ライフサイエンスコーパス: cellular respiration

1 thus has lost the ability to perform aerobic cellular respiration.

2 igest food to fuel brain neurometabolism via cellular respiration.

3 tegral membrane protein complex essential to cellular respiration.

4 ochondrial membrane is essential for coupled cellular respiration.

5 lar signal transduction to the regulation of cellular respiration.

6 regulation of the innate immune response and cellular respiration.

7 y, activate astrocyte signaling, and control cellular respiration.

8 eneration of reactive oxygen species through cellular respiration.

9 the oxidative phosphorylation machinery and cellular respiration.

10 assays use population growth as a proxy for cellular respiration.

11 s change is fueled by seasonal adaptation in cellular respiration.

12 on of genes related to muscle remodeling and cellular respiration.

13 enhanced activity of the glycolysis and the cellular respiration.

14 capacity as a terminal electron acceptor for cellular respiration.

15 range disrupt bird orientation and mammalian cellular respiration.

16 supercomplexes responsible for carrying out cellular respiration.

17 on of dysfunctional mitochondria to maintain cellular respiration.

18 epletion resulted in reduced CI activity and cellular respiration.

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

20 ivities, including energy generation through cellular respiration.

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

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

23 s a biosynthetic hub as well as a center for cellular respiration.

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

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

26 ogical processes, such as photosynthesis and cellular respiration.

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

28 rally fluorescent metabolite associated with cellular respiration.

29 ermogenic genes and a reduction in uncoupled cellular respiration.

30 generated through electron transport during cellular respiration.

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

32 ons may be directly responsible for impaired cellular respiration.

33 ochondrial membrane potential, and decreased cellular respiration.

34 e oxygen species production while increasing cellular respiration.

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

36 M contains the protein machinery crucial for cellular respiration and ATP generation, and loss of fun

37 st by intoxicating their TCA cycle, lowering cellular respiration and ATP production.

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

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

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

41 play an important role in the regulation of cellular respiration and cell death.

42 encoded mitochondrial (NEM) genes related to cellular respiration and Complex I.

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

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

45 genomes must be co-adapted to ensure proper cellular respiration and energy production.

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

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

48 owed an upregulation of proteins involved in cellular respiration and general stress pathways that ma

49 Both cellular respiration and glycolysis were reduced in OGT/

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

51 anion (O(2)(-.)) is generated during normal cellular respiration and has fundamental roles in a wide

52 rolling essential functions for life such as cellular respiration and homoeostasis.

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

54 Cellular respiration and metabolism were all accelerated

55 es and translational machinery essential for cellular respiration and metabolism.

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

57 NO inhibits cellular respiration and mitochondrial electron transpor

58 Experimental studies of cellular respiration and mitochondrial function were per

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

60 nctional impacts, as evidenced by changes in cellular respiration and mitochondrial membrane potentia

61 ath, transport-related genes associated with cellular respiration and mitochondrial respiratory chain

62 FAS-associated processes, leading to reduced cellular respiration and mitochondrial translation.

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

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

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

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

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

68 O-GlcNAcylation enhanced cellular respiration and promoted mitochondrial superoxi

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

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

71 dent enzymes ultimately resulting in loss of cellular respiration and sensitivity to mild glucose sta

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

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

74 We performed cellular respiration and toxicity assays using PrimPol o

75 al and bacterial respiratory chains, driving cellular respiration and transducing the free energy fro

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

77 This reveals IMM fluidity to be linked to cellular-respiration and responsive to stimuli.

78 tion null cells restored lipoylation levels, cellular respiration, and growth in low glucose conditio

79 (50(O2)), the O(2) pressure for half-maximal cellular respiration, and has pleiotropic effects on oxi

80 ondrial biogenesis, antioxidant defense, and cellular respiration, and its downstream effectors in bo

81 to its essential role in energy metabolism, cellular respiration, and oxygen transport.

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

83 s associated with increased ATP consumption, cellular respiration, and reactive oxygen species (ROS)

84 knockdown induces oxidative stress, hinders cellular respiration, and reduces the survival of GBM ce

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

86 on of genes related to muscle remodeling and cellular respiration, and there were changes in the rela

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

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

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

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

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

92 Inhibition of cellular respiration by knockout of the cytochrome oxida

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

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

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

96 rRNA processing machinery, and mitochondrial cellular respiration capacity, termed the Ribo-dominant

97 n of PGC-1alpha attenuates the inhibition in cellular respiration caused by 3-oxo-C12-HSL.

