ライフサイエンスコーパス: metabolic inhibitor

1 g workflows for discovering off-targets of a metabolic inhibitor.

2 2B receptors were somewhat diminished by the metabolic inhibitor.

3 d mammalian cells treated with and without a metabolic inhibitor.

4 ct targets, clarify mechanisms, and optimize metabolic inhibitors.

5 redict sensitivity of tumors to a variety of metabolic inhibitors.

6 covery of novel antiviral therapies based on metabolic inhibitors.

7 the development of cancer therapies based on metabolic inhibitors.

8 ation could explain the protective effect of metabolic inhibitors.

9 by transmission electron microscopy and with metabolic inhibitors.

10 provides an archetype for development of DNA metabolic inhibitors.

11 D-aspartate from synaptosomes exposed to the metabolic inhibitors.

12 with recombinant PKCalpha in the absence of metabolic inhibitors.

13 TCR downregulation was resistant to various metabolic inhibitors.

14 ed transferrin and reduced by weak bases and metabolic inhibitors.

15 being significantly (P < 0.01) inhibited by metabolic inhibitors.

16 equired to maintain the beneficial effect of metabolic inhibitors.

17 odulates their metabolism in the presence of metabolic inhibitors.

18 ipocytes of fructose 1,6-bisphosphate or the metabolic inhibitor 2-deoxyglucose, two agents that disr

19 tions in tone and pHi were observed with the metabolic inhibitors 2,4-dinitrophenol (DNP) and sodium

20 treated for 10 min with a combination of the metabolic inhibitors 2-deoxyglucose and rotenone, 100 mM

21 ndrial proton uncoupler, FCCP, and a glucose metabolic inhibitor, 2-DG, activated AMPK and inhibited

22 i-spinal) delivery of fluorocitrate, a glial metabolic inhibitor; (2) prevented and reversed by intra

23 The metabolic inhibitor 3-bromopyruvate blocks the transcrip

24 olic substrates (25/28 cells) or exposure to metabolic inhibitors (32/40 cells) opened K+-selective c

25 ely overexpressed before exposing cells to a metabolic inhibitor, an insult sufficient to cause mitoc

26 showed that melatonin acted both as a tumor metabolic inhibitor and a circadian-regulated kinase inh

27 n corresponding diseases, are susceptible to metabolic inhibitors and are effective targets for thera

28 The use of metabolic inhibitors and blocking antibodies revealed th

29 reduction of ATP by various combinations of metabolic inhibitors and by ouabain was closely parallel

30 n early target of injury in cells exposed to metabolic inhibitors and demonstrate that hsp72 reduces

31 While various metabolic inhibitors and microbiome-modulating approache

32 ls were applied to PANC-1 cells treated with metabolic inhibitors and patient-derived cancer organoid

33 brain slices, in the presence and absence of metabolic inhibitors and physiological energy substrates

34 aches that minimize the systemic toxicity of metabolic inhibitors and reduce the risk of drug resista

35 Furthermore, treatment of cells with metabolic inhibitors and uncouplers of photosynthetic el

36 sm of 2D and 3D cell cultures in response to metabolic inhibitors, and chemotherapeutics.

37 hen cytosolic ATP levels were lowered by the metabolic inhibitors azide or FCCP.

38 p72 prevents apoptosis caused by exposure to metabolic inhibitors by protecting the mitochondrial mem

39 Exposure of the cells to a metabolic inhibitor causes the periodic motion to cease.

40 Here we review small-molecule metabolic inhibitors currently in clinical development f

41 However, the metabolic inhibitors did not change the anisotropy of GF

42 he enhancement in HSC development; likewise, metabolic inhibitors diminished nascent HSC production a

43 The specific metabolic inhibitors for sugar metabolism (2-DG), fatty

44 sed to evaluate the therapeutic responses of metabolic inhibitors (glycolysis pathway inhibitor STF 3

45 Metabolic inhibitors have been used in oncology for deca

46 ombined action of inflammatory mediators and metabolic inhibitors, having tumoricidal functions.

47 Pharmacological studies with kinase and metabolic inhibitors implicated class II/III phosphatidy

48 s to provide an overview of the landscape of metabolic inhibitors in clinical development for oncolog

49 However, we found that channel activation by metabolic inhibitors in norpAP24 was strictly dependent

50 nd normal cells is an exploitable target for metabolic inhibitors in the in vitro setting and in vivo

51 tly reduced cell death caused by exposure to metabolic inhibitors in vitro and preserved kidney funct

52 nd normal cells is an exploitable target for metabolic inhibitors in vitro.

53 or myocytes treated with known mitochondrial metabolic inhibitors, including carbonyl cyanide m-chlor

54 ing [3H]D-aspartate to either L-glutamate or metabolic inhibitors increased the efflux of the radiola

55 Renal injury with metabolic inhibitors increased the mean secretion of 2',

56 The metabolic inhibitors iodoacetate and 6-aminonicotinamide

57 r, the relative susceptibility of cells to a metabolic inhibitor is dictated by their metabolic deman

58 causes metabolic inhibition, and the use of metabolic inhibitors is one experimental method of simul

59 combined use of an anti-HIV drug (NVR) and a metabolic inhibitor (ML355).

