogen content reduction from healthy to tumor tissue

78 ubility, troponin-T degradation products and glycogen content than did other muscles.

79 T co-treatment led to an increase in hepatic glycogen content that coincides with heavier liver in fe

80 e glucose disposal related to lower starting glycogen content, and increased glycogen synthase activi

81 The digestion-resistant glycogen correlates with the disease-pathogenic insolubl

82 llow-up: -6.9 +/- 4.6; P = 0.17] and hepatic glycogen (Deltaglycogen_baseline: 64.4 +/- 14.1 compared

83 eplenish these stores more readily following glycogen depleting exercise, the idea that hepatic glyco

84 the recovery duration between a first muscle glycogen-depleting exercise and a second exercise sessio

85 howed excessive hepatic fat accumulation and glycogen depletion.

86 In the central nervous system, glycogen-derived bioenergetic resources in astrocytes he

87 the result was verified by the conventional glycogen detection assays.

88 Despite the availability of various glycogen detection methods, selective visualization of g

89 Glycogen determination and periodic acid-Schiff-diastase

90 aused by a defect in the enzyme required for glycogen digestion.

91 o upregulated by the inability to synthesise glycogen, either when storage is inhibited in knock-down

92 Toxoplasma genome encodes a suite of likely glycogenes expected to assemble N-glycans, O-glycans, a

93 ion method, we measure degradation-resistant glycogen in as little as 30 mg of skeletal muscle or a s

94 The pathways for biosynthesis of glycogen in bacteria and starch in plants are evolutiona

95 exercise session started with reduced muscle glycogen in both approaches but was performed either 2 o

96 rates metabolic reprogramming that preserves glycogen in favor of fatty acid oxidation and mitochondr

97 There was less glycogen in hepatocytes in the diet group (PAS stain sco

98 We revealed the subcellular enrichment of glycogen in live cancer cells and achieved specific glyc

99 ent an optical imaging strategy to visualize glycogen in live cancer cells with minimal perturbation

100 etection methods, selective visualization of glycogen in living cells with high spatial resolution ha

101 buted to the accumulation of glucose-6-P and glycogen in primary rat hepatocytes.

102 rom the PYGM mutation to the accumulation of glycogen in the muscle fibers.

103 myofibril loss), accumulation of perinuclear glycogen, interstitial fibrosis, and myocardial gap junc

104 of cytokines in regulating the expression of glycogenes involved in the biosynthesis of N-glycans.

105 The soluble alpha-polyglucan glycogen is a central metabolite enabling transient gluc

106 Glycogen is a high-density glucose polymer, which provid

107 GDPGP1/mcp-1 and consequent loss of neuronal glycogen is a maladaptive response that limits neuronal

108 The defective autophagic degradation of glycogen is associated with abnormal ubiquitination and

109 Moreover, glycogen is measured within the metabolomics workflow.

110 lycolytic and mitochondrial pathways such as glycogen, ketone bodies and nucleosides.

111 caused markedly increased postprandial liver glycogen levels (in a HNF4alpha-dependent fashion), indi

112 d hepatic and renal triglyceride and hepatic glycogen levels found in control G6pc -/- mice.

113 genic mutations, however, result in elevated glycogen levels with no changes in mTORC1 or GSK3beta ac

114 mRNA, glycogen phosphorylase (gpn) mRNA, and glycogen levels, accumulate with a daily rhythm controll

115 n expression resulted in high and arrhythmic glycogen levels, and deletion of gpn abolished gsn mRNA

116 xygen consumption rates, suppressing hypoxic glycogen levels, and inhibiting the expression of the so

117 GDPGP1/mcp-1 regulates neuronal glycogen levels, indicating a key role for this metaboli

118 depletion and loss of rhythmicity in hepatic glycogen levels.

119 ucose for energy needs and stores glucose as glycogen mainly in astrocytes.

120 n in live cancer cells and achieved specific glycogen mapping through distinct spectral identificatio

121 Using this method, different glycogen metabolic phenotypes were characterized in a se

122 patic glucose output associated with altered glycogen metabolism and elevated hepatic glycogen conten

123 Mutations in PGM1 cause impairment in glycogen metabolism and glycosylation, the latter manife

124 otect from AHR-mediated steatosis, but alter glycogen metabolism and increase the risk of TCDD-elicit

125 possibility for noninvasive study of complex glycogen metabolism at subcellular resolution and may he

126 Reprogramming of glycogen metabolism has recently been suggested to play

127 ultiple pathways regulating glucose, fat and glycogen metabolism in Gprc6a(Liver-cko) mice.

