ライフサイエンスコーパス: metabolic inhibitor

1 2B receptors were somewhat diminished by the metabolic inhibitor.

2 ation could explain the protective effect of metabolic inhibitors.

3 equired to maintain the beneficial effect of metabolic inhibitors.

4 by transmission electron microscopy and with metabolic inhibitors.

5 provides an archetype for development of DNA metabolic inhibitors.

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

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

8 with recombinant PKCalpha in the absence of metabolic inhibitors.

9 TCR downregulation was resistant to various metabolic inhibitors.

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

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

12 covery of novel antiviral therapies based on metabolic inhibitors.

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

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

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

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

17 The metabolic inhibitor 3-bromopyruvate blocks the transcrip

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

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

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

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

22 The use of metabolic inhibitors and blocking antibodies revealed th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 The metabolic inhibitors iodoacetate and 6-aminonicotinamide

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

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

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

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

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

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

48 Using metabolic inhibitors of the plastidic and cytosolic isop

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

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

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

52 Metabolic inhibitors or omission of amino acids in the c

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

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

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

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

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

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

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

60 The use of metabolic inhibitors revealed that mevalonic acid biosyn

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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