ライフサイエンスコーパス: cellular respiration

1 supercomplexes responsible for carrying out cellular respiration.

2 on of dysfunctional mitochondria to maintain cellular respiration.

3 epletion resulted in reduced CI activity and cellular respiration.

4 complex I (NADH dehydrogenase) activity and cellular respiration.

5 ivities, including energy generation through cellular respiration.

6 n their redox properties, leading to loss of cellular respiration.

7 istent with a pivotal role in the control of cellular respiration.

8 ed by previous results from Biolog assays of cellular respiration.

9 lated the expression of PGC1alpha, UCP1, and cellular respiration.

10 ogical processes, such as photosynthesis and cellular respiration.

11 in, plays several important roles in aerobic cellular respiration.

12 rally fluorescent metabolite associated with cellular respiration.

13 enhanced activity of the glycolysis and the cellular respiration.

14 ermogenic genes and a reduction in uncoupled cellular respiration.

15 generated through electron transport during cellular respiration.

16 capacity as a terminal electron acceptor for cellular respiration.

17 COX) crucial to the production of ATP during cellular respiration.

18 ons may be directly responsible for impaired cellular respiration.

19 ochondrial membrane potential, and decreased cellular respiration.

20 e oxygen species production while increasing cellular respiration.

21 lpha-mediated effects on gene regulation and cellular respiration.

22 tegral membrane protein complex essential to cellular respiration.

23 ochondrial membrane is essential for coupled cellular respiration.

24 lar signal transduction to the regulation of cellular respiration.

25 identifies a link between antibiotic-induced cellular respiration and bactericidal lethality and demo

26 egulates a large family of genes involved in cellular respiration and carbon metabolism during condit

27 timepoints after injection and analyzed for cellular respiration and caspase activation.

28 lar processes and is especially critical for cellular respiration and division.

29 nown biological modulating activity of MT in cellular respiration and energy metabolism in a tissue-s

30 mitochondrial oxidative capacity measured by cellular respiration and fatty acid oxidation.

31 We investigated changes in the cellular respiration and gene expression diversity resul

32 Both cellular respiration and glycolysis were reduced in OGT/

33 tion of a variety of different metal ions to cellular respiration and growth.

34 isoprenylated quinone that is essential for cellular respiration and is synthesized in mitochondria

35 Because NO regulates cellular respiration and mitochondrial biogenesis, we hy

36 NO inhibits cellular respiration and mitochondrial electron transpor

37 ling, cell cycle, transcription/translation, cellular respiration and mitochondrial function, cell su

38 ated lens cells, including genes involved in cellular respiration and mRNA and peptide processing.

39 ced MB as measured by increases in uncoupled cellular respiration and PGC-1alpha and NDUFS1 mRNA expr

40 tegral membrane protein complex essential to cellular respiration and photosynthesis.

41 egral membrane protein complex essential for cellular respiration and photosynthesis; it couples elec

42 Defects in COX assembly alter cellular respiration and produce severe human encephalom

43 ddition to vasodilation, in enhancing tissue cellular respiration and provides a possible physiologic

44 a cells increased OGA expression and reduced cellular respiration and ROS generation.

45 ata demonstrate that arginine flux preserves cellular respiration and suppresses pathological signali

46 s demonstrated in living cell culture, where cellular respiration and topography were simultaneously

47 of frataxin in yeast, YFH1, is required for cellular respiration and was suggested to regulate mitoc

48 nockdown of SIRT4 resulted in increased FAO, cellular respiration, and pAMPK levels.

49 f NO that can regulate hypoxic vasodilation, cellular respiration, and signaling.

50 anoic acid, revealed SW-induced increases in cellular respiration as the principal consequence of gil

51 ilus and is the preferred terminal enzyme of cellular respiration at low dioxygen tensions.

52 Loss of mNEET decreased cellular respiration, because of a reduction in the tota

53 Carbon monoxide (CO) can arrest cellular respiration, but paradoxically, it is synthesiz

54 arbon dioxide is produced as a by-product of cellular respiration by all aerobic organisms and thus s

55 Inhibition of cellular respiration by knockout of the cytochrome oxida

56 in the regulation of complex I activity and cellular respiration by nitric oxide.