128 shes methodological advancements relevant to glycogen metabolism investigations generally, and GSDs.

129 A reduction in glycogen metabolism was attributed to loss of glycogen p

130 ed the molecular links between the clock and glycogen metabolism, a conserved glucose homeostatic pro

131 involving defects in adenosine, fructose and glycogen metabolism, as well as disruptions in the membr

132 oding critical insulin-responsive enzymes in glycogen metabolism, glycolysis and TCA cycle were hypom

133 educed the levels of metabolites involved in glycogen metabolism, glycolysis, and the Krebs cycle, bu

134 Since physical activity potently modulates glycogen metabolism, this provides a rationale for consi

135 zed or tissue-specific defects in enzymes of glycogen metabolism.

136 the genes have, therefore, mostly focused on glycogen metabolism.

137 decreased glycolysis but possibly including glycogen mobilization and other metabolic changes.

138 Recently, glycogen mobilization has been shown to play a role in t

139 We show in vitro that the glycogen NOE (glycoNOE) signal is correlated linearly wi

140 We report an MRI method for imaging glycogen noninvasively with enhanced detection sensitivi

141 orage of the excess nutrients in the form of glycogen or fat.

142 sion, but this approach did not reduce brain glycogen or LBs to levels below those at the time of int

143 However, LC1Hm could not metabolize either glycogen or starch (both alpha-glucans) or other polysac

144 and these changes are similarly reflected in glycogen oscillations.

145 It represents a potential therapy for glycogen overload and hepatosteatosis associated with GS

146 Lafora disease caused by the absence of the glycogen phosphatase laforin or its interacting partner

147 ibitors against muscle and liver isoforms of glycogen phosphorylase (GP).

148 We show that phosphorylated glycogen phosphorylase (GPa), glycogen synthase (GSa) -

149 a We find that glycogen synthase (gsn) mRNA, glycogen phosphorylase (gpn) mRNA, and glycogen levels,

150 t this communication bridge is essential for glycogen phosphorylase (PYG) activation through the cano

151 regulatory pathway of the muscle isoform of glycogen phosphorylase (PYGM) that plays an important ro

152 lycogen metabolism was attributed to loss of glycogen phosphorylase and phosphoglucomutase at the pro

153 The glycogen phosphorylase isoenzyme BB (GPBB) was detected

154 c studies with rabbit muscle and human liver glycogen phosphorylases showed that the (R)-imidazolinon

155 Glycogen plays a central role in glucose homeostasis and

156 These studies indicate that glycogen plays an important role in glucose homeostasis

157 FA, triglycerides, and cholesterol), whereas glycogen production was comparatively low.

158 demonstrate that while gsn was necessary for glycogen production, constitutive gsn expression resulte

159 solution and may help reveal new features of glycogen regulation in cancer systems.

160 o direct glucose into the muscles in need of glycogen replenishment.

161 on can also accelerate post-exercise (liver) glycogen repletion rates, which may be relevant when rap

162 essions and accelerate post-exercise (liver) glycogen repletion.

163 al to homeostasis, their roles in generating glycogen rhythms were investigated.

164 tion over signaling or allosteric control of glycogen rhythms, a mechanism that is potentially conser

165 yocyte myocytolysis, cardiomyocyte diameter, glycogen score or Cx43 distribution at the time of surge

166 The ability to noninvasively image glycogen should allow assessment of diseases in which gl

167 12 glycogenes showed unique expression in 231BR, which coul

168 muscle and brain that demonstrates that the glycogen shunt functions to maintain homeostasis of glyc

169 en depleting exercise, the idea that hepatic glycogen storage and hepatic de novo lipogenesis are lin

170 As expected, impaired hepatic glycogen storage and increased ectopic lipid storage in

171 Glycogen storage disease (GSD) type 1a is an inborn erro

172 cell line from a child with Pompe disease, a glycogen storage disease caused by a defect in the enzym

173 dy describes the first example of a dominant glycogen storage disease in humans, and elucidates the u

174 Glycogen storage disease type Ia (GSD Ia) is caused by a

175 iency, also known as von Gierke's Disease or Glycogen storage disease type Ia (GSD Ia), is characteri

176 infections and inflammatory bowel disease in glycogen storage disease type Ib (GSD-Ib).

