ライフサイエンスコーパス: glutaminolysis

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

2 ctivated T cells to switch to glycolysis and glutaminolysis.

3 r cells exhibit high rates of glycolysis and glutaminolysis.

4 intermediates in glycolysis, TCA cycle, and glutaminolysis.

5 s that participate in aerobic glycolysis and glutaminolysis.

6 ce, mitochondrial biogenesis, apoptosis, and glutaminolysis.

7 hydrogenase kinase, fatty acid oxidation, or glutaminolysis.

8 e levels were decreased, suggesting enhanced glutaminolysis.

9 chanism of resistance to therapies targeting glutaminolysis.

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

11 Glutaminolysis, an anaplerotic pathway, replenished aspa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 How mitochondrial glutaminolysis contributes to redox homeostasis in cance

40 Glutaminolysis converts Gln into alpha-ketoglutarate (al

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

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

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

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

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

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

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

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

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

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

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

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

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

54 The role of glutaminolysis in providing metabolites to support tumou

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

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

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

58 Finally, glutaminolysis inhibition activated mitochondrial apopto

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

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

61 Glutaminolysis is a metabolic pathway adapted by many ag

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

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

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

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

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

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

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

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

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

71 turally and functionally to derive energy by glutaminolysis only.

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

73 The glutaminolysis pathway follows the citric acid cycle, wh

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

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

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

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

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

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

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

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

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

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

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

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

86 8 hours resulted in reduction in glycolysis, glutaminolysis, the citric acid (TCA) cycle as well as t

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

88 Inhibition of glutaminolysis, the essential component of ferroptosis,

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

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

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

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

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

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

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

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

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