60 tylated 4-fluoro-glucosamine (4-F-GlcNAc), a metabolic inhibitor of N-acetyllactosamine biosynthesis,

61 mbrane cholesterol dependent and impaired by metabolic inhibitors of G(i), Src family, and the GTPase

62 d the efficacy of several well-characterized metabolic inhibitors of glycosylation and of a novel flu

63 agonists, glucagon-receptor antagonists, and metabolic inhibitors of hepatic glucose output are being

64 Using metabolic inhibitors of the plastidic and cytosolic isop

65 , we found an unappreciated impact of a host metabolic inhibitor on the pathogen, and show that infla

66 listic approach that considers the effect of metabolic inhibitors on major tumor-resident cell popula

67 The confounding role of metabolic inhibitors on our interpretation of myeloid me

68 The effects of metabolic inhibitors on the activity of inward rectifier

69 hts the potential confounding effect of host metabolic inhibitors on the pathogen and uncoupling of M

70 consideration when contemplating anticancer metabolic inhibitor options, especially in the context o

71 ridamole, a nucleoside inhibitor; or NaN3, a metabolic inhibitor or under Ca(2+)-free conditions.

72 e have found that inhibition of NF-kappaB by metabolic inhibitors or a constitutively active mutated

73 Metabolic inhibitors or omission of amino acids in the c

74 Aggregates formed in the presence of metabolic inhibitors or signal transduction inhibitors b

75 sponse gene hsp70 in response to arsenite, a metabolic inhibitor, or cadmium, a heavy metal.

76 ultiple assays in the presence or absence of metabolic inhibitors, or in cells genetically depleted o

77 PAG administration of the general glial cell metabolic inhibitor propentofylline or the astrocyte act

78 deficient culture medium or a combination of metabolic inhibitors reduces the efficiency of the trans

79 sterols, total lipid storage, sensitivity to metabolic inhibitors, response to altered sterol structu

80 fection of cells with PrV in the presence of metabolic inhibitors revealed that cycloheximide a prote

81 The use of metabolic inhibitors revealed that mevalonic acid biosyn

82 Use of highly specific enzymes and metabolic inhibitors reveals that LS174T CD44 binding to

83 lized and requires inclusion of a CYP450 3A4 metabolic inhibitor, ritonavir, to boost levels of the a

84 treated with glucose-free medium or with the metabolic inhibitor rotenone.

85 ombination of anti-metastatic approaches and metabolic inhibitors selected specifically for different

86 Addition of metabolic inhibitors showed that living cells were requi

87 Depletion of ATP by metabolic inhibitors similarly prevented the cell killin

88 Carbon monoxide did not act as a general metabolic inhibitor, since growth of a strain deleted fo

89 donuclease inhibitor zinc acetate and by the metabolic inhibitor sodium azide.

90 preconditioned with 2 episodes of either the metabolic inhibitor, sodium cyanide (NaCN), or the mitoK

91 Low temperature or metabolic inhibitors, sodium azide or iodoacetamide, hav

92 iscuss the therapeutic targeting of Cav-1 by metabolic inhibitors such as betulinic acid and Cav-1 mo

93 s, and this movement is greatly reduced when metabolic inhibitors such as sodium azide are added.

94 e presence of other L- and D-amino acids and metabolic inhibitors, such as ouabain and sodium azide,

95 This study raises the possibility that metabolic inhibitors, such as those that target glycolys

96 quired for growth in the presence of certain metabolic inhibitors, suggesting that Ess1 is important

97 tin diffusion was found to be insensitive to metabolic inhibitors, suggesting that it results from cl

98 Ac), potentially establishing a new class of metabolic inhibitors targeting bacterial glycosylation.

99 Of the metabolic inhibitors tested (F-, malonate, and arsenite)

100 ated with 75 microM iodoacetic acid (IAA), a metabolic inhibitor that induces rapid depletion of cell

101 cal administration of fluorocitrate (a glial metabolic inhibitor), TNF antagonist, and IL-1 antagonis

102 a suggest that 4F-GalNAc may be applied as a metabolic inhibitor to reduce O-linked glycosylation, si

103 de biosynthetic pathways in conjunction with metabolic inhibitors to better define the inducing signa

104 abolic pathways could improve the ability of metabolic inhibitors to suppress cancers with limited tr

105 Catalase overexpression and metabolic inhibitors were used to determine the role of

106 ateral intrastriatal infusion of malonate, a metabolic inhibitor which decreases ATP levels.

107 Combination therapies involving metabolic inhibitors with immune checkpoint blockade (IC

108 alpha can be therapeutically exploited using metabolic inhibitors with lactate as a biomarker to iden

109 ene group, and show that it acts as a potent metabolic inhibitor within cells to antagonize protein f