ライフサイエンスコーパス: glutaminolysis

1 tion from glutamine was essentially zero (no glutaminolysis).

2 otency by affecting stem cell activation and glutaminolysis.

3 s and increases mitochondrial respiration by glutaminolysis.

4 chanism of resistance to therapies targeting glutaminolysis.

5 airway inflammation, and Th17 cells rely on glutaminolysis.

6 sic and accompanied by a metabolic switch to glutaminolysis.

7 cated a unique role for p15/16 in regulating glutaminolysis.

8 n by increasing pyruvate-alanine cycling and glutaminolysis.

9 uamous cell carcinoma (HNSCC) is addicted to glutaminolysis.

10 esults in a shift from aerobic glycolysis to glutaminolysis.

11 etabolism facilitated by hyperglycolysis and glutaminolysis.

12 1 (GLS1), which catalyzes the first step in glutaminolysis.

13 xPhos induces a metabolic reprogramming into glutaminolysis.

14 glutaminase (GLS), inhibiting glycolysis and glutaminolysis.

15 luding glycolysis, one-carbon metabolism and glutaminolysis.

16 mal stem cells (MSCs) through suppression of glutaminolysis.

17 bolism towards pentose phosphate pathway and glutaminolysis.

18 bolism which is compensated for by increased glutaminolysis.

19 ce ATP and to inhibit AMPK, independently of glutaminolysis.

20 le alpha-ketoglutarate production as part of glutaminolysis.

21 phosphorylation and increased glycolysis and glutaminolysis.

22 e levels were decreased, suggesting enhanced glutaminolysis.

23 ctivated T cells to switch to glycolysis and glutaminolysis.

24 r cells exhibit high rates of glycolysis and glutaminolysis.

25 intermediates in glycolysis, TCA cycle, and glutaminolysis.

26 s that participate in aerobic glycolysis and glutaminolysis.

27 ce, mitochondrial biogenesis, apoptosis, and glutaminolysis.

28 hydrogenase kinase, fatty acid oxidation, or glutaminolysis.

29 ry tumors revealed a significant increase in glutaminolysis, a critical metabolic pathway that genera

30 Glutaminolysis, an anaplerotic pathway, replenished aspa

31 It is therefore concluded that glutaminolysis and aerobic glycolysis are important for

32 egulators CB-839 or GSK2837808A that inhibit glutaminolysis and aerobic glycolysis, respectively, als

33 These changes were largely dependent on glutaminolysis and aerobic glycolysis.

34 owth and migration through YAP/TAZ-dependent glutaminolysis and anaplerosis, and thereby link mechani

35 uding glycolysis, oxidative phosphorylation, glutaminolysis and anti-oxidant response.

36 ons, modifying expression of genes linked to glutaminolysis and DNA replication.

37 es that determine mitochondrial respiration, glutaminolysis and fatty acid synthesis.

38 served upon loss of FoxO3 revealed a drop in glutaminolysis and filling of the tricarboxylic acid (TC

39 The contributions of MUC5AC to glutaminolysis and gemcitabine resistance were examined

40 Here, we focused on glutaminolysis and genetically blocked this process thro

41 including glutaminase (GLS1), to coordinate glutaminolysis and glycolysis.

42 n the thymus promotes aerobic glycolysis and glutaminolysis and increases allocation of glutamine car

43 Consequently, inhibition of glutaminolysis and inhibition of autophagy strongly and

44 itochondrial dynamics, increased glycolysis, glutaminolysis and lactic acidosis, and neurotransmitter

45 The degree of glutaminolysis and lipid synthesis was specific to the c

46 In this study, we explored the role of glutaminolysis and metabolites of TCA in supporting myof

47 cy shifts ILC2 metabolism toward glycolysis, glutaminolysis and methionine catabolism.

