ライフサイエンスコーパス: GLUT4

1 xpressing myc epitope at the exofacial loop (GLUT4).

2 sponsive facilitative glucose transporter 4 (GLUT4).

3 ave a role in the specialized trafficking of GLUT4.

4 calization of Rab13 with ACTN4 or Rab13 with GLUT4.

5 ivo, concomitant with decreased abundance of GLUT4.

6 there is no three-dimensional structure for GLUT4.

7 ed receptor (PPAR) gamma target genes beyond Glut4.

8 location by interacting with IRAP as well as GLUT4.

9 the broader therapeutic utility of targeting GLUT4.

10 volve an increased cell surface abundance of GLUT4.

11 e proliferator-activated receptor gamma, and GLUT4.

12 y the major facilitative glucose transporter Glut4.

13 of the pathways from IR to translocation of GLUT4.

14 d glucose uptake and impaired endocytosis of GLUT4.

15 ous fat, and increased adipose expression of GLUT4.

16 gradation, increasing total and cell surface Glut4 3-fold.

17 In contrast, S-acylation of GLUT4, a glucose transporter that extensively co-localis

18 xocytic translocation of vesicles containing GLUT4, a glucose transporter, and insulin-regulated amin

19 r significance for type 2 diabetes (in which GluT4 activity in the periphery is impaired) and Alzheim

20 Glut4 in fibroblasts but predominantly with Glut4 after differentiation.

21 GLUT4, Akt protein content and insulin-stimulated Akt ph

22 in insulin signalling and glucose transport (GLUT4, Akt1 and Akt2) were unaffected by extended mornin

23 Glut4 also cycles through a slow constitutive endosomal

24 ipose-specific knockout or overexpression of Glut4 alters systemic insulin sensitivity.

25 lysed for mRNA levels of selected genes, and GLUT4 and Akt protein content.

26 intraperitoneal glucose tolerance test; and Glut4 and ApoE expression in VAT.

27 but decreases the stability of sortilin and Glut4 and blocks their entry into the small vesicular ca

28 AnkB binds directly to GLUT4 and clathrin and promotes their association in adi

29 the distinct physiologic programs related to Glut4 and Glut1-mediated glucose uptake.

30 e transport in liposomes containing purified GLUT4 and GLUT3.

31 on enhanced the translocation of GSV cargos, GLUT4 and insulin-regulated aminopeptidase (IRAP), and A

32 se included established GSV proteins such as GLUT4 and insulin-responsive aminopeptidase, as well as

33 on reduced TUG acetylation and redistributed GLUT4 and IRAP to the plasma membrane in 3T3-L1 adipocyt

34 that DHHC7 represents the principal PAT for Glut4 and that this mechanism is essential for insulin-r

35 pha2-macroglobulin receptor LRP1 cycles with Glut4 and the Tf receptor through all three exocytic pat

36 embrane and cytosolic domains from GLUT1 and GLUT4 and/or point mutations were generated and expresse

37 te markers, including glucose transporter 4 (GLUT4) and adiponectin expression and Oil Red O staining

38 ion of insulin-regulated glucose transporter GLUT4, and (iii) changed feedback from mammalian target

39 gar transporters SGLT1, GLUT1, GLUT2, GLUT3, GLUT4, and GLUT5.

40 abolic genes, including Ogt, Oga, Pdk4, H19, Glut4, and Ptpn1, in offspring skeletal muscle.

41 lin interacts with the first luminal loop of Glut4, and the cytoplasmic tail of sortilin binds to ret

42 proximately 32%) and repressed the levels of GLUT4 ( approximately 50%) in cultured myotubes from C57

43 in translocation of the glucose transporter GLUT4 are associated with peripheral insulin resistance,

44 ve terminals rely on the glucose transporter GLUT4 as a glycolytic regulatory system to meet the acti

45 we identify the insulin downstream effector GLUT4 as a key modulator of podocyte function in diabeti

46 They identify GluT4 as a key regulator of hippocampal memory processin

47 and reduced abundances of insulin receptor, GLUT4, AS160, ribosomal protein S6, and FOXO1.