177 e-alpha (G6Pase-alpha or G6PC) deficiency in glycogen storage disease type-Ia (GSD-Ia) leads to impai

178 own animal models or storage is saturated in glycogen storage disease.

179 Glycogen storage diseases (GSDs) are severe human disord

180 Glycogen storage diseases (GSDs) comprise over 15 entiti

181 of glycogen appears as a hallmark in various glycogen storage diseases (GSDs), including Pompe, Cori,

182 eview is the development of gene therapy for glycogen storage diseases (GSDs).

183 iac disease, muscular disorders, cancer, and glycogen storage diseases.

184 n of this technology is for the treatment of glycogen storage disorders (GSDs) via an antibody-enzyme

185 ction with decreased glycolytic activity and glycogen storage in skeletal muscle, resulting in accumu

186 Ectopic lipid deposition and postprandial glycogen storage in the liver and skeletal muscle were n

187 gy as the driving causes underlying abnormal glycogen storage in TSC irrespective of the underlying m

188 ts indicate that cell lines manifesting high glycogen storage level showed increased tolerance to glu

189 lism to support complete oxidation of FA and glycogen storage regardless of Met supply.

190 ng glutathione biosynthesis and upregulating glycogen storage, and may respond to low pH by increasin

191 ctose has the capacity to upregulate hepatic glycogen storage, and replenish these stores more readil

192 ished TSC function is associated with excess glycogen storage, but the causative mechanism is unknown

193 dient during differentiation induced zonated glycogen storage, which was higher in the hepatocytes gr

194 ructose ingestion, and saturation of hepatic glycogen stores could exacerbate the negative metabolic

195 mice exhibited a greater decrease in muscle glycogen stores during exercise and elevated circulating

196 We propose that hepatic glycogen stores may be a key factor in determining the m

197 Endurance exercise begun with reduced muscle glycogen stores seems to potentiate skeletal muscle prot

198 Hepatic glycogen stores were evaluated using periodic acid Schif

199 stasis, balancing the degradation of hepatic glycogen stores, and gluconeogenesis (GNG).

200 se session is necessary to reduce the muscle glycogen stores.

201 ormance, presumably because of lower hepatic glycogen stores.

202 lucose is processed in muscle, for energy or glycogen stores.

203 Three homologous candidate genes, glycogen synthase (glys), atp-binding cassette transport

204 bitors of the key glycogen synthetic enzyme, glycogen synthase (GS), we identified a substituted imid

205 phosphorylated glycogen phosphorylase (GPa), glycogen synthase (GSa) - respectively activated and ina

206 c process, in Neurospora crassa We find that glycogen synthase (gsn) mRNA, glycogen phosphorylase (gp

207 ulation of glucose transporter 2 (GLUT2) and glycogen synthase 2 (GYS2); while expression of gluconeo

208 wer starting glycogen content, and increased glycogen synthase activity, together with increased musc

209 rved that phosphorylation of Gpa2 depends on glycogen synthase kinase (GSK).

210 contrast, phosphomimetic substitution of the glycogen synthase kinase (GSK3beta) site in the Pro/Ala-

211 but REDD1-mediated Nrf2 degradation required glycogen synthase kinase 3 (GSK3) activity and Ser-351/S

212 Glycogen synthase kinase 3 (GSK3) alpha and beta are 2 h

213 maller receptor-mediated vesicles containing glycogen synthase kinase 3 (GSK3) and protein arginine e

214 ion in p-AKT (S473), which in turn activated glycogen synthase kinase 3 (GSK3) and reduced beta-caten

215 rt the evolutionary importance of the enzyme Glycogen Synthase Kinase 3 (GSK3) for maintaining podocy

216 in collagen I 3D cultures in the absence of glycogen synthase kinase 3 (GSK3) inhibition, hPSC-deriv

217 ptor (D2R) and protein kinase B (PKB or Akt)/glycogen synthase kinase 3 (GSK3) signaling in the ventr

218 sites and secondary casein kinase 1 (CK1) or glycogen synthase kinase 3 (GSK3) sites was carefully ev

219 here show a novel mode of eIF6 regulation by glycogen synthase kinase 3 (GSK3) that is predominantly

220 Glycogen synthase kinase 3 (GSK3) was identified as an e

221 ation of proteins (Wnt/STOP), which inhibits glycogen synthase kinase 3 (GSK3)-dependent protein ubiq

222 Arabidopsis GLYCOGEN SYNTHASE KINASE 3 (GSK3)-like kinases play vari

223 al domain, priming it for phosphorylation by glycogen synthase kinase 3 (GSK3).