48 r basis for cancer therapy through targeting glutaminolysis and mitochondrial respiration in ESCC wit

49 a consequence of the aberrant activation of glutaminolysis and mTORC1 signaling during nutritional i

50 ograms cellular metabolic pathways to favour glutaminolysis and oxidative metabolism, which are requi

51 asing mitochondrial and glycolytic capacity, glutaminolysis and polyamine synthesis, and reprogrammed

52 glucose and glutamine catabolites, promoting glutaminolysis and preserving the TCA cycle and hexosami

53 dependency of leukemic cells, causes reduced glutaminolysis and profound tumor reduction in pre-clini

54 mation that enables glutaminases to catalyze glutaminolysis and support cancer progression.

55 ycolysis, thereby increasing dependence upon glutaminolysis and the pentose phosphate pathway.

56 ronounced metabolic features of tumor cells: glutaminolysis and the Warburg effect.

57 Serine biosynthesis intersects glutaminolysis and together with this pathway provides s

58 This was associated with elevated levels of glutaminolysis and tricarboxylic acid (TCA)-related meta

59 bolic shutdown, with prominent inhibition of glutaminolysis and triggers autophagy as a salvage pathw

60 duce a transcriptional program that promotes glutaminolysis and triggers cellular addiction to glutam

61 ether, the data define a mechanism to induce glutaminolysis and uncover a survival pathway engaged du

62 enables malignant cells to undergo increased glutaminolysis and utilization of glutamine as an altern

63 etabolism (e.g. activation of glycolysis and glutaminolysis) and changes in histone methylation, acet

64 or nucleotide biosynthesis and substrate for glutaminolysis), and arginine (an essential amino acid f

65 amycin signaling axis; increased glycolysis, glutaminolysis, and cholesterol synthesis; epigenetic ch

66 We found that glycolysis, glutaminolysis, and FAS are all required for maximal KSH

67 etabolic pathways, including the glycolysis, glutaminolysis, and fatty acid synthesis (FAS) pathways,

68 ar metabolic pathways, including glycolysis, glutaminolysis, and fatty acid synthesis.

69 ent uptaking, increased glycolysis, elevated glutaminolysis, and heightened synthesis of fatty acids

70 change their metabolism to favor glycolysis, glutaminolysis, and lactate generation.

71 IL-17A-mediated increases in HPK glycolysis, glutaminolysis, and lipid uptake, which were validated u

72 ied by increased glutamine uptake, increased glutaminolysis, and rewired cellular metabolism, as evid

73 pulmonary glutamine assimilation, activating glutaminolysis, and thereby restrain detrimental inflamm

74 f2-mutant cancers are dependent on increased glutaminolysis, and this property can be therapeutically

75 ging in patients showed enhanced glycolysis, glutaminolysis, and tricarboxylic acid cycle metabolism

76 ically flexible and sustained growth through glutaminolysis, another metabolic process frequently imp

77 Aerobic glycolysis and glutaminolysis are two of the most essential characteris

78 e (GLS), a target of MYC and a key enzyme in glutaminolysis, are intrinsically resistant to platinum-

79 and glucose oxidation, fatty acid oxidation, glutaminolysis, arginine metabolism, one-carbon metaboli

80 Here we identify glutaminolysis as a critical pathway for leukemia cell g

81 Overall, these results identify glutaminolysis as a major node in cancer metabolism cont

82 vidence implicating increased glycolysis and glutaminolysis as mediators of fibrosis is presented, wi

83 toglutarate and malate despite high rates of glutaminolysis, as determined by flux studies with isoto

84 ohol consumption and RORgammat deficiency on glutaminolysis, biosynthesis, and tumor growth in vivo.

85 logue analysis, we showed that LND increased glutaminolysis but decreased reductive carboxylation of

86 rload also led to inefficient glycolysis and glutaminolysis but heightened activity in the hexosamine

87 Glycolysis and glutaminolysis, but not FAS, inhibit viral genome replic

88 vidence for the importance of glycolysis and glutaminolysis, but not fatty acid beta-oxidation, as an

89 Glycolysis can provide energy and glutaminolysis can provide carbon for anaplerosis and re

90 ession is dependent on sufficient amounts of glutaminolysis catabolites particularly alpha-ketoglutar

91 Here, we report that aerobic glycolysis and glutaminolysis co-operatively reduce UDP-GlcNAc biosynth

92 ells from male humans and mice had decreased glutaminolysis compared with female individuals, and tha

93 How mitochondrial glutaminolysis contributes to redox homeostasis in cance

94 Glutaminolysis converts Gln into alpha-ketoglutarate (al

95 glutamine utilization and the inhibition of glutaminolysis could have clinical implications.

