ライフサイエンスコーパス: glycolysis

1 rter protein type 1-mediated arginolysis and glycolysis.

2 egulates pro-tumorigenic programs, including glycolysis.

3 P, while bloodstream cells switch to aerobic glycolysis.

4 nd a metabolic profile skewed toward aerobic glycolysis.

5 low CSE environment enhances the reliance on glycolysis.

6 kinase A, leading to enhanced malignant cell glycolysis.

7 CD4+ and CD8+ T cells had impaired resting glycolysis.

8 ediating mTOR inactivation and inhibition of glycolysis.

9 y enhancing Toll-like receptor (TLR)-induced glycolysis.

10 on, which is a critical regulator in aerobic glycolysis.

11 ciated to NAD(+) regeneration, essential for glycolysis.

12 tabolic reprogramming inducing shifts toward glycolysis.

13 the enhancement of key indicators of aerobic glycolysis.

14 in oxidative phosphorylation, and increased glycolysis.

15 d with enhanced FAO and a modest increase in glycolysis.

16 t that mediates exquisite control of aerobic glycolysis.

17 d protein response rather than by inhibiting glycolysis.

18 to uncouple rapid proliferation from aerobic glycolysis.

19 tive phosphorylation and metabolic shifts to glycolysis.

20 isolation of cells with different levels of glycolysis.

21 elationships of hypoxia, glucose uptake, and glycolysis.

22 combination of oxidative phosphorylation and glycolysis.

23 t protein/min, representing ~0.003-0.006% of glycolysis.

24 ted with an apparent inability to upregulate glycolysis.

25 tate, which can be reversed by inhibition of glycolysis.

26 vity towards 2-deoxyglucose, an inhibitor of glycolysis.

27 V, metabolic tumour volume, and total lesion glycolysis.

28 d, but not quiescent, HSCs relied readily on glycolysis.

29 ity due to diverse pathologies with enhanced glycolysis.

30 Concurrent inhibition of glycolysis (2-deoxy-D-glucose, 2DG) and mitochondrial re

31 ts for the fermentative component of aerobic glycolysis, a near ubiquitous metabolic alteration in ca

32 tions indicate that a metabolic shift toward glycolysis accompanies collective cellular migration but

33 phages undergo a metabolic switch to aerobic glycolysis, accumulating Krebs' cycle intermediates that

34 icantly colocated with prior maps of aerobic glycolysis (AG), AG-related gene expression, postnatal c

35 g electrons away from the respiratory chain, glycolysis also enables thiol/disulfide exchange-mediate

36 ynthesis and central carbon pathways such as glycolysis and amino acid metabolism are shown to synchr

37 roteins, alarmins, protease inhibitors); and glycolysis and antioxidant defense enzymes.

38 sulfatase Sulf-2), and TIGAR (TP53-inducible glycolysis and apoptosis regulator).

39 nced differentiation towards effector cells, glycolysis and apoptosis.

40 exposure to cigarette smoke extract enhances glycolysis and attenuates AMP-activated protein kinase (

41 Both glycolysis and basal respiration were reduced in DM, and

42 hepatic ChREBP knockdown reduced downstream glycolysis and de novo lipogenesis but also strongly sup

43 binding protein (ChREBP), a key regulator of glycolysis and de novo lipogenesis, is increased in GSD

44 but rather failure to recoup the ATP cost of glycolysis and diversion of glucose metabolites to the p

45 ls is mediated by reduction of viral-induced glycolysis and enhanced innate antiviral responses.

46 olase A and ERK signaling which up-regulates glycolysis and especially the non-oxidative pentose phos

47 nvestigated the metabolic control of cardiac glycolysis and explored the potential of glucose 6-phosp

48 HUVEC were reliant on glycolysis and FAO, and inhibition of either pathway dis

49 oxidation (FAO), whereas GW0742 reduced both glycolysis and FAO.