48 Of note, GLUT4 associated with the complex in response to insulin

49 is critically dependent on palmitoylation of Glut4 at Cys-223.

50 ts importance, a selective knockout of brain GLUT4 (BG4KO) was generated by crossing Nestin-Cre mice

51 r studies have shown that prolonged systemic GluT4 blockade causes insulin resistance.

52 ation and memory acquisition was impaired by GluT4 blockade.

53 As a result, Glut4 cannot reach the insulin-responsive compartment, a

54 117 binding envelopes of exofacial GLUT1 and GLUT4 conformers differ significantly.

55 e activated by insulin in muscle to mobilize GLUT4-containing vesicles to the muscle cell surface.

56 The fusion of GLUT4-containing vesicles with the plasma membrane of ad

57 contraction-induced increases in sarcolemmal GLUT4 content and glucose uptake were lower in the white

58 rapidly increased (p < 0.05) plasma membrane GLUT4 content in both red and white gastrocnemius muscle

59 ed pyruvate dehydrogenase activity, membrane GLUT4 content, and insulin-stimulated Akt phosphorylatio

60 Because GLUT4 continually cycles between the PM and intracellula

61 This slow constitutive pathway is the only Glut4 cycling pathway in undifferentiated fibroblasts.

62 In summary, GLUT4 deficiency in podocytes affects podocyte nutrient

63 Differentiation also decreases Glut4 degradation, increasing total and cell surface Glu

64 ce were decreased, indicating that increased GLUT4-dependent glucose flux decreases nutrient stress b

65 Impaired GLUT4-dependent glucose uptake is a contributing factor

66 revent muscle-specific AMPK failure, restore GLUT4 disposition, and diminish protein breakdown.

67 olism, suggesting the possibility that brain GluT4 dysregulation may be one cause of cognitive impair

68 a 1.4-fold increase in the rate constant of Glut4 endocytosis (ken).

69 re ubiquitously expressed in normal tissues, GLUT4 exhibits more limited normal expression profiles.

70 ly to a 62% decrease in the rate constant of Glut4 exocytosis (kex), although Rab10 knockdown also ca

71 m sequestration in GSVs is rate-limiting for Glut4 exocytosis in basal adipocytes.

72 ocytic pathways including insulin secretion, GLUT4 exocytosis, and neurotransmitter release.

73 2) GLUT1 and GLUT4 exofacial conformers present multiple, adjacent gl

74 5 mm glucose pulse increased adiponectin and GLUT4 expression and accumulation of neutral lipids via

75 ulin activation of glycogen synthase by 60%, GLUT4 expression by 16%, and 5' AMPK-alpha1 expression b

76 Importantly, exercise upregulates muscle GLUT4 expression in an insulin-independent manner under

77 which accompanies a significant elevation of Glut4 expression in iBAT.

78 ent mechanism responsible for rescued muscle GLUT4 expression is poorly understood.

79 brain, reduced in vivo brain glucose uptake, GLUT4 expression, and spatial memory.

80 PPARgamma agonist rosiglitazone to increase Glut4 expression, but was not sufficient to increase exp

81 The glucose transporter GLUT4 facilitates insulin-stimulated glucose uptake in p

82 reasing the exocytic trafficking rate of the GLUT4 facilitative glucose transporter from intracellula

83 s generated by crossing Nestin-Cre mice with GLUT4-floxed mice.

84 0 promote insulin-stimulated mobilization of GLUT4 from a perinuclear recycling endosome/TGN compartm

85 tes, sortilin together with retromer rescues Glut4 from degradation in lysosomes and retrieves it to

86 the translocation of the glucose transporter GLUT4 from intracellular vesicles to the cell surface.