96 sphocholine level together with increases in glutaminolysis, de novo fatty acid synthesis and pyruvat

97 l pyruvate carrier, fatty acid oxidation, or glutaminolysis, demonstrating a compensatory role of mit

98 AR signaling thus attenuates glutaminolysis, demonstrating sex-specific metabolic reg

99 tion enhances mitochondrial dysfunction in a glutaminolysis-dependent and autophagy-independent manne

100 These findings identify glutaminolysis-derived Asp as a regulator of mTORC1-depe

101 al angiogenesis, endothelial cells (ECs) use glutaminolysis-derived glutamate to produce aspartate (A

102 Since inhibition of glutaminolysis did not prevent the PDS-induced morphogen

103 ability of Myc-expressing cells to engage in glutaminolysis does not depend on concomitant activation

104 high production of ROS, balanced by PPP- and glutaminolysis-driven synthesis of glutathione, as a pri

105 Specifically, aberrant glycolysis, glutaminolysis, fatty acid and glycosphingolipid metabol

106 pment of small molecule inhibitors to target glutaminolysis for cancer therapy.

107 le intermediates, leading to a dependence on glutaminolysis for cell survival.

108 d that females had a selective reliance upon glutaminolysis for Th17-mediated airway inflammation, an

109 cells depend on high rates of glycolysis and glutaminolysis for their growth and survival.

110 nd the peritoneum to be rich in glutamate, a glutaminolysis-fuel that is exploited by peritoneal-resi

111 suppressed the expression of glycolysis and glutaminolysis genes and blocked metabolic adaptation in

112 nd c-Myc, control most of the glycolytic and glutaminolysis genes.

113 for long-chain fatty acid oxidation (Cpt2), glutaminolysis (Gls), or mitochondrial pyruvate import (

114 t transcriptionally controls a key enzyme of glutaminolysis, glutaminase-2 (GLS-2).

115 Blockage of glutaminolysis had the same inhibitory effect, which was

116 d metabolism, but no molecular connection to glutaminolysis has been reported.

117 As the first enzyme in catalyzing glutaminolysis, human kidney-type glutaminase isoform (K

118 As a result, MPC inhibition led to decreased glutaminolysis in DLBCLs, opposite to previous observati

119 addition, EGFR activation did not accelerate glutaminolysis in ELK1 knockdown or ELK1 Ser383-mutated

120 owth by coordinating cycles of autophagy and glutaminolysis in invasive hyphae.

121 The proposed model for glutaminolysis in IS is based on GDH providing NADH and

122 g reactive oxygen production, glycolysis and glutaminolysis in lymphoma cells have been described.

123 ated Th17 cell mitochondrial respiration and glutaminolysis in mice.

124 nt with the hypothesis that glucose inhibits glutaminolysis in pancreatic beta-cells in a concentrati

125 poiesis under steady-state conditions, while glutaminolysis in progenitors promotes emergency myelopo

126 The role of glutaminolysis in providing metabolites to support tumou

127 inhibited activation-induced glycolysis and glutaminolysis in T cells.

