ライフサイエンスコーパス: GLUT4

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

2 aB, resulting in the decreased expression of GLUT4.

3 ivo, concomitant with decreased abundance of GLUT4.

4 of the pathways from IR to translocation of GLUT4.

5 d glucose uptake and impaired endocytosis of GLUT4.

6 ous fat, and increased adipose expression of GLUT4.

7 ave a role in the specialized trafficking of GLUT4.

8 calization of Rab13 with ACTN4 or Rab13 with GLUT4.

9 there is no three-dimensional structure for GLUT4.

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

11 ble cardiomyocyte-specific expression of the GLUT4.

12 ng, stability, and insulin responsiveness of Glut4.

13 pathways, DNA methylation, and expression of GLUT4.

14 rt in general rather than being specific for GLUT4.

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

16 r CHC22 in addition to retrograde sorting of GLUT4 after endocytic recapture, enhancing pathways for

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

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

19 Glut4 also cycles through a slow constitutive endosomal

20 xpression in the liver and also up-regulated GLUT4 and adiponectin expression in adipose tissue.

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

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

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

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

25 5 from adipocytes reduces cellular levels of GLUT4 and concomitantly blunts the ability of insulin to

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

27 e transport in liposomes containing purified GLUT4 and GLUT3.

28 scle of CON but not PCOS, training increased GLUT4 and HKII mRNA and protein expressions.

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

30 lpha and PPARbeta, and reversing HFD-induced GLUT4 and pAKT reductions.

31 Here, we show that IRAP, similar to Glut4 and sortilin, is retrieved from endosomes to the t

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

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

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

35 ase (IRAP) along with glucose transporter 4 (Glut4) and sortilin, represents a major component protei

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

37 IVAS also up-regulated GLUT1, GLUT4, and PI3K p85alpha protein, and increased phosphor

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

39 not mobilize ATP7A nor does copper mobilize GLUT4, and RAB10 is not required for copper-elicited ATP

40 CHC22 complexes with ERGIC tether p115, GLUT4, and sortilin, and downregulation of either p115 o

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

42 lucose transport through glucose transporter GLUT4- and PI3K-dependent mechanisms.

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

44 Glycogen and glucose transporter GLUT4 are decreased.

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

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 The phenomenon was specific to GLUT4 because other recycling proteins were unaffected.

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

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

53 ation and memory acquisition was impaired by GluT4 blockade.

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

55 117 binding envelopes of exofacial GLUT1 and GLUT4 conformers differ significantly.

56 n in delivery of glucose transporter type 4 (GLUT4)-containing vesicles to the plasma membrane in res

57 Our results define the GLUT4-containing region of the TGN as a sorting and stor

58 ion to regulating the PM proximal effects of GLUT4-containing vesicles docking to and fusion with the

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

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

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

62 Because GLUT4 continually cycles between the PM and intracellula

63 GLUT4 controls glucose transport into fat and muscle tis

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

65 PM, also directly regulates the behavior of GLUT4 deeper within the cell.

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

67 Impaired GLUT4-dependent glucose uptake is a contributing factor

68 Here, we reflect on the importance of the GLUT4 discovery and chronicle additional key findings ma

69 The surfacing of the glucose transporter GLUT4 driven by insulin receptor activation provides the

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

71 methylation in the evaluated regions of the GLUT4-encoding gene Slc2a4.

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

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

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

75 5 mm glucose pulse increased adiponectin and GLUT4 expression and accumulation of neutral lipids via

76 ma FGF21 and white adipocyte tissue-specific GLUT4 expression and raised plasma glucose levels in LKO

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

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

79 tion of inflammatory pathways, and decreased GLUT4 expression in the GM of adult offspring.

80 mechanism that may be involved in decreasing GLUT4 expression is DNA methylation.

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

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

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 net redistribution of glucose transporter 4 (GLUT4) from intracellular storage to the plasma membrane

87 Remaining gaps in our understanding of GLUT4 function and regulation are highlighted here, alon

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

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

90 AMPK and plasma membrane localization of the GLUT4 glucose transporter in skeletal muscle, but are no

91 n, which stimulates the translocation of the GLUT4 glucose transporter to cell membranes.

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

93 ery of intracellular vesicles containing the GLUT4 glucose transporter to the plasma membrane.