50 cid (TCA) cycle converts the end products of glycolysis and fatty acid beta-oxidation into the reduci

51 ant CSC- and EMT-like phenotype with aerobic glycolysis and fatty acid beta-oxidation-mediated oxidat

52 e bioenergetics by shifting redox balance to glycolysis and fermentation, thereby diminishing electro

53 ine biosynthesis pathway (HBP) branches from glycolysis and forms UDP-GlcNAc, the moiety for O-linked

54 es adapt their metabolism rapidly to enhance glycolysis and fuel specialized antimicrobial effector f

55 to study the metabolic control of myocardial glycolysis and G6P levels.

56 fatty acid metabolism toward oxygen-sparing glycolysis and glucose oxidation and to increase cAMP le

57 Aerobic glycolysis and glutaminolysis are two of the most essent

58 K/ERK pathways, suppressed the expression of glycolysis and glutaminolysis genes and blocked metaboli

59 tudy provides evidence for the importance of glycolysis and glutaminolysis, but not fatty acid beta-o

60 creased 2.1-fold, indicating an inability of glycolysis and glycogen synthesis to process glucose at

61 eoclasts heavily relies on increased aerobic glycolysis and glycolysis-derived lactate production.

62 -type, VHL-deficient Th17 cells had elevated glycolysis and glycolytic capacity.

63 Collectively, our data identify enhanced glycolysis and HIF-1alpha activation as drivers of low-g

64 the saturated fatty acid palmitate increased glycolysis and HIF-1alpha expression, which culminated i

65 state acetate (PMA) upregulated fermentative glycolysis and increased cellular ROS accumulation under

66 n cellular levels of citrate would stimulate glycolysis and inhibit gluconeogenesis.

67 ose involved in cell survival, angiogenesis, glycolysis and invasion/metastasis.

68 to reprogramming of cell metabolism towards glycolysis and lactate dehydrogenase A (LDHA).

69 ation has been previously linked to impaired glycolysis and mitochondrial dysfunction.

70 ectively, this study reveals a role for both glycolysis and mitochondrial metabolism in cytokine-stim

71 nd associated with the metabolic coupling of glycolysis and mitochondrial oxidation that is necessary

72 e is a direct readout of the balance between glycolysis and mitochondrial oxidative metabolism.

73 Metabolic shifting between glycolysis and mitochondrial oxidative phosphorylation h

74 We analyzed glycolysis and mitochondrial respiration in resting and

75 with a marked increase in energy metabolism (glycolysis and mitochondrial respiration) of peripheral

76 The association of citrin with glycolysis and NAD+/NADH ratio led us to hypothesize tha

77 and is essential for supplementing NAD+ for glycolysis and NADH for oxidative phosphorylation.

78 2 to M1 continuum and appear to utilize both glycolysis and OX PHOS in obesity.

79 lso acquire a hybrid phenotype in which both glycolysis and oxidative phosphorylation (OXPHOS) can be

80 Recent studies support the notion that glycolysis and oxidative phosphorylation are rheostats i

81 This coincided with an increase in glycolysis and oxidative phosphorylation measured with S

82 metabolic profiles characterized by elevated glycolysis and oxidative phosphorylation, distinct from

83 ork demonstrated a post-LVAD dissociation of glycolysis and oxidative-phosphorylation characterized b

84 s that allow more direct assessment of tumor glycolysis and oxygenation status quantitatively.

85 endent metabolic pathway, leading to aerobic glycolysis and polarization of macrophages.

86 bility (migration and invasion) through anti-glycolysis and pro-autophagy.

87 educe HIF-1alpha levels, thereby suppressing glycolysis and production of IL-1beta, IL-6, and IL-12,

88 phosphorylation, cause a metabolic switch to glycolysis and reduce ATP production in TNBC cells.

89 deficiency also results in defective aerobic glycolysis and reduced lactate production.

90 which shifts metabolism from respiration to glycolysis and reduces energy production, is known to be

91 e associated with altered glucose metabolism/glycolysis and report here that TG2 expression and activ

92 tic measurement and metabolomics upregulated glycolysis and suppressed oxidative phosphorylation.