98 If reduced cellular respiration contributes to muscle atrophy in th

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

100 biological processes such as photosynthesis, cellular respiration, DNA repair, cellular homeostasis,

101 of cyanobacteria, including photosynthesis, cellular respiration, DNA replication, and the biosynthe

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

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

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

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

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

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

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

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

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

111 ifferential methylation analyses showed that cellular respiration genes were differentially methylate

112 gen presentation and decreased expression of cellular respiration genes.

113 sses integral to cellular function including Cellular Respiration (GO:0045333; FDR 5.05E-08), Ion Tra

114 mplex interplay between mRNA translation and cellular respiration has been recently unveiled, but its

115 generated as a metabolic intermediate during cellular respiration, have led to suggestions that prote

116 ein levels, respectively, ultimately raising cellular respiration; however, this was only observed wh

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

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

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

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

121 he molecular level, isofalcarintriol affects cellular respiration in mammalian cells, C. elegans, and

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

123 the uFFE separation of important players of cellular respiration in operando.

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

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

126 as metabolism, mitochondrial biogenesis, and cellular respiration in the ECs.

127 Cellular respiration in the presence of glucose was foun

128 slightly reduced, but all other measures of cellular respiration, including oxygen consumption rate

129 Analysis of cellular respiration indicated similar metabolic profile

130 th SLC35A4-MP significantly diminish maximal cellular respiration, indicating a vital role for this m

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

132 Cellular respiration is essential for multiple bacterial

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

134 and for glucose as the primary substrate for cellular respiration is met by the breakdown of complex

135 Cellular respiration is monitored through O2 consumption

136 Cellular respiration is powered by membrane-bound redox

137 for adenosine triphosphate synthesis during cellular respiration is the primary goal of research on

138 activity measured spectrophotometrically and cellular respiration measured polarographically are unde

139 r enzymes for ATP generation in a simplified cellular respiration mimic.

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

141 Recovery of cellular respiration, mitochondrial biogenesis, and func

142 in mouse models of kidney disease stimulated cellular respiration, mitochondrial dynamics, and tubula

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

144 actor in enzymes involved in photosynthesis, cellular respiration, nitrate assimilation, nitrogen fix

145 h that pUL13 alone is sufficient to increase cellular respiration, not requiring the presence of othe

146 0.5 microm), which immediately inhibited the cellular respiration of cocultured neurons, as did authe

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

148 maintain critical bioenergetic gradients for cellular respiration, oxidative mitochondrial reactions,

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

150 Cellular respiration plays an important role during this

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

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

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

154 tal metabolic activities in cells, including cellular respiration, regulation, and repair.

155 ia, which hold clues regarding mechanisms of cellular respiration relevant to early life.

156 Coupled cellular respiration requires that ATP and ADP be effici

157 er mitochondria to myeloma cells to increase cellular respiration, resulting in increased proliferati

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

159 umption rate assay as a measure of increased cellular respiration, SHO1122147 (7m) displayed an EC(50

160 Other agents also inhibit cellular respiration, sometimes irreversibly.

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

162 ed lights on ascorbate, ethylene signalling, cellular respiration, sugar accumulation, and softening

163 tive oxygen species (ROS) are by-products of cellular respiration that can promote oxidative stress a

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

165 ced tricarboxylic acid cycling, and elevated cellular respiration that ultimately conferred vulnerabi

166 erichia coli aerotaxis receptor Aer monitors cellular respiration through a redox-sensitive flavin ad

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

168 tatic cofactor in fundamental processes from cellular respiration to pigmentation, working through cy

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

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

171 ies, cytokinin and cell cycle regulation and cellular respiration under LDs and short days, whereas H

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

173 Mitochondria, the seat of cellular respiration, undergo profound changes in post m

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

175 ion longevity pathways but is due to altered cellular respiration via increased mitochondrial uncoupl

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

177 Cellular respiration was followed polarographically.

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

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

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

181 id metabolism, cell envelope biogenesis, and cellular respiration were predominantly impacted by the

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

183 ota's production of sulfide, an inhibitor of cellular respiration, which is key to host invasion by n

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