87 GLUT4 function is impaired in obesity and type 2 diabete

88 To better understand the regulation of GLUT4 function, a targeted siRNA screen was performed an

89 Mice with a podocyte-specific deletion of GLUT4 (G4 KO) did not develop albuminuria despite having

90 mediated by glucose-dependent activation of GLUT4 gene transcription through the cis-acting GLUT4-li

91 nsgenic mice engineered to express the human GLUT4 gene under the control of the human GLUT4 promoter

92 HA-GLUT4-GFP redistribution to the plasma membrane (PM) was

93 In obesity and type 2 diabetes, Glut4 glucose transporter expression is decreased select

94 Mice overexpressing the Glut4 glucose transporter in adipocytes have elevated li

95 r of insulin-stimulated translocation of the GLUT4 glucose transporter to the plasma membrane (PM) of

96 This effect is mediated by the Glut4 glucose transporter.

97 eavage liberates intracellularly sequestered GLUT4 glucose transporters for translocation to the cell

98 Insulin causes the exocytic translocation of GLUT4 glucose transporters to stimulate glucose uptake i

99 rs, CD36 (cluster of differentiation 36) and GLUT4 (glucose transporter type 4), are also unchanged.

100 ocytes appear to express glucose transporter GLUT4, glucose entry across the astrocyte plasma membran

101 lows the order of potency: insulin-regulated GLUT4 >> GLUT1 approximately neuronal GLUT3.

102 e insulin signal transduction between IR and GLUT4 has been thoroughly studied with modeling and time

103 , Cycs, Ucp3) and glucose metabolism (Glut1, Glut4, Hk2) was increased.

104 ied that determine steady state cell surface Glut4: (i) endocytosis, (ii) degradation, (iii) sorting,

105 el needed three distinct pathways from IR to GLUT4: (i) via protein kinase B (PKB) and Akt substrate

106 nexpectedly, whereas long-term inhibition of GluT4 impaired long-term memory, short-term memory was e

107 Mice overexpressing GLUT4 in adipocytes (AG4OX) have elevated AT lipogenesis

108 of the insulin-sensitive glucose transporter Glut4 in adipocytes.

109 LRP1 cycles with the Tf receptor and Glut4 in fibroblasts but predominantly with Glut4 after

110 Rab10 knockdown decreased cell surface Glut4 in insulin-stimulated adipocytes by 65%, but not i

111 that RabGAP deficiency impairs retention of GLUT4 in intracellular vesicles in the basal state.

112 s results support a model in which TUG traps GLUT4 in intracellular, insulin-responsive vesicles term

113 GLUT4 in muscle and adipose tissue is important in maint

114 onsible for exercise-dependent regulation of GLUT4 in muscle.

115 Rab8A colocalizes with GLUT4 in perinuclear but not submembrane regions visuali

116 ensing, indicating a critical role for brain GLUT4 in sensing and responding to changes in blood gluc

117 se that increased cell surface expression of GLUT4 in skeletal muscle and fatty tissue of AnkbR1788W/

118 d expression of IL-1 receptor antagonist and Glut4 in skeletal muscles after MSC transplantation resu

119 However, the role of insulin-responsive GLUT4 in the central nervous system has not been well ch

120 and also suggest differential regulation of GluT4 in the hippocampus from that in peripheral tissues

121 and muscle cells by regulating the amount of GLUT4 in the plasma membrane.

122 ts, the maintenance of elevated cell-surface GLUT4 in the presence of insulin requires accelerated bi

123 ent cell surface glucose transporter type 4 (GLUT4) in adipocytes resulting from impaired function of

124 brane localization of glucose transporter 4 (GLUT4) in skeletal muscle and adipocytes.

125 evaluate the role of glucose transporter-4 (GLUT4) in the anti-diabetic effects of methanol, hexane

126 of insulin-regulated glucose transporter-4 (GluT4) in the brain is unclear.

127 eletal muscle in vivo and ex vivo, increased GLUT4, increased ChREBP and markers of adipose tissue li

128 GLUT4 inhibition also caused sensitization to metformin

129 Inhibition of glucose metabolism with the GLUT4 inhibitor ritonavir elicits variable cytotoxicity

130 Activity at synapses triggers insertion of GLUT4 into the axonal plasma membrane driven by activati

131 ults in insertion of the glucose transporter GLUT4 into the plasma membrane and subsequent glucose up

132 that was previously shown to be critical for GLUT4 intracellular retention.