93 nt cells lose the WE but continue to conduct glycolysis and surprisingly remain dependent on glucose

94 ls and mammalian cells to initiate anaerobic glycolysis and survive hypoxia.

95 Glycolysis and the generation of mitochondrial reactive

96 -/-) macrophages show increased flux through glycolysis and the pentose phosphate pathway, thereby es

97 increased glucose uptake and utilization by glycolysis and the pentose shunt, but no changes in glut

98 expression patterns of the genes involved in glycolysis and the synthesis of FAs, 2-MAG, TAG, and mem

99 ine, and citrate) were mapped to pathways of glycolysis and the TCA cycle demonstrating tumor metabol

100 onists, a downregulation of genes related to glycolysis and the TCA cycle, and a lower rate of cell c

101 gly, numerous NCLDV encode the components of glycolysis and the TCA cycle, suggesting that they can r

102 gh cytosolic NAD levels in supporting robust glycolysis and to transfer electrons to the electron tra

103 de range of human cancers and drives aerobic glycolysis and tumor growth by inhibiting pyruvate kinas

104 racrine signals that increase malignant cell glycolysis and tumour growth.

105 We observed perturbed glycolysis and visibly reduced markers of Warburg effect

106 imary mammary epithelial cells, fermentative glycolysis, and intracellular concentration of reactive

107 ore, changes in pathways of lipid oxidation, glycolysis, and mitochondrial oxidative phosphorylation

108 atment with CoCl(2), leads to an increase in glycolysis, and more dangerous tumors.

109 ndance in tubular epithelial cells, enhanced glycolysis, and suppression of fatty acid oxidation.

110 metabolites involved in glycogen metabolism, glycolysis, and the Krebs cycle, but the levels of pento

111 in a decrease in lactate transport, reduced glycolysis, and ultimately reduced cell proliferation.

112 ism in mice and inhibiting CSE or modulating glycolysis are potential targets for host-directed TB co

113 n this light, single cells that exhibit high glycolysis are specific targets for therapy.

114 Increased glucose uptake and aerobic glycolysis are striking features of many cancers.

115 d to high glucose, which stimulates cellular glycolysis as measured by Seahorse analysis.

116 fatty acid oxidation and strikingly promoted glycolysis, as evidenced by our transcriptomic and metab

117 available in vitro data showed a decrease of glycolysis-associated genes after treatment with the EP3

118 cells from patients with ME/CFS had reduced glycolysis at rest, whereas CD8+ T cells also had reduce

119 flux analysis revealed that VEGF-A promoted glycolysis at the expense of fatty acid oxidation (FAO),

120 t with this, 2-deoxyglucose, an inhibitor of glycolysis, augmented AMPK activity and attenuated ZIKV

121 In CD8 + splenic T cells from the HFS mice, glycolysis/basal respiration ratio was significantly red

122 In hypoxia, however, glycolysis becomes critical for cytokine production and

123 We show that reducing glycolysis both lowers steady-state levels of ATP and st

124 FBP1 inhibits glycolysis but also directly interferes with PRC2 functi

125 d that S47 cells exhibit decreased catabolic glycolysis but increased use of the pentose phosphate pa

126 elevated 50-fold, consistent with decreased glycolysis but possibly including glycogen mobilization

127 ROS generated by NOX2 in AML cells promotes glycolysis by activating PFKFB3 and suggest PFKFB3 as a

128 allenged with high glucose by stimulation of glycolysis by an AMP-activated protein kinase-independen

129 PNC synchronizes mitochondrial activity with glycolysis by balancing electron transfer to mitochondri

130 ly, skewing T cell metabolism toward aerobic glycolysis by deleting mitochondrial pyruvate carrier re

131 Citrate is known to suppress glycolysis by inhibiting phosphofructokinase-1 and activ

132 Our study suggests that inhibiting glycolysis by targeting Gpi1 could be an effective thera

133 a lower glucose uptake (deceased > 40%) and glycolysis capacity (reduced approximately 50%).