224 pathways including phosphoinositide 3-kinase/glycogen synthase kinase 3 (PI3K/GSK3) signaling, with s

225 atenin was required for BRB restoration, but glycogen synthase kinase 3 alpha/beta (GSK-3alpha/beta)

226 We demonstrate that inhibitors of glycogen synthase kinase 3 alpha/beta (GSK3alpha/beta) e

227 ing protein, p53, which is phosphorylated by glycogen synthase kinase 3 at serine 33 and then ubiquit

228 through a kinome-wide screen, we found that glycogen synthase kinase 3 beta (GSK-3beta) was robustly

229 he virulence of P. gingivalis (Pg) affecting glycogen synthase kinase 3 beta (GSK-3beta)/nuclear fact

230 we found that CAMK4 phosphorylates GSK3beta (glycogen synthase kinase 3 beta), activates the Wnt path

231 d THC-induced downregulation of local GSK-3 (glycogen synthase kinase 3) and Akt signaling pathways d

232 cked cortical downregulation of local GSK-3 (glycogen synthase kinase 3) and Akt signaling pathways,

233 an inhibitor of cyclin-dependent kinases and glycogen synthase kinase 3, as a modulator of parkin rec

234 screen for anti-fibrotic compounds targeting glycogen synthase kinase 3, which has a consistent role

235 ave been some reports on MTDLs targeting the glycogen synthase kinase 3beta (GSK-3beta) enzyme, due t

236 osphorylation on p53 at Ser-33 and Ser-37 by glycogen synthase kinase 3beta (GSK3beta) and DNA-depend

237 tes diminished inhibitory phosphorylation of glycogen synthase kinase 3beta (GSK3beta) at Ser-9 in th

238 Glycogen synthase kinase 3beta (GSK3beta) deactivation a

239 ppress many signaling pathways that activate glycogen synthase kinase 3beta (GSK3beta) implicated in

240 g pathway involving AKT Ser/Thr kinase (AKT)/glycogen synthase kinase 3beta (GSK3beta) or paxillin.

241 ide 3-kinase (PI3K)-AKT Ser/Thr kinase (AKT)-glycogen synthase kinase 3beta (GSK3beta) signaling path

242 peractivation and subsequent inactivation of glycogen synthase kinase 3beta (GSK3beta), a negative re

243 ivation, which results in hyperactivation of glycogen synthase kinase 3beta (GSK3beta), followed by p

244 CUGBP1 activity is controlled by glycogen synthase kinase 3beta (GSK3beta), which is elev

245 the canonical regulation of beta-catenin via glycogen synthase kinase 3beta (GSK3beta)-dependent degr

246 at S199 (hTau-S199-P) by the protein kinase glycogen synthase kinase 3beta (GSK3beta).

247 n (mTOR) signaling pathway and inhibition of glycogen synthase kinase 3beta (GSK3beta).

248 al nuclear factor kappaB pathway and the Akt-glycogen synthase kinase 3beta signaling axis, respectiv

249 bound IRF1 turnover is promoted by GSK3beta (Glycogen Synthase Kinase 3beta) via phosphorylation of t

250 cocorticoid kinase 1 (SGK1), an inhibitor of glycogen synthase kinase 3beta, as part of this pathway.

251 ead box protein O1 transcription factors and glycogen synthase kinase 3beta.

252 signal-regulated protein kinase modules and glycogen synthase kinase 3beta.