133 pogenic genes, and glucose metabolism genes (Glut4, Irs1).

134 sociated with glucose and lipid homeostasis (GLUT4, IRS1, FASN, ACACA, FATP2, CD36, and G6PC) in live

135 Endocytosis of Glut4 is 3 times slower than the Tf receptor in fibrobla

136 In the current study, we demonstrate that GluT4 is a critical component of hippocampal memory proc

137 gether, a moderate increase in expression of GLUT4 is a good target for treatment of insulin resistan

138 GluT4 is also expressed in some hippocampal neurons, but

139 In adipocytes, Glut4 is also sorted from endosomes into a second exocyt

140 reviously determined that insulin-responsive GLUT4 is constitutively localized on the plasma membrane

141 Glut4 is internalized and recycled through a highly regu

142 GLUT4 is necessary for acute insulin- and contraction-in

143 Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle gluco

144 ific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes.

145 of endogenous glucose production even though Glut4 is not present in the liver.

146 In fibroblasts, Glut4 is recycled from endosomes through a slow constitu

147 Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake.

148 0 in GLUT1 to the corresponding positions in GLUT4 is sufficient to completely transform GLUT1 into G

149 The insulin-regulated glucose transporter-4 (GluT4) is critical for insulin- and contractile-mediated

150 Differentiation decreases Glut4 ken 40% (ken = 0.12 min(-1)).

151 growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not nec

152 e adipose tissue (WAT) from adipose-specific Glut4-knockout or adipose-specific Glut4-overexpressing

153 urthermore, we show that genetic ablation of GLUT4 leads to an arrest of synaptic vesicle recycling d

154 d Akt, endothelial nitric oxide synthase and GLUT4 levels were also induced in hypertrophied muscles,

155 NA expression of glucose transporter type 4 (GLUT4), lipoprotein lipase (LpL), peroxisome proliferato

156 T4 gene transcription through the cis-acting GLUT4-liver X receptor element (LXRE) promoter element.

157 ail to restore normal lipid accumulation and GLUT4 localization in adipocytes are present in 1.3% of

158 ion, which was paralleled by increased basal GLUT4 localization in the sarcolemma, as assessed throug

159 which are required for the activation of the GLUT4 locus.

160 60 substrates on the trafficking kinetics of Glut4, LRP1, and the Tf receptor were measured in adipoc

161 exists whereby other Gluts such as Glut3 and Glut4 may also support the influx of glucose into activa

162 te, selective intrahippocampal inhibition of GluT4-mediated glucose transport impaired memory acquisi

163 We show that insulin-stimulated Glut4-mediated glucose uptake requires PDPK1 phosphoryla

164 cose clearance by increasing skeletal muscle GLUT4-mediated glucose uptake.

165 theless, an intact HM domain is required for Glut4-mediated glucose uptake.

166 terization showed that PIMT was recruited to GLUT4, MEF2A and HDAC5 promoters and overexpression of P

167 muscle via the transcriptional modulation of GLUT4, MEF2A, PGC-1alpha and HDAC5 genes.

168 T differentially regulated the expression of GLUT4, MEF2A, PGC-1alpha and HDAC5 in cultured cells and

169 Elevating CCR5/CCL5 activity induced GLUT4 membrane translocation and reduced phospho-IRS-1(S

170 its knockdown suppressed, insulin-dependent Glut4 membrane translocation in both 3T3-L1 adipocytes a

171 vation of DHHC7 suppressed insulin-dependent Glut4 membrane translocation in both 3T3-L1 adipocytes a

172 lmo2 is a new regulator of insulin-dependent Glut4 membrane translocation through modulating Rac1 act

173 c1 have been implicated in insulin dependent Glut4 membrane translocation, we hypothesize here that E

174 t Elmo2 may play a role in insulin-dependent Glut4 membrane translocation.