134 method to reform the metabolic shift toward glycolysis caused by glucose oversupply by integrating N

135 atures in distinct pathways such as hypoxia, glycolysis, cell metabolism, translation initiation, cel

136 ed, including starch and sucrose metabolism, glycolysis, citrate cycle, amino acids synthesis, and pl

137 ncreased oxidative phosphorylation and basal glycolysis compared to WT cells and correlated with moto

138 y relies on increased aerobic glycolysis and glycolysis-derived lactate production.

139 While pharmacological inhibition of glycolysis did not affect osteoclast differentiation or

140 t with a role for metabolic intermediates in glycolysis-driven biomass production, dietary amino acid

141 on on host cell metabolism as an increase in glycolysis during infection has been defined.

142 lize a range of carbohydrates that feed into glycolysis ending in pyruvate, which is catabolized by s

143 Notably, in vivo inhibition of glycolysis enhanced the competitive repopulation ability

144 We found decreased flux from glycolysis entering the tricarboxylic acid cycle in Mull

145 alternative arrestin-1 binding partners, the glycolysis enzyme enolase-1, to map the molecular contac

146 s of cancer cells, characterized by enhanced glycolysis even under aerobic conditions.

147 , NF-kappaB2 played a key role in regulating glycolysis, exhibiting a metabolic shift when MGs had an

148 aling, mitochondrial oxygen consumption, and glycolysis extracellular acidification rate assays.

149 Glycolysis, FA and membrane lipid biosynthesis were repr

150 developing nodules revealed highly activated glycolysis, fatty acid (FA), 2-monoacylglycerol (2-MAG),

151 amycin (AKT-mTOR) pathway, increased aerobic glycolysis, favored Th17 cell differentiation over that

152 ignant tumors are characterized by increased glycolysis followed by lactic acid fermentation, even in

153 rest, whereas CD8+ T cells also had reduced glycolysis following activation.

154 d used fatty acid oxidation (FAO) instead of glycolysis for energy.

155 cells, we discovered that S. aureus requires glycolysis for survival in bone.

156 Quiescent HSCs are thought to rely on glycolysis for their energy, but the overall metabolic p

157 l retina metabolizes glucose through aerobic glycolysis generating large amounts of lactate.

158 lytic intermediates, increased expression of glycolysis genes, and increased ethanol production.

159 C-13) had opposite effects from metformin on glycolysis, gluconeogenesis, and cell G6P.

160 ent in central metabolic pathways, including glycolysis, gluconeogenesis, the tricarboxylic acid (TCA

161 associations of baseline and 1-y changes in glycolysis/gluconeogenesis and TCA cycle metabolites wit

162 Glycolysis/gluconeogenesis and tricarboxylic acid (TCA)

163 ion, oocyte meiosis, cholesterol metabolism, glycolysis/gluconeogenesis, and MAPK, PI3K-AKT, HIPPO an

164 ic changes in the levels of intermediates of glycolysis/gluconeogenesis, the tricarboxylic acid cycle

165 We identified a panel of glycolysis/gluconeogenesis-related metabolites that was

166 D-1 deficiency shifts ILC2 metabolism toward glycolysis, glutaminolysis and methionine catabolism.

167 in vivo imaging in patients showed enhanced glycolysis, glutaminolysis, and tricarboxylic acid cycle

168 Specifically, aberrant glycolysis, glutaminolysis, fatty acid and glycosphingol

169 lic fitness characterized by increased basal glycolysis, glycolytic capacity, maximal mitochondrial r

170 Targeting glycolysis has been considered therapeutically intractab

171 Hypoxia and glycolysis have long been appreciated to promote immune

172 , G6PD-deficient RBCs demonstrated increased glycolysis, impaired glutathione homeostasis, and increa

173 alyses revealed that HDAC inhibitors blunted glycolysis in a c-Myc-dependent manner and lowered ATP l

174 ssue, and up-regulation of miR-203-3p limits glycolysis in adipose under conditions of metabolic stre

175 he activity of the PI3K/AKT/mTOR pathway and glycolysis in B-cell lymphomas.