128 we show that the enhanced proliferation and glutaminolysis in the absence of ephrin-A1 were attribut

129 C (GAC), which are rate-limiting enzymes of glutaminolysis in the central carbon metabolism in neuro

130 Upregulation of glycolysis and glutaminolysis in this manner causes the brain to enter

131 d inhibition of key enzymes in glycolysis or glutaminolysis increased H3K27me3, altered chromatin acc

132 creatic beta cells show an increased rate of glutaminolysis, increased insulin release in response to

133 gested SC-144 reduced glycolytic dependence, glutaminolysis induction, and enhanced fatty acid metabo

134 Finally, glutaminolysis inhibition activated mitochondrial apopto

135 Consequently, either ATF4 agonists or glutaminolysis inhibitors potently induce apoptosis in v

136 Coadministration of B-catenin and glutaminolysis inhibitors with gemcitabine abrogated the

137 Coadministration of beta-catenin and glutaminolysis inhibitors with gemcitabine abrogated the

138 emcitabine in combination with B-catenin and glutaminolysis inhibitors.

139 itabine in combination with beta-catenin and glutaminolysis inhibitors.

140 nated seizure-like activity, we propose that glutaminolysis is a causative process linking neuronal m

141 Together, these data demonstrate that glutaminolysis is a critical component of myofibroblast

142 Glutaminolysis is a metabolic pathway adapted by many ag

143 ecessary for early gene transcription, while glutaminolysis is necessary for early gene translation b

144 the precise regulation and role of beta-cell glutaminolysis is probably central to our concept of nor

145 A consequence of this Myc-dependent glutaminolysis is the reprogramming of mitochondrial met

146 a primary function of aerobic glycolysis and glutaminolysis is to co-operatively limit metabolite sup

147 oward glycolysis and mitochondrial-dependent glutaminolysis, leading to accumulation of glycolytic me

148 Up-regulated xCT, in combination with glutaminolysis, leads to increased extracellular glutama

149 uding regulation of genes leading to reduced glutaminolysis, like overexpression of GLUL and reductio

150 t MHV-68 lytic infection induces glycolysis, glutaminolysis, lipid metabolism, and nucleotide metabol

151 species reversed IL-17A-mediated glycolysis, glutaminolysis, lipid uptake, and HPK hyperproliferation

152 e phosphorylation to aerobic glycolysis plus glutaminolysis, markedly increasing glucose and glutamin

153 ich GDH1-mediated metabolic reprogramming of glutaminolysis mediates lung cancer metastasis and offer

154 the suppressive impact on cancer glycolysis, glutaminolysis, mitochondrial biogenesis and other major

155 at 968 selectively blocks the enhancement in glutaminolysis necessary for satisfying the glutamine ad

156 Glutaminolysis not only provides sufficient ATP to suppo

157 ulate that in the basal interprandial state, glutaminolysis of beta-cells is partly turned on because

158 sequently, we studied the effect of blocking glutaminolysis on M. tuberculosis-induced cytokines.

159 turally and functionally to derive energy by glutaminolysis only.

160 Finally, inhibiting glycolysis and glutaminolysis or activating Ppara in Pkd1-mutant cells

161 In accord, a pharmacological inhibition of glutaminolysis or oxidative phosphorylation arrests the

162 Viruses may hijack glycolysis, glutaminolysis, or fatty acid beta-oxidation of host cel

163 , and memory T cells), including glycolysis, glutaminolysis, oxidative phosphorylation, fatty acid sy

164 The glutaminolysis pathway follows the citric acid cycle, wh

165 er cells depend on glutamine as they use the glutaminolysis pathway to generate building blocks and e

166 precursor and propose an alternative to the glutaminolysis pathway where flux of glutamine to lipoge

167 e glutaminase (GLS), the first enzyme in the glutaminolysis pathway, catalyzes the hydrolysis of glut

168 iver biopsies to study how HCV modulates the glutaminolysis pathway, which is known to play an import

169 h may be due to an increased activity of the glutaminolysis pathway.

170 mine-fueled intracellular metabolic pathway, glutaminolysis, played crucial roles in the death proces

171 A) catalyzes the first step in mitochondrial glutaminolysis playing a key role in cancer metabolic re

172 timulated insulin secretion (AASIS) in which glutaminolysis plays a key role.

173 ays of oxidative metabolism, glycolysis, and glutaminolysis preferentially fuel the cell fate decisio

174 cing substrates such as glucose and enhances glutaminolysis, preventing the mitochondrial accumulatio

175 nd YAP-dependent mechanotransduction altered glutaminolysis, pulmonary vascular proliferation, and ma

176 k (3), a surrogate biomarker for glutaminolysis rate, was relatively low in about 50% of

177 e inhibitor CB-839 substantially reduced the glutaminolysis rates as measured by k (3) Conclusion: (1

178 intracellular glutamine pool size and tumor glutaminolysis rates.

179 lper 17 (Th17) cell metabolism, specifically glutaminolysis, reducing airway inflammation in males.

180 ation of pyruvate dehydrogenase kinase), and glutaminolysis (reflecting ischemia-induced cMyc activat

181 rlying mechanism of oncogenic alterations of glutaminolysis remains unclear.

182 B cells in vitro suggests, however, that the glutaminolysis requirement is not B cell-intrinsic.

183 , we genetically blocked both glycolysis and glutaminolysis simultaneously and found the abrogation o

184 Key enzymes involved in glutaminolysis, specifically, glutamic-pyruvic transamin

185 Glutaminolysis stimulated by the leucine analogue d,l-be

186 own of Id1 suppressed aerobic glycolysis and glutaminolysis, suggesting that Id1 promotes a metabolic

187 of adult HSCs, which rely on glycolysis and glutaminolysis, suggests a potential role for the post-t

188 of Th17 cells with implications for Th17 or glutaminolysis targeted therapeutics.

189 ndrial function for metabolism, specifically glutaminolysis that catabolizes glutamine to generate AT

190 8 hours resulted in reduction in glycolysis, glutaminolysis, the citric acid (TCA) cycle as well as t

191 is) requires induction of enzymes to promote glutaminolysis, the conversion of glutamine to alpha-ket

192 Inhibition of glutaminolysis, the essential component of ferroptosis,

193 lls or in cells treated with an inhibitor of glutaminolysis, the pathway of glutamine catabolism, cou

194 suggest that GPT2 is a critical link between glutaminolysis, the TCA cycle, and OXPHOS and is a poten

195 duced the secretion of insulin by augmenting glutaminolysis through activating glutaminase and GDH.

196 ux was achieved through enhanced reliance on glutaminolysis through malic enzyme and pyruvate dehydro

197 ates ELK1 to activate GDH1 transcription and glutaminolysis through MEK/ERK pathway, providing new in

198 pentose phosphate pathway, malic enzyme, and glutaminolysis thus confer layered protection against ox

199 While HCV induces glutaminolysis to create an environment favorable for vi

200 red glucose metabolism, cancer cells undergo glutaminolysis to meet their energy demands.

201 dation of free fatty acids to glycolysis and glutaminolysis to meet these demands.

202 glutamine uptake and its metabolism through glutaminolysis to provide the cancer cell with a replace

203 ed a Myc-dependent metabolic pathway linking glutaminolysis to the biosynthesis of polyamines.

204 se (AADR) and not due to the contribution of glutaminolysis to the TCA cycle.

205 agic flux liberate alpha-ketoglutarate - via glutaminolysis - to reactivate TOR signaling and fuel bi

206 Metabolites involved in glutaminolysis, tryptophan catabolism, pyrimidine, lipid

207 ated c-Myc activation coupled with increased glutaminolysis underscore the critical role of RORgammat

208 ng the two key CCEM pathways, glycolysis and glutaminolysis, viral replication was inhibited in vitro

209 Furthermore, we showed that GDH1-mediated glutaminolysis was involved in EGF-promoted cell prolife

210 First, conversion of glutamine to lactate (glutaminolysis) was rapid enough to produce sufficient N

211 cells by modulating targets associated with glutaminolysis, which leads to decreased production of l

212 and MCT-4), Krebs cycle redox metabolism, or glutaminolysis will synergistically abrogate tumor cell

213 In contrast, the inhibition of glutaminolysis with 6-diazo-5-oxo-l-norleucine had a gre

214 sed glycolysis feeding anabolic pathways and glutaminolysis yielding increased alpha-ketoglutarate (a