175 Therefore, we hypothesized that hippocampal GluT4 might be involved in memory processes.

176 first to show the cognitive impact of brain GluT4 modulation.

177 4 was due to both decreased transcription of Glut4 mRNA and decreased efficiency of Glut4 pre-mRNA sp

178 deficiency was attributed to a reduction in GLUT4 mRNA and protein levels.

179 Furthermore, GLUT4 mRNA expression was mediated by glucose-dependent

180 nce, which was associated with increased VAT Glut4 mRNA levels (P < 0.05).

181 esulting in opposing effects on steady-state Glut4 mRNA levels.

182 Persistent reduction in Glut4 mRNA suggests that a posttranscriptional mechanism

183 ription with an increase in the stability of Glut4 mRNA, resulting in opposing effects on steady-stat

184 sue, the abundance of GLUT4 protein, but not GLUT4 mRNA, was substantially reduced.

185 lglyceride levels, but did not rescue muscle Glut4 mRNA.

186 Glut4 neuron ablation affects orexigenic melanin-concent

187 After Glut4 neuron ablation, mice demonstrate altered hormone

188 Glut4 neuron-ablated mice show peripheral metabolic defe

189 ion to selectively remove basal hypothalamic Glut4 neurons and investigate the resulting phenotypes.

190 The apparent heterogeneity of Glut4 neurons has thus far thwarted attempts to understa

191 We conclude that Glut4 neurons integrate hormonal and nutritional cues an

192 porters (Glut4) often colocalize in neurons (Glut4 neurons) in anatomically and functionally distinct

193 and insulin-responsive glucose transporters (Glut4) often colocalize in neurons (Glut4 neurons) in an

194 Consequently, suppression of GLUT4 or inhibition of glucose transport with the HIV pr

195 Despite 68% homology between GLUT1 and GLUT4, our virtual screen identified two potent compound

196 ural basis for the selectivity of PIs toward GLUT4 over GLUT1 that can be used in ongoing novel drug

197 -specific Glut4-knockout or adipose-specific Glut4-overexpressing mice with their respective controls

198 gain further insights into the regulation of Glut4 palmitoylation, we set out to identify the palmito

199 e that ectopic expression of DHHC7 increased Glut4 palmitoylation, whereas DHHC7 knockdown in 3T3-L1

200 C7 KO in adipose tissue and muscle decreased Glut4 palmitoylation.

201 mammalian DHHC proteins, DHHC7 is the major Glut4 PAT, based on evidence that ectopic expression of

202 l from endosomes may represent a step in the Glut4 pathway vulnerable to the development of insulin r

203 enes related to insulin sensitivity (ADIPOQ, GLUT4, PPARG2, and SIRT1) and lipogenesis (SREBP1c, ACC,

204 on of Glut4 mRNA and decreased efficiency of Glut4 pre-mRNA splicing.

205 o potent compounds that were shown to target GLUT4 preferentially over GLUT1 and block glucose transp

206 an GLUT4 gene under the control of the human GLUT4 promoter (i.e., transgenic [TG] mice) are resistan

207 of WT but not MEF2A binding defective mutant GLUT4 promoter.

208 scued high-fat diet-induced decreased muscle GLUT4 protein and improved both fasting plasma insulin a

209 chanism regulated insulin-independent muscle GLUT4 protein expression in response to exercise in lean

210 BG4KO mice had a 99% reduction in GLUT4 protein expression throughout the brain.

211 However, no difference in GLUT4 protein expression was observed in VWR-exercised m

212 In contrast, GLUT4 protein expression was only partially restored by

213 -independent upregulation of skeletal muscle GLUT4 protein expression with exercise is through increa

214 Reduction of GLUT4 protein in sedentary animals upon treatment with r

215 RabGAP TBC1D1 plays a key role in regulating GLUT4 protein levels and in exercise-mediated glucose up

216 GLUT4 protein levels were reduced by approximately 40% i

217 e and white adipose tissue, the abundance of GLUT4 protein, but not GLUT4 mRNA, was substantially red

218 GLUT4 recruitment to the plasma membrane of skeletal mus

219 eases the rate constant for sorting into the Glut4 recycling pathway (ksort) 3-fold.