176 K2 promotes PI3K/AKT and HIF-1alpha-mediated glycolysis in bladder cancer cells.

177 High rates of glycolysis in cancer cells are a well-established charac

178 a DeltahemB SCV prototype potently activate glycolysis in host cells.

179 ethyltransferase 6 (PRMT6) regulates aerobic glycolysis in human hepatocellular carcinoma (HCC) throu

180 STING agonists activated STAT3 and promoted glycolysis in IECs.

181 lating cross talk between mTOR signaling and glycolysis in liver cancer progression is not fully unde

182 Similarly, pharmacological inhibition of glycolysis in mammalian cells induces ciliary translocat

183 ia GLUT (glucose transporter)-1 and enhanced glycolysis in neutrophils promoted the production of S10

184 TGF-beta treatment increased glycolysis in PASMCs, but did not recapitulate the PAEC

185 an and mouse macrophages undergo a switch to glycolysis in response to IgG IC stimulation, mirroring

186 AMs did not upregulate glycolysis in response to LPS, irrespective of LKB1 pres

187 (OXPHOS), the rates of utilization of OXPHOS/glycolysis in response to metabolic stress, and mitochon

188 ast fusion, cellular oxygen consumption, and glycolysis in skeletal muscle cells.

189 Liraglutide blocked glycolysis in T cells and decreased their Glut1 mRNA exp

190 We show that CRISPR-mediated targeting of glycolysis in T cells in mice results in global loss of

191 veal a novel role for TRIM32 for controlling glycolysis in the context of both normal development and

192 ionship between hypoxia, glucose uptake, and glycolysis in three human pancreatic ductal adenocarcino

193 VEGF-A was a potent inducer of glycolysis in tubulogenic HUVEC, while FAO was maintaine

194 High rates of glycolysis in tumors have been associated with cancer me

195 abolic changes have been compared to aerobic glycolysis in tumour cells.

196 ectively, these results demonstrate that the glycolysis-inactive form of PKM2 plays a crucial role in

197 lude restoring oxidative phosphorylation and glycolysis, increasing insulin sensitivity, correcting m

198 sms responsible for the beneficial effect of glycolysis induction during the recovery of failing huma

199 sensing promotes adipocyte glycolysis, while glycolysis inhibition impeded IFNbeta-driven intra-adipo

200 In vivo, glycolysis inhibition led to a reduction in kidney macro

201 tected from MMS-induced NAD(+) depletion and glycolysis inhibition.

202 treated or not with sodium iodoacetate (IAA; glycolysis inhibitor) plus 2,4-dinitrophenol (DNP; oxida

203 apeutic potential of using 2-deoxyglucose, a glycolysis inhibitor, to reverse tumorigenicity and sora

204 Although glycolysis is a main driver of allogeneic T cell-driven

205 These findings reveal that aerobic glycolysis is a process functionally distinct from conve

206 ing glucose transporters to regulate aerobic glycolysis is an attractive approach to identify potenti

207 s not fuel mitochondrial ATP generation, and glycolysis is dispensable for blastocyst formation.

208 Moreover, glycolysis is essential for V-ATPase-mediated proton pum

209 T-cell glycolysis is inhibited at the low pH observed in LNs.

210 Glycolysis is one of the primordial pathways of metaboli

211 T1 expression and activity, and GnRH-induced glycolysis is recapitulated in primary gonadotropes.

212 ngly, when ECs become quiescent, endothelial glycolysis is repressed, and GLUT1 expression increases

213 lic switch from oxidative phosphorylation to glycolysis is required for tumorigenesis in order to pro

214 We show that glycolysis is required to maintain the plasma membrane p

215 Glycolysis is the main HIF-regulated pathway that drives

216 osynthesis pathway (HBP), a shunt pathway of glycolysis, is a metabolic node in cancer cells that can

217 Glucose, the starting material for glycolysis, is transported through the cellular membrane

218 ations of a range of metabolites relating to glycolysis (lactate, pyruvate, succinate).