94 This effect is mediated by the Glut4 glucose transporter.

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

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

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

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

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

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

101 ly increase or rapidly decrease cell-surface Glut4 in adipocytes stimulated with submaximal insulin c

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

103 We investigated the role of GLUT4 in adipose tissue and muscle in whole-body insulin

104 quester the facilitative glucose transporter GLUT4 in an intracellular compartment from where it can

105 f the insulin-responsive glucose transporter GLUT4 in humans.

106 and Tankyrase interact, and colocalise with GLUT4 in insulin-sensitive cells.

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

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

109 GLUT4 in muscle and adipose tissue is important in maint

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

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

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

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

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

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

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

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

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

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

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

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

122 agonists/antagonists decreased cell-surface Glut4 independently of insulin.

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

124 these data support our model that sorting of GLUT4 into its insulin-sensitive store involves a cycle

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

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

127 Consequently, GLUT4 intracellular sequestration and mobilization by in

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

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

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

131 GluT4 is also expressed in some hippocampal neurons, but

132 Glut4 is internalized and recycled through a highly regu

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

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

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

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

137 We also show that GLUT4 is retained in an element/domain of the TGN from w

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

139 Glucose transporter 4 (GLUT4) is sequestered inside muscle and fat and then rel

140 om adipose-specific GLUT4-overexpressing and GLUT4 knockout mice to find reciprocally regulated genes

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

142 ing tissue-specific GLUT4-overexpressing and GLUT4 knockout mice.

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

144 chronic nerve constriction causes increased GLUT4 levels in conjunction with decreased glycolytic ac

145 ular GLUT4 protein and enhanced cell surface GLUT4 levels in response to AMPK activation.

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

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

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

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

150 GLUT4 localization was scattered as opposed to clearly a

151 h into G(1) Of note, glucose transporter 4 (glut4) localized on the RMC surface at G(0)/G(1) and was

152 60 substrates on the trafficking kinetics of Glut4, LRP1, and the Tf receptor were measured in adipoc

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

154 TAZ upregulates IRS1 and stimulates Akt- and Glut4-mediated glucose uptake in muscle cells.

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

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

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

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

159 6-CHC22 and is less effective at controlling GLUT4 membrane traffic, altering its insulin-regulated r

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

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

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

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

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

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

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

167 trate that TBC1D4-RAB10 functions to control GLUT4 mobilization from a trans-Golgi network (TGN) stor

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

169 4 was due to both decreased transcription of Glut4 mRNA and decreased efficiency of Glut4 pre-mRNA sp

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

171 t and real-time PCR(qAMP); and expression of GLUT4 mRNA in the GM by real-time PCR.

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

173 Persistent reduction in Glut4 mRNA suggests that a posttranscriptional mechanism

174 65, and NF-kappaBp50 decreased expression of GLUT4 mRNA were observed in the PED-o rats.

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

176 Moreover, exposure of GLUT4-Myc-labeled L6 myoblasts to compound A increased G

177 Glut4 neuron-ablated mice show peripheral metabolic defe

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

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

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

181 Manipulation of the expression of GLUT4 or GLUT4-regulating molecules in mice has revealed

182 rays on adipose tissue from adipose-specific GLUT4-overexpressing and GLUT4 knockout mice to find rec

183 insulin sensitivity, making tissue-specific GLUT4-overexpressing and GLUT4 knockout mice.

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

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

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

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

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

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

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

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

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

193 a post-transcriptional increase in cellular GLUT4 protein and enhanced cell surface GLUT4 levels in

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

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

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

197 sity, intramuscular triglyceride content and GLUT4 protein expression using quantitative immunofluore

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

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

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

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

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

203 Despite the altered localization, we found GLUT4 protein levels to be increased 7.8-fold while GLUT

204 sulin-responsive glucose transporter type 4 (GLUT4) protein in 1988 inspired its molecular cloning in

205 GLUT4 recruitment to the plasma membrane of skeletal mus

206 Manipulation of the expression of GLUT4 or GLUT4-regulating molecules in mice has revealed the impa

207 ent with rapamycin revealed mTORC1-dependent GLUT4 regulation.

208 30 or sortilin, abrogates insulin-responsive GLUT4 release.

209 o noted that, under high-glucose conditions, glut4 remained on the RMC surface for at least 2 h into

210 on translocation of a glucose transporter 4 (Glut4) reporter expressed in murine 3T3-L1 adipocytes.