253 Additionally, in the current study, glycogen synthase kinase appears to attenuate tau pathol

254 In both cell types, insulin blocks glycogen synthase kinase beta (GSK3beta) activity.

255 plex 1 (mTORC1) inhibitor rapamycin, and the glycogen synthase kinase-3 (GSK-3) inhibitor lithium act

256 Activation of glycogen synthase kinase-3 (GSK-3) interferes with micro

257 bition of the histone deacetylase (HDAC) and glycogen synthase kinase-3 (GSK-3) pathways, which cause

258 nt oxazole-4-carboxamide-based inhibitors of glycogen synthase kinase-3 (GSK-3).

259 ia containing fetal bovine serum (FBS) and a glycogen synthase kinase-3 (GSK3) inhibitor, and in seru

260 e describe a cell-engineering strategy using glycogen synthase kinase-3 (GSK3) inhibitor-loaded nanop

261 Glycogen synthase kinase-3 (GSK3) is an important signal

262 We found that glycogen synthase kinase-3 (GSK3) is overactivated in co

263 Glycogen synthase kinase-3 (GSK3) was found to be an ups

264 Glycogen synthase kinase-3 beta (GSK-3beta), a serine/th

265 PSC-CMs in vitro (i.e., 100- to 250-fold) by glycogen synthase kinase-3beta (GSK-3beta) inhibition us

266 Glycogen synthase kinase-3beta (GSK3beta) controls many

267 ith emerin and beta-actin, and activation of glycogen synthase kinase-3beta (GSK3beta).

268 GSK-3beta (glycogen synthase kinase-3beta) is highly associated wit

269 ABA increases expression of important glycogen synthase, glucose, fatty acid and mitochondrial

270 Constitutive reduction of glycogen synthase-1 (GYS1) activity prevents murine LD,

271 Recent evidence suggests that glycogen-synthase kinase 3beta (GSK3beta) plays a key ro

272 nase B phosphorylation and increased hepatic glycogen synthesis after an oral glucose challenge.

273 owever, regulation of metabolic rewiring for glycogen synthesis and breakdown in cancer cells remains

274 or glucose homeostasis through regulation of glycogen synthesis and glucose output.

275 such conditions, fructose lowers whole-body glycogen synthesis and impairs subsequent exercise perfo

276 ia, which occurs in many cancers, results in glycogen synthesis and increased survival under stressed

277 miR-20b-5p overexpression increased basal glycogen synthesis in human skeletal muscle cells.

278 ated to glycogenin, an enzyme that may prime glycogen synthesis in yeast and animals.

279 t assay suitable for assessment of candidate glycogen synthesis inhibitors, and 2) discovery of alpha

280 Importantly, blocking glycogen synthesis permits reactive oxygen species (ROS)

281 complete loss of TSC2 causes an increase in glycogen synthesis through mTORC1 hyperactivation and su

282 d, indicating an inability of glycolysis and glycogen synthesis to process glucose at sufficient rate

283 was evident from reduced insulin-stimulated glycogen synthesis, glucose oxidation, glucose uptake, i

284 hepatic insulin resistance prevents hepatic glycogen synthesis, preserving glucose for glucose-depen

285 insulin to dramatically increase the rate of glycogen synthesis.

286 pleted simultaneously, and markedly elevated glycogen synthesis.

287 se 3beta (GSK3beta), a negative regulator of glycogen synthesis.

288 The blockade of both glycogen synthetase kinase 3beta and cyclin-dependent ki

289 The blockade of both glycogen synthetase kinase 3beta and cyclin-dependent ki

290 designed to screen for inhibitors of the key glycogen synthetic enzyme, glycogen synthase (GS), we id

291 approaches to map the connections between 67 glycogenes, their enzyme products, the glycans to which

292 We identified a Raman biomarker from glycogen to distinguish iPSCs from their neural derivati

293 phage (hMDMs) and amoebae to rapidly degrade glycogen to generate cytosolic hyper-glucose.

294 dicators of nutritional physiology including glycogen, total sugar, lipids, and protein were associat

295 esses such as the NAD(+) salvage pathway and glycogen turnover.

296 ompanied by decreased ATP demand and reduced glycogen usage.

297 omolecules, such as DNA, protein, lipids and glycogen, via the enrichment and distinct spectra of car

298 Glucose export was decreased, but cellular glycogen was increased by the presence of CC and increas

299 Muscle glycogen was reduced to ~200 mmol kg(-1) dw in all trial

300 By editing 17 glycogenes, we discovered novel Glc(0-2)-Man(6)-GlcNAc(2