219 the endothelium by enhancing PFKFB3-mediated glycolysis, leading to a proadhesive state, which can be

220 ation is characterized by an upregulation of glycolysis, leading to an augmentation in lactate produc

221 ion of GLUT1 decreases EC glucose uptake and glycolysis, leading to energy depletion and the activati

222 el phosphorylation via genetic disruption of glycolysis leads to rapid sterilization.

223 Consequently, this altered state of glycolysis led to differential metabolic activity and re

224 ial signalling intermediary for TLR4-induced glycolysis, macrophage metabolic reprogramming and infla

225 n glucose limitation, Vitamin K2-upregulated glycolysis markedly induced metabolic stress, along with

226 Our findings support a novel role for glycolysis-mediated TG2 induction and tissue fibrosis as

227 Surprisingly for a gatekeeper of glycolysis, no fine control mechanism of betaPGM has yet

228 promoter, and drives NE differentiation and glycolysis of prostate cancer.

229 unctionally different during fully oxidative glycolysis or during the WE is unknown.

230 3)C]lactate conversion rates, independent of glycolysis or LDHA activity.

231 dependent of increased ATP synthesis through glycolysis or oxidative phosphorylation, but dependent o

232 Aerobic glycolysis or the Warburg effect (WE) is characterized b

233 Inhibition of glycolysis, or genetic depletion of HIF1alpha, attenuate

234 Aerobic glycolysis, originally identified by Warburg as a hallma

235 viding lymphocytes typically rely on aerobic glycolysis over oxidative phosphorylation for energy.

236 and metabolically reprogram to favor aerobic glycolysis over oxidative phosphorylation.

237 es involved in oxidative phosphorylation and glycolysis (OXPHOG) as a critical predictor of patient s

238 This includes the glycolysis pathway (composed of 10 genes) and inducible

239 that the most potent modifiers refer to the glycolysis pathway and that, more broadly, they show str

240 Diseased PAECs had increased proximate glycolysis pathway intermediates, less pentose shunt flu

241 nversion into DATPs via a HIF1alpha-mediated glycolysis pathway, which is required for mature AT1 cel

242 ehydrogenase (GAPDH), a critical node in the glycolysis pathway.

243 Glycolysis plays an important role in the metabolic plas

244 creatine, IECs transition toward a stressed, glycolysis-predominant form of metabolism; this resulted

245 Pharmacological inhibition of glycolysis preferentially impedes tumorigenicity of huma

246 ve metabolic remodeling to engage in aerobic glycolysis prior to delamination.

247 cancer cells by PI3K/AKT/HIF-1alpha-mediated glycolysis promotion.

248 How glycolysis regulates WNT signalling in the tail bud is c

249 elanin inside the phagosome and induction of glycolysis required for efficient innate immune response

250 inhibition of oxidative phosphorylation and glycolysis, respectively, in murine immune cells.

251 ing ASS1- and GLUT1-mediated arginolysis and glycolysis, respectively, which may provide insights int

252 Our data reveal a mechanism by which glycolysis responds to architectural features of the act

253 romoted effector-like metabolism and aerobic glycolysis, robustly inducing lactate dehydrogenase (LDH

254 Glycolysis shifted towards the pentose phosphate and gly

255 on of PI3K/AKT/HIF-1alpha and attenuation of glycolysis significantly blocked Vitamin K2-induced AMPK

256 Inhibition of STAT3 pathway and glycolysis suppressed STING-induced REG3gamma production

257 isotopologues of intermediate metabolites of glycolysis, TCA cycle, amino acids, pentose phosphate pa

258 ongation(1), exhibit a high level of aerobic glycolysis that is reminiscent of the metabolic status o

259 Most tumor cells use aerobic glycolysis (the Warburg effect) to support anabolic grow

260 ral pathways of energy metabolism, including glycolysis, the tricarboxylic acid cycle, and electron t

261 rate and kinetics of glucose consumption and glycolysis throughout IVM.