211 Insulin-stimulated trafficking of GLUT4 requires the myosin motor Myo1C and signaling adap

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

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

214 Unlike Glut4, retrograde transport of IRAP does not require sor

215 indicates that CHC22 traffic initiates human GLUT4 sequestration from the ERGIC and defines a role fo

216 endocytic recapture, enhancing pathways for GLUT4 sequestration in humans relative to mice, which la

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

218 n a HFD but not those heterozygous (+/-) for Glut4 (Slc2a4) on the same diet had an increase in decid

219 Here, we discuss GLUT4 sorting in different species and how studies of CH

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

221 nd assaying the effect on insulin-stimulated GLUT4 surface expression in differentiated L6 rat myocyt

222 Oylation had no effect on insulin-responsive GLUT4 surface trafficking using any of the tools we empl

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

224 mportant for infection, as overexpression of GLUT4, the high capacity glucose transporter, partially

225 In the late 1980s, when GLUT4, the major insulin-regulated glucose transporter,

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

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

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

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

230 3-L1 adipocytes shifts the endosomal pool of Glut4 to more acidic endosomes, but does not affect IRV

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

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

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

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

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

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

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

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

239 Here, we map the biogenesis of this GLUT4 traffic pathway in humans, which involves clathrin

240 tion to the PM, although where it intersects GLUT4 traffic was unknown.

241 cells have been invaluable in understanding GLUT4 traffic, evolutionary plasticity must be considere

242 identified species-specific distinctions in GLUT4 traffic, notably the participation of a novel clat

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

244 udy aimed to identify proteins that regulate GLUT4 trafficking and homeostasis via TBC1D1.

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

246 th and disease, our data strongly argue that GLUT4 trafficking in response to insulin is not regulate

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

248 - and exercise-stimulated glucose uptake and GLUT4 trafficking is TBC1D1.

249 Thus, investigation of regulated GLUT4 trafficking provides a major means by which to map

250 involved in the spaciotemporal regulation of GLUT4 trafficking represent potential therapeutic target

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

252 GLUT4 trafficking was altered in animals expressing muta

253 Mechanisms of action include effects on Glut4 trafficking, signal transduction, inhibition of pr

254 3B, and SEC31, in the insulin stimulation of GLUT4 trafficking, suggesting that vesicles derived from

255 lin signal transduction to the regulation of GLUT4 trafficking.

256 dies of CHC22 have identified new routes for GLUT4 trafficking.

257 labeled L6 myoblasts to compound A increased GLUT4 trafficking.

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

259 xpression with exercise is through increased Glut4 transcription.

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

261 We observe that GLUT4 transits through the early secretory pathway more

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

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

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

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

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

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

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

269 1D4 play a crucial role in the regulation of GLUT4 translocation in response to insulin and contracti

270 lin action in nonexercised muscle may reduce GLUT4 translocation in response to insulin.

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

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

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

274 GLUT4 translocation to the plasma membrane was elevated

275 als also a novel role of DNAJB3 in eliciting Glut4 translocation to the plasma membrane.

276 ng module is required for insulin-stimulated GLUT4 translocation to the PM, although where it interse

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

278 Two pathways that acutely regulate Glut4 translocation were discovered: de novo protein syn

279 , protein synthesis, FOXO nuclear exclusion, GLUT4 translocation, and glucose uptake were attenuated

280 Furthermore, insulin signaling, SkM GLUT4 translocation, hexokinase activity, and glycolysis

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

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

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

284 ownstream of AMPK and AKT, and the resultant GLUT4 translocation.

285 (IRS1, Akt, TBC1D4), and insulin-stimulated GLUT4 translocation.

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

287 lly, it was thought that 14-3-3beta promotes GLUT4 transport by binding the Myo1C lever arm and activ

288 es accelerated biogenesis of the specialized GLUT4 transport vesicles.

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

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

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

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

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

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

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 Glucose transporter 4 (GLUT4) was lower in IUGR and IUGR-AR skeletal muscle tha

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

299 that this process requires ubiquitination of GLUT4 while numerous other studies have identified sever

300 tent inhibitor of GLUT1 as well as GLUT3 and GLUT4, with an IC(50) value of low nanomolar for GLUT1.