57 In contrast, impairment of cellular respiration by the addition of the nitric oxide

58 In combination, suppression of cellular respiration by the bacteriostatic antibiotic wa

59 oma cells, which was determined by decreased cellular respiration, decreased ATP production, and incr

60 osomal NAD(+) also preserved DeltaPsi(m) and cellular respiration during oxidative stress.

61 rocytes to mitochondria, thereby maintaining cellular respiration during periods of high physiologica

62 We next developed a method to quantify cellular respiration dynamically and found that bacteric

63 in host cells including electron transport, cellular respiration, energy metabolism, gene expression

64 l cells, identifying a greater dependence on cellular respiration for energy in control cells.

65 s were tested for their ability to carry out cellular respiration, for their growth rates on non-ferm

66 Ionizing radiation and normal cellular respiration form reactive oxygen species that d

67 Ureagenic substrates increased cellular respiration from 15.8 +/- 0.9 nmol O(2)/min/10(

68 preserves mitochondria, a key organelle for cellular respiration, from reperfusion injury and limits

69 s also present in mitochondria and regulates cellular respiration in a transcriptional-independent ma

70 benzamide (1 mM) prevented the inhibition of cellular respiration in cells exposed to ONOO-.

71 that allows for the real-time assessment of cellular respiration in intact skeletal muscle fibre bun

72 and provide further evidence for disordered cellular respiration in KD/SBMA skeletal muscle.

73 ahorse XF24 flux analyzer revealed unaltered cellular respiration in neurons derived from R6/2 mice c

74 ich is key for STAT3 induction and increased cellular respiration in Sirt1-KO cells.

75 We evaluated the role of defective cellular respiration in sporadic GIST lacking mutations

76 Cellular respiration in the presence of glucose was foun

77 ur functional pathways within the Br module (cellular respiration, intracellular transport, energy co

78 Here, we show that when cellular respiration is inhibited by depleting oxygen or

79 Cellular respiration is monitored through O2 consumption

80 activity measured spectrophotometrically and cellular respiration measured polarographically are unde

81 mote apoptosis, which includes impairment of cellular respiration (mitochondrial O(2) consumption).

82 Recovery of cellular respiration, mitochondrial biogenesis, and func

83 lated regions and gene ontologies related to cellular respiration, mRNA binding and translation.

84 0.5 microm), which immediately inhibited the cellular respiration of cocultured neurons, as did authe

85 is known about the roles of beta-catenin in cellular respiration or mitochondria of hepatocytes.

86 t present in all tissues and is required for cellular respiration, peptide amidation, neurotransmitte

87 Cellular respiration plays an important role during this

88 potential (DeltaPsi(m)), NAD(+) content, and cellular respiration, prevented release of apoptosis-ind

89 mitochondrial [NADH] ([NADH]m) may regulate cellular respiration rate and energetic state, it is not

90 sed to detect ferrocyanide or which affected cellular respiration rates.

91 Coupled cellular respiration requires that ATP and ADP be effici

92 roles in brain function: it is generated in cellular respiration, serves as a modulator of dopaminer

93 Other agents also inhibit cellular respiration, sometimes irreversibly.

94 in vivo We propose a model wherein impaired cellular respiration stimulates SaeRS via an as yet unde

95 due to an intrinsic acquired derangement in cellular respiration that is caused, at least in part, b

96 SIRT5 represses biochemical activity of, and cellular respiration through, two protein complexes iden

97 l model to evaluate the EPR oximetry data on cellular respiration to quantify related parameters usin

98 many crucial biogeochemical processes, from cellular respiration to rock weathering, makes reconstru

99 bunit succinate dehydrogenase-B, maintaining cellular respiration under low-nutrient conditions, and

100 a new approach for quantitative analysis of cellular respiration using EPR oximetry.

101 e reductase activity of neuroglobin inhibits cellular respiration via NO binding to cytochrome c oxid

102 Cellular respiration was followed polarographically.

103 The loss of cellular respiration was rapid, peaking 1-3 h after ONOO

104 While the clamp was maintained, cellular respiration was unaffected but, as it failed, r

105 ial dehydrogenase activity, and therefore of cellular respiration, was measured in isolated mitochond

106 c antibiotics was associated with suppressed cellular respiration whereas cell death from most bacter

107 urs) demonstrated a reversible inhibition of cellular respiration with maintenance of cell viability,