262 umor was based on the change in total lesion glycolysis (TLG) between baseline and follow-up and was

263 abolic tumour volume (MTV), and total lesion glycolysis (TLG) obtained by PET/CT, and also to compare

264 x), metabolic tumor volume, and total lesion glycolysis (TLG) were determined for the primary tumor,

265 ard glucose uptake (SUVmax) and total lesion glycolysis (TLG), nutritional risk as measured by the ma

266 in the tumor, and the second is total lesion glycolysis (TLG), which is the TLV multiplied by the ave

267 the ability to undergo a metabolic switch to glycolysis to allow them to perform rapid plastic respon

268 metabolism of amino acids and a switch from glycolysis to gluconeogenesis while those of cells carry

269 Tumor cells rely on glycolysis to meet their elevated demand for energy.

270 A metabolic transition from glycolysis to oxidative phosphorylation is often associa

271 rogenase, which controls the transition from glycolysis to the citric acid cycle, effectively reduces

272 ripts of the genes and pathways of immunity, glycolysis, tricarboxylic acid cycle, OX-PHOS, nicotinam

273 olic changes might be indicative of enhanced glycolysis triggered by hypoxia conditions as a conseque

274 lpha protein levels and a metabolic shift to glycolysis under normoxic conditions.

275 homeostatic Th17 cells, partial blockade of glycolysis upon Gpi1 inactivation was compensated by pen

276 state, serving as a carbon source that fuels glycolysis (Varahan et al., 2019).

277 based on the opposing enzyme requirements of glycolysis versus gluconeogenesis.

278 o soft substrates causes a downregulation of glycolysis via proteasomal degradation of the rate-limit

279 nd basal respiration were reduced in DM, and glycolysis was increased by metformin.

280 Glycolysis was inhibited in cells and mice by administra

281 Increased glycolysis was likely a response to perturbation of mito

282 A general reduction in oxidative glycolysis was observed in accordance with the Warburg t

283 p-regulation of PFKFB3 protein and increased glycolysis were early and sustained events during HSC ac

284 LUT4 translocation, hexokinase activity, and glycolysis were increased.

285 te production from glucose, known as aerobic glycolysis when oxygen is abundant, is also critical for

286 This argues that cells engage in aerobic glycolysis when the demand for NAD(+) is in excess of th

287 M1 macrophages primarily rely on glycolysis, whereas M2 macrophages rely on the tricarbox

288 ting lactose synthesis to acute fermentative glycolysis which caused increased flux of glucose metabo

289 nd rats) have increased levels of PFKFB3 and glycolysis, which are essential for activation of HSCs.

290 nse, hMDMs shift their metabolism to aerobic glycolysis, which directly triggers an M1-like pro-infla

291 ed from oxidative phosphorylation to aerobic glycolysis, which is considered important for proinflamm

292 Since EP300 is a promoter of glycolysis, which negatively affects anti-tumor immune r

293 ic analyses reveal that HIF-1alpha regulates glycolysis while HIF-2alpha regulates genes associated w

294 IFNbeta-sensing promotes adipocyte glycolysis, while glycolysis inhibition impeded IFNbeta-

295 ochondrial pyruvate metabolism and inhibited glycolysis, while MPC-1-specific inhibitor UK5099 attenu

296 Inhibition of glycolysis with 2-deoxy-D-glucose (2-DG) reduced osteocl

297 es an immunometabolic signaling axis towards glycolysis with activation of hypoxia-inducible factor 1

298 t1 in osteoclast progenitors reduces aerobic glycolysis without compromising OXPHOS, but nonetheless

299 hosphorylation characterized by induction of glycolysis without subsequent increase in pyruvate oxida

300 isolate cancer cell subpopulations based on glycolysis without the use of labels or active sorting c