220 ent with rapamycin revealed mTORC1-dependent GLUT4 regulation.

221 lin stimulates proteolytic processing of the GLUT4 retention protein, TUG, to promote GLUT4 transloca

222 suggest that sortilin- and retromer-mediated Glut4 retrieval from endosomes may represent a step in t

223 s strongly bolster the utility of developing GLUT4-selective inhibitors as anti-cancer therapeutics.

224 ess that requires skeletal muscle SIRT3-AMPK-GLUT4 signaling.

225 ecialized intracellular compartments, termed GLUT4 storage vesicles (GSVs), to the plasma membrane.

226 cellular, insulin-responsive vesicles termed GLUT4 storage vesicles (GSVs).

227 somes into a second exocytic pathway through Glut4 storage vesicles (GSVs).

228 Rab10 and RalA reside in the same pool of Glut4-storage vesicles in untreated cells, and, together

229 We have generated a homology model for GLUT4 that we utilized to screen for drug-like compounds

230 The trafficking kinetics of Glut4, the transferrin (Tf) receptor, and LRP1 were quan

231 n triggers TUG cleavage to release the GSVs; GLUT4 then recycles through endosomes during ongoing ins

232 r of insulin-activated Rab13, which links to GLUT4 through ACTN4, localizing GLUT4 vesicles at the mu

233 red function of ankyrin-B (AnkB) in coupling GLUT4 to clathrin-mediated endocytosis.

234 ted for the signaling network between IR and GLUT4 to create a model also for their interconnections.

235 y sought to identify selective inhibitors of GLUT4 to develop a more potent cancer chemotherapeutic w

236 etal muscle by blocking the translocation of GLUT4 to the cell surface.

237 The active mTORC2 causes translocation of GLUT4 to the plasma membrane and glucose uptake without

238 ce and contraction-mediated translocation of GLUT4 to the plasma membrane in skeletal muscle.

239 Delivery of GLUT4 to the plasma membrane is mediated by formation of

240 Insulin controls the trafficking of Glut4 to the plasma membrane via regulation of a series

241 of the insulin-regulated glucose transporter GLUT4 to the plasma membrane, where it sustains the ATP

242 o promote the translocation of intracellular GLUT4 to the plasma membrane.

243 elerate formation of the vesicles that ferry GLUT4 to the PM during insulin stimulation.

244 ated translocation of exofacially myc-tagged GLUT4 to the surface of muscle cells.

245 dent translocation of glucose transporter 4 (Glut4) to the plasma membrane of fat and skeletal muscle

246 dent translocation of glucose transporter 4 (Glut4) to the plasma membrane plays a key role in the dy

247 hrough recruitment of glucose transporter 4 (GLUT4) to the plasma membrane.

248 the redistribution of glucose transporter 4 (GLUT4) to the plasma membrane.

249 cade in the regulation of insulin-stimulated Glut4 trafficking and glucose uptake.

250 rs of memory processing regulate hippocampal GluT4 trafficking and hippocampal memory formation is li

251 t TBC1D1 is not required for insulin-induced GLUT4 trafficking events.

252 tylated residues impaired insulin-responsive GLUT4 trafficking in 3T3-L1 adipocytes.

253 The function of SEC16A in GLUT4 trafficking is independent of its previously chara

254 t glucose uptake, associated with defects in GLUT4 trafficking to the plasma membrane.

255 that VAMP2 is the major v-SNARE involved in GLUT4 trafficking to the surface of 3T3-L1 adipocytes.

256 GLUT4 trafficking was altered in animals expressing muta

257 These findings functionally link TUSC5 to GLUT4 trafficking, insulin action, insulin resistance, a

258 3B, and SEC31, in the insulin stimulation of GLUT4 trafficking, suggesting that vesicles derived from

259 lin signal transduction to the regulation of GLUT4 trafficking.

260 ansport by regulating glucose transporter 4 (GLUT4) trafficking from specialized intracellular compar

261 erestingly, mathematical modeling shows that Glut4 traffics predominantly through the specialized Rab

262 xpression with exercise is through increased Glut4 transcription.

263 letal muscle samples revealed that increased GLUT4 transgene expression was associated with decreased

264 ere, we show that, in male rats, hippocampal GluT4 translocates to the plasma membrane after memory t

265 e adiponectin administration-induced cardiac GLUT4 translocation and endothelial nitric oxide synthas

266 the GLUT4 retention protein, TUG, to promote GLUT4 translocation and glucose uptake.

267 Memory training increased hippocampal GluT4 translocation and memory acquisition was impaired

268 es in the absence of insulin by upregulating GLUT4 translocation by PI3K mediated activation of Akt s

269 e, Rab10, is required for insulin-stimulated GLUT4 translocation in cultured 3T3-L1 adipocytes.

270 ogenesis and elongation, glucose uptake, and GLUT4 translocation in cultured murine and human adipocy

271 D4 (AS160) were previously shown to regulate GLUT4 translocation in response to activation of AKT and

272 ncomplete disruption of stimulated adipocyte GLUT4 translocation on whole-body glucose homeostasis is

273 ive or negative regulators of the ISP, using GLUT4 translocation to the cell surface as an output for

274 a defect in one of the components regulating GLUT4 translocation to the cell surface in response to i

275 t both insulin-stimulated glucose uptake and GLUT4 translocation to the plasma membrane are reduced b

276 GLUT4 translocation to the plasma membrane was elevated

277 n signaling and effect on glucose uptake and Glut4 translocation were decreased, and lipolysis was in

278 uppressed insulin-stimulated glucose uptake, GLUT4 translocation, and Akt signaling in 3T3-L1 adipocy

279 SEC16A knockdown attenuates insulin-induced GLUT4 translocation, phenocopying RAB10 knockdown.

280 red Rlf compensates for the loss of Rab10 in Glut4 translocation, suggesting that Rab10 recruits Rlf

281 rylation was the RabGAP AS160 that regulates GLUT4 translocation.

282 L2 (MICAL-L2-CT) impaired insulin-stimulated GLUT4 translocation.

283 pha-actinin-4 (ACTN4), a protein involved in GLUT4 translocation.

284 drolase-mediated glucose transporter type 4 (GLUT4) translocation.

285 ctivation that regulates the accumulation of GLUT4 transport vesicles at the plasma membrane.

286 es accelerated biogenesis of the specialized GLUT4 transport vesicles.

287 campal blockade of glucose transport through GluT4-upregulated markers of hippocampal insulin signali

288 e C2-domain factor Doc2b plays a key role in GLUT4 vesicle fusion, but its molecular mechanism has be

289 ng triggers actin remodeling, which promotes GLUT4 vesicle translocation and glucose uptake into skel

290 quired for localized F-actin polymerization, GLUT4 vesicle translocation, and glucose uptake.

291 -cortactin-mediated actin polymerization and GLUT4 vesicle translocation.

292 and Rab13 is necessary for insulin-regulated GLUT4-vesicle exocytic translocation in muscle cells.

293 ich links to GLUT4 through ACTN4, localizing GLUT4 vesicles at the muscle cell periphery to enable th

294 cts with the motor protein MyoVa to mobilize GLUT4 vesicles toward the muscle cell plasma membrane.

295 The decrease in GLUT4 was due to both decreased transcription of Glut4 m

296 cating that exercise-dependent regulation on GLUT4 was mTOR independent.

297 ) was upregulated but glucose transporter 4 (GLUT4) was unaffected, and adipose triglyceride lipase (

298 ufficient to completely transform GLUT1 into GLUT4 with respect to indinavir inhibition of 2-DOG upta

299 le protein levels of the glucose transporter GLUT4, with increasing number of p.Arg684Ter alleles.

300 %) the levels of glucose transporter type 4 (GLUT4) without affecting the Akt pathway.