ライフサイエンスコーパス: adenosine triphosphate

1 ies on oxidative phosphorylation to generate adenosine triphosphate.

2 phase accompanied by a drop in intracellular adenosine triphosphate.

3 tochondria was directly inhibited by p-JNK + adenosine triphosphate.

4 ted by the intracytoplasmatic application of adenosine triphosphate.

5 the hypotension but enhanced skeletal muscle adenosine triphosphate.

6 ting to mitochondria as their main source of adenosine triphosphate.

7 an ectonucleotidase that generates PPi from adenosine triphosphate.

8 host crucial metabolic pathways and produce adenosine triphosphate.

9 bstrate molecules, we employed (18)O-labeled adenosine triphosphate ((18)O-ATP) as the phosphate dono

10 In addition, M110 hydrolyzes adenosine triphosphate 2.5-fold faster in the presence o

11 uption of the parasite's sodium efflux pump (adenosine triphosphate 4).

12 hly specific and does not bind to adenosine, adenosine triphosphate, adenosine 5'-diphosphate, or str

13 ide adenine dinucleotide redox potential and adenosine triphosphate/adenosine diphosphate failed to r

14 are decreased in frequency, exhibit limited adenosine triphosphate/adenosine diphosphate hydrolysis

15 ne triphosphate levels in the liver, whereas adenosine triphosphate/adenosine diphosphate ratios rema

16 se in adenosine triphosphate levels, whereas adenosine triphosphate/adenosine diphosphate ratios were

17 y beneficial in restoring cellular levels of adenosine triphosphate after kidneys have been subjected

18 deposits, were quantified and identified by adenosine triphosphate analysis and pyrosequencing, resp

19 example, tri- and diorganophosphates (e.g., adenosine triphosphate and adenosine diphosphate) were r

20 AMP is converted to adenosine triphosphate and coupled to firefly luciferase

21 in DeltaPsim, resulting in reduced cellular adenosine triphosphate and increased necrosis.

22 as altered biliary composition with reduced adenosine triphosphate and lysosomal enzyme release.

23 o a single turnover autophosphorylation with adenosine triphosphate and magnesium (MgATP) and trap bo

24 ic machinery for hydrolysis of extracellular adenosine triphosphate and nicotinamide adenine dinucleo

25 xylic acids to aldehydes using the cofactors adenosine triphosphate and nicotinamide adenine dinucleo

26 r neurons-acetylcholine and a combination of adenosine triphosphate and nitric oxide, respectively.

27 or two representative small molecule targets-adenosine triphosphate and tobramycin.

28 f-disinfecting coatings for disinfecting and adenosine triphosphate and ultraviolet/fluorescent surfa

29 GPCR ligands such as lysophosphatidic acid, adenosine triphosphate, and allergens that activate GPCR

30 ine 3',5'-cyclic monophosphate, depletion of adenosine triphosphate, and depolarization of mitochondr

31 s were incubated with lipopolysaccharide and adenosine triphosphate, and levels of IL1beta production

32 educed levels of intracellular G6P, lactate, adenosine triphosphate, and reduced NAD phosphate, where

33 n serum and soleus muscle, hepatic levels of adenosine triphosphate, and systemic and hepatic insulin

34 ze the hydrolysis of chemical fuels, such as adenosine triphosphate, and use the energy released to d

35 ver, it is now clear that both adenosine and adenosine triphosphate are (i) abundant biochemical comp

36 a enzyme complexes may enhance production of adenosine triphosphate at rates beyond that possible wit

37 s helicase function, RecBCD unwinding at low adenosine triphosphate (ATP) (2-4 muM) was measured usin

38 Here, we utilized an adenosine triphosphate (ATP) affinity probe coupled with

39 in mammals where, by monitoring cellular AMP:adenosine triphosphate (ATP) and adenosine diphosphate (

40 , Darbousset et al define opposing roles for adenosine triphosphate (ATP) and adenosine in regulating

41 Nucleotides and nucleosides-such as adenosine triphosphate (ATP) and adenosine-are famous fo

42 Nucleotides (NTs), such as adenosine triphosphate (ATP) and guanosine triphosphate

43 haracterized the association of lithium with adenosine triphosphate (ATP) and identified a bimetallic

44 a key purinergic enzyme in the hydrolysis of adenosine triphosphate (ATP) and increased CD39 enzymati

45 and accurate method for the determination of adenosine triphosphate (ATP) and its first five cataboli

46 Adenosine triphosphate (ATP) and its metabolite, adenosi

47 ucleotide phosphate (NADP(+) and NADPH), and adenosine triphosphate (ATP) and its precursors, adenosi

48 erified by neuropathological analysis and by Adenosine Triphosphate (ATP) and Phosphocreatine (PCr) l

49 sly showed that patients with BD show normal adenosine triphosphate (ATP) and phosphocreatine levels

50 n the presence of stabilizing agents such as adenosine triphosphate (ATP) and polyethylene glycol (PE

51 analysis; we also measured mucosal levels of adenosine triphosphate (ATP) and reactive oxygen species

52 try, as well as an increase in intracellular adenosine triphosphate (ATP) and the accumulation of ter

53 Adenosine triphosphate (ATP) and the TLR2 ligand lipotei

54 adenosine (ADO) in the presence of exogenous adenosine triphosphate (ATP) as well as A(1), A2A, A2B,

55 ows no significant structural changes due to adenosine triphosphate (ATP) binding, but two different

56 Extracellular adenosine triphosphate (ATP) binds as a danger signal to

57 ermeability, protein synthesis activity, and adenosine triphosphate (ATP) biosynthesis pathways such

58 as well as the decrease of succinate-driven adenosine triphosphate (ATP) biosynthesis rates.

59 ole of creatine, an organic acid involved in adenosine triphosphate (ATP) buffering, in oligodendrocy

60 methodology is extended to the detection of adenosine triphosphate (ATP) by aptamer recognition.

61 ization resulting in a highly CHK1 selective adenosine triphosphate (ATP) competitive inhibitor.

62 tumors will be resistant or sensitive to new adenosine triphosphate (ATP) competitive mTOR inhibitors

63 The PCr to adenosine triphosphate (ATP) concentration ratio (PCr/AT

64 how a significant depletion of intracellular adenosine triphosphate (ATP) content and cell-membrane l

65 lexed [two end points in one screen; MMP and adenosine triphosphate (ATP) content] quantitative high

66 These data indicate that adenosine triphosphate (ATP) contributes to polymorphonu

67 denosine 5'-monophosphate (AMP) degradation, adenosine triphosphate (ATP) diphosphohydrolase (CD39) a

68 ication of group I or I/II mGluR agonists or adenosine triphosphate (ATP) elicited global astrocytic

69 es on host cells for essential nutrients and adenosine triphosphate (ATP) for a productive infection.

70 nd 2 (ERK-1/2), which promotes the efflux of adenosine triphosphate (ATP) from the macrophage.

71 ibited lower OXPHOS coupling respiration and adenosine triphosphate (ATP) generation.

72 rophage activation by lipopolysaccharide and adenosine triphosphate (ATP) has been studied extensivel

73 Here, we show that adenosine triphosphate (ATP) has properties of a biologi

74 Intravitreal administration of adenosine triphosphate (ATP) has recently been found to

75 pped-flow methods to monitor the coupling of adenosine triphosphate (ATP) hydrolysis and DNA transloc

76 Based on experimental data, we propose that adenosine triphosphate (ATP) hydrolysis by CglI produces

77 se binding sites required multiple rounds of adenosine triphosphate (ATP) hydrolysis in vitro, which

78 are members of the AAA+ superfamily and use adenosine triphosphate (ATP) hydrolysis to remodel initi

79 lti-subunit complexes that use the energy of adenosine triphosphate (ATP) hydrolysis to remodel nucle

80 This process relies on adenosine triphosphate (ATP) hydrolysis.

81 teps and enables the real-time monitoring of adenosine triphosphate (ATP) in a quantitative manner ov

82 of RBCs to release the vasoactive substance adenosine triphosphate (ATP) in response to reductions i

83 Finally, nu(max) obtained by injecting adenosine triphosphate (ATP) in the microchannel chamber

84 he concentration of a target small molecule, adenosine triphosphate (ATP) in this work, in the range

85 Here, we show that extracellular adenosine triphosphate (ATP) indirectly modulates the ex

86 Adenosine triphosphate (ATP) induces pain via activation

87 Diffusion of magnesium adenosine triphosphate (ATP) into these crystals trapped

88 ctrochemical aptasensor for the detection of adenosine triphosphate (ATP) is investigated in the pres

89 After tissue injury, adenosine triphosphate (ATP) is released and acts as a d

90 ntation, the proinflammatory "danger signal" adenosine triphosphate (ATP) is released from damaged ce

91 Adenosine triphosphate (ATP) is the energy currency of l

92 itochondrial membrane potential, and reduces adenosine triphosphate (ATP) levels in a concentration-d

93 Renal adenosine triphosphate (ATP) levels were reduced by 48%

94 species, cellular integrity or intracellular adenosine triphosphate (ATP) levels were unaffected.

95 hepatic mitochondrial content, function, and adenosine triphosphate (ATP) levels, in conjunction with

96 the unidirectional phosphocreatine (PCr) to adenosine triphosphate (ATP) metabolic fluxes in muscles

97 ldalkalibacillus thermarum, which hydrolyzes adenosine triphosphate (ATP) poorly.

98 cell stimulation up-regulates mitochondrial adenosine triphosphate (ATP) production to fuel purinerg

99 ental pulpal nerve fibers express ionotropic adenosine triphosphate (ATP) receptors, suggesting that

100 Adenosine triphosphate (ATP) release and autocrine purin

101 EVs cause adenosine triphosphate (ATP) release from platelets and

102 membrane mechanical stability, and cellular adenosine triphosphate (ATP) release.

103 In the immune system, extracellular adenosine triphosphate (ATP) released by dying cells is

104 Adenosine triphosphate (ATP) resynthesis during oxygenat

105 In contrast, transcripts of adenosine triphosphate (ATP) synthase and ribosomal prot

106 aquiline to treat tuberculosis has validated adenosine triphosphate (ATP) synthase as an attractive t

107 dentified a novel association with AD in the adenosine triphosphate (ATP) synthase, H+ transporting,

108 osed of four respiratory-chain complexes and adenosine triphosphate (ATP) synthase.

109 se (SA-beta-gal) activity but an increase in adenosine triphosphate (ATP) synthesis and mitochondrial

110 METHOD: Mitochondrial O2 consumption and adenosine triphosphate (ATP) synthesis rates of osteosar

111 heart failure (HF) and increases the rate of adenosine triphosphate (ATP) synthesis through creatine

112 minimal electron transport chain capable of adenosine triphosphate (ATP) synthesis, combining Escher

113 F), which provides the driving force for the adenosine triphosphate (ATP) synthesis.

114 xygen-glucose deprivation and contained less adenosine triphosphate (ATP) than WT nerves.

115 es have demonstrated that in the presence of adenosine triphosphate (ATP) the human RAD51 (HsRAD51) r

116 monitoring of enzymatic reactions converting adenosine triphosphate (ATP) to adenosine diphosphate or

117 nases (CK) catalyze the transfer of HEP from adenosine triphosphate (ATP) to PCr and from PCr back to

118 Tumor cells require increased adenosine triphosphate (ATP) to support anabolism and pr

119 lectrostatic lock to prevent coordination of adenosine triphosphate (ATP) to the catalytic site.

120 rch for underpinning molecular mechanisms of adenosine triphosphate (ATP) utilisation.

121 Extracellular adenosine triphosphate (ATP), a potent danger molecule,

122 +) and NADPH); coenzymes of energy including adenosine triphosphate (ATP), adenosine diphosphate (ADP

123 In the presence of adenosine triphosphate (ATP), all three components bind

124 slocase stress-sensitive B (SesB), increased adenosine triphosphate (ATP), and a reduction in autopha

125 Acetyl coenzyme A (CoA), malonyl-CoA, adenosine triphosphate (ATP), and adenosine diphosphate

126 NRPS module in the presence of ornithine and adenosine triphosphate (ATP), and we detected the same p

127 Nucleotides, such as adenosine triphosphate (ATP), are released by cellular i

128 produced by microglia, such as cytokines and adenosine triphosphate (ATP), have been directly linked

129 arget molecules, such as ochratoxin A (OTA), adenosine triphosphate (ATP), or thrombin, the aptamer s

130 d by chemical gradients or the hydrolysis of adenosine triphosphate (ATP), so far there are no synthe

131 Adenosine triphosphate (ATP), the chemical energy curren

132 pendent vasodilators acetylcholine (ACh) and adenosine triphosphate (ATP), the endothelium-independen

133 sing applications such as the measurement of adenosine triphosphate (ATP), the energy unit in biologi

134 (CO), and carbon dioxide (CO2) without using adenosine triphosphate (ATP), when samarium(II) iodide (

135 member of the family of structurally related adenosine triphosphate (ATP)-binding cassette (ABC) prot

136 ABCB4 (MDR3) is an adenosine triphosphate (ATP)-binding cassette (ABC) tran

137 nalysis of exporters from the superfamily of adenosine triphosphate (ATP)-binding cassette (ABC) tran

138 re harboring disease-causing variants in the adenosine triphosphate (ATP)-binding cassette subfamily

139 on of two of the most relevant transporters: adenosine triphosphate (ATP)-binding cassette subfamily

140 le salt export pump (BSEP), a liver-specific adenosine triphosphate (ATP)-binding cassette transporte

141 or that expresses the photoreceptor-specific adenosine triphosphate (ATP)-binding cassette transporte

142 rol secretion and hepatic gene expression of adenosine triphosphate (ATP)-binding cassette, subfamily

143 We discovered an N676K mutation in the adenosine triphosphate (ATP)-binding domain (tyrosine ki

144 plex loaded onto DNA directly interacts with adenosine triphosphate (ATP)-bound DnaA and stimulates t

145 In contrast, Tregs devoid of the adenosine triphosphate (ATP)-degrading ecto-enzyme CD39

146 Given the implications for adenosine triphosphate (ATP)-dependent Ca(2+) signaling

147 al part of the chromatin landscape shaped by adenosine triphosphate (ATP)-dependent chromatin remodel

148 recently, were only known to participate in adenosine triphosphate (ATP)-dependent proteolysis in ba

149 ir activities also include duplex annealing, adenosine triphosphate (ATP)-dependent RNA binding, and

150 f subunits confers functional specificity to adenosine triphosphate (ATP)-dependent SWI/SNF-like Brg/

151 NDPKs) NM23-H1/H2, which produce GTP through adenosine triphosphate (ATP)-driven conversion of guanos

152 and protein degradation by proteasomes in an adenosine triphosphate (ATP)-independent manner.

153 nt study, H2O2 dose-dependently impaired the adenosine triphosphate (ATP)-induced Ca(2+) response, wh

154 cells requires Toll-like receptor (TLR) and adenosine triphosphate (ATP)-mediated P2X purinoceptor 7

155 ve cation channel activated by extracellular adenosine triphosphate (ATP).

156 lysis by the Mtb proteasome independently of adenosine triphosphate (ATP).

157 by thousands of dynein motors that hydrolyze adenosine triphosphate (ATP).

158 tory effects when activated by extracellular adenosine triphosphate (ATP).

159 rgic receptors and impaired migration toward adenosine triphosphate (ATP).

160 ed astrocytes to release the gliotransmitter adenosine triphosphate (ATP).

161 by increasing the synthesis and secretion of adenosine triphosphate (ATP).

162 t robust pRNA synthesis as it initiates with adenosine triphosphate (ATP).

163 hile maintaining or increasing production of adenosine triphosphate (ATP).

164 fically, ketamine tended to downregulate the adenosine triphosphate (ATP)/adenosine diphosphate (ADP)

165 LR-L-KO mice contained low levels of ALR and adenosine triphosphate (ATP); they had reduced mitochond

166 ble of converting a chosen biological input, adenosine triphosphate (ATP; that does not directly bind

167 te-containing compounds (phosphocreatine and adenosine triphosphate [ATP]), inorganic phosphate, and

168 y-mass spectrometry for energetic cofactors (adenosine triphosphate [ATP]/adenosine diphosphate [ADP]

169 reduced lung injury associated with restored adenosine triphosphate availability and turnover.

170 i and the acidic milieu) might promote hyper-adenosine triphosphate-bilia, lipopolysaccharide overloa

171 This mutation impairs adenosine triphosphate binding and reduces catalytic act

172 l lumen via the sterol-exporting heterodimer adenosine triphosphate binding cassette subfamily G memb

173 Ibrutinib and A419259 also blocked adenosine triphosphate binding to HCK, whereas transduct

174 ing their conformations during the course of adenosine triphosphate binding, hydrolysis and product r

175 on with another Type ISP enzyme and requires adenosine triphosphate binding/hydrolysis but, surprisin

176 The adenosine triphosphate-binding cassette (ABC) sterol tra

177 cleotide polymorphisms nor expression of the adenosine triphosphate-binding cassette (ABC) transporte

178 By characterization of a Petunia hybrida adenosine triphosphate-binding cassette (ABC) transporte

179 eptors (LXRs) regulate the expression of the adenosine triphosphate-binding cassette (ABC) transporte

180 to a sequence within Clostridium perfringens adenosine triphosphate-binding cassette (ABC) transporte

181 d cholesterol efflux via the upregulation of adenosine triphosphate-binding cassette (ABC) transporte

182 rug resistance 2 (Mdr2)-knockout (KO) mouse (adenosine triphosphate-binding cassette b4(-/-) ), a mod

183 in; KCNN4, the Gardos channel; and ABCB6, an adenosine triphosphate-binding cassette family member, i

184 ss the transport activity of P-glycoprotein (adenosine triphosphate-binding cassette subfamily B, mem

185 BCB1]) and breast cancer resistance protein (adenosine triphosphate-binding cassette subfamily G, mem

186 nding cassette (ABC) transporters, including adenosine triphosphate-binding cassette transporter A1 (

187 -binding cassette transporter A1 (ABCA1) and adenosine triphosphate-binding cassette transporter G1 (

188 recessive disease caused by mutations in the adenosine triphosphate-binding cassette transporter gene

189 logous sequence of a Clostridium perfringens adenosine triphosphate-binding cassette transporter.

190 in other genes including SLC28A1 and several adenosine triphosphate-binding cassette transporters (AB

191 The adenosine triphosphate-binding cassette transporters P-g

192 e (HK) by focusing on their highly conserved adenosine triphosphate-binding domain.

193 he acquisition of secondary mutations in the adenosine triphosphate-binding pocket of the JAK mutant.

194 s not depend on cyclophilin A, but rather on adenosine-triphosphate-binding cassette transporters and

195 d that the fluorescence of BODIPY-conjugated adenosine triphosphate (BODIPY-ATP) was quenched by Fe(I

196 Sperm motility is powered by adenosine triphosphate but the relative importance of la

197 Because adenosine triphosphate-citrate lyase and adenosine monop

198 markers as they relate to the inhibition of adenosine triphosphate-citrate lyase and the activation

199 ETC-1002 is an adenosine triphosphate-citrate lyase inhibitor/adenosine

200 re, the aim of this study was to investigate adenosine triphosphate-competitive inhibitors of mTOR ki

201 JNK1 or JNK2 or treatment with JNK-IN-8, an adenosine triphosphate-competitive irreversible pan-JNK

202 and coincide with two peaks of intracellular adenosine triphosphate concentration.

203 02, compared to NE), whereas skeletal muscle adenosine triphosphate concentrations were increased.

204 m patients with COPD have reduced DeltaPsim, adenosine triphosphate content, complex expression, basa

205 incubations with radiolabelled phosphate and adenosine triphosphate coupled with cell sorting flow cy

206 ionally silent complex requiring specialized adenosine triphosphate-dependent activators for initiati

207 Adenosine triphosphate-dependent chromatin remodeling ma

208 s key enzymatic features with LlaGI; namely, adenosine triphosphate-dependent DNA translocation ( app

209 d threaded through the helicase domain in an adenosine triphosphate-dependent manner.

210 we found that eIF4A functions instead as an adenosine triphosphate-dependent processive helicase whe

211 as Rho-dependent termination relies upon the adenosine triphosphate-dependent RNA translocase Rho, wh

212 however, its transport activity, assessed by adenosine triphosphate-dependent taurocholate transport

213 brane potential (DeltaPsim) and, ultimately, adenosine triphosphate depletion and necrosis.

214 on against UVA-induced mitochondrial damage, adenosine triphosphate depletion, and the ensuing necrot

215 itochondria leads to necrotic cell death via adenosine triphosphate depletion.

216 hiamin pyrophosphate transporter, leading to adenosine triphosphate depletion.

217 eltapsi-driven presequence translocation and adenosine triphosphate-driven import motor activity.

218 e leaving group of the native substrate with adenosine triphosphate, enabling sensitive detection via

219 pressed in liver facilitating the release of adenosine triphosphate from hepatocytes.

220 s, where they act as powerhouses to generate adenosine triphosphate from oxidation of nutrients.

221 -immobilized enzymes that are independent of adenosine triphosphate function as self-powered micropum

222 nd interference with proteins normally using adenosine triphosphate/guanosine triphosphate, probably

223 studies have demonstrated that extracellular adenosine triphosphate has the ability to initiate infla

224 gnaling molecule in a pathway that maintains adenosine triphosphate homeostasis.

225 nses of HSCs are increased by CD39-dependent adenosine triphosphate hydrolysis and adenosine signalin

226 the hydrolytic nuclease reaction instead of adenosine triphosphate hydrolysis as in conventional hel

227 ibit markedly lower catalytic efficiency for adenosine triphosphate hydrolysis compared to WT.

228 sidues defines a sequential, around-the-ring adenosine triphosphate hydrolysis cycle that results in

229 that adopts two distinct folds, and the post-adenosine triphosphate hydrolysis state of KaiC create a

230 ae condensin is a molecular motor capable of adenosine triphosphate hydrolysis-dependent translocatio

231 asmid segregation events by stimulating ParF adenosine triphosphate hydrolysis.

232 lls by walking along microtubules powered by adenosine triphosphate hydrolysis.

233 mal P2X4 forms channels activated by luminal adenosine triphosphate in a pH-dependent manner.

234 njury and evaluate the role of extracellular adenosine triphosphate in ischemic injury in specific or

235 IL1beta production by lipopolysaccharide and adenosine triphosphate in PBMCs.

236 ssion levels were suppressed; also levels of adenosine triphosphate in the intestine of animals with

237 nent role is to facilitate the production of adenosine triphosphate in the mitochondria by participat

238 and decreased the productions of lactate and adenosine triphosphate in tumor cells and in the Ras-tra

239 Adenosine triphosphate is a well-defined intracellular e

240 Within the liver vasculature, adenosine triphosphate is converted into pyrophosphate,

241 The adenosine triphosphate level of the cell is predictive o

242 SRT1720 treatment increased adenosine triphosphate levels and survival of cultured h

243 but neither agent alone, slightly decreased adenosine triphosphate levels in AR42J cells, but induce

244 rial mass, enhanced autophagy, and preserved adenosine triphosphate levels in the liver after ischemi

245 restored the fall in oxygen consumption and adenosine triphosphate levels in the liver, whereas aden

246 by 65.5% +/- 14% (P < 0.05 vs. control), but adenosine triphosphate levels were maintained.

247 rences in APAP serum levels, glutathione, or adenosine triphosphate levels were noted.

248 -reperfusion for analyses of hepatic injury, adenosine triphosphate levels, mitochondrial mass, autop

249 result of pneumonia, but with an increase in adenosine triphosphate levels, whereas adenosine triphos

250 ty and flagellar motility and an increase in adenosine triphosphate levels.

251 ced 25% when values were less than 130 ng/mL adenosine triphosphate (low immune cell response) and in

252 m to discuss the molecular mechanisms behind adenosine triphosphate-mediated ischemic tissue injury a

253 hannel's regulation by magnesium (Mg) and Mg.adenosine triphosphate (Mg.ATP).

254 wn to form a common underlying extracellular adenosine triphosphate molecular mechanism in ischemic o

255 Adenosine triphosphate molecule has been implicated in v

256 iallyldimethylammonium chloride) with either adenosine triphosphate or carboxymethyl-dextran using a

257 from cationic peptides/polyelectrolytes and adenosine triphosphate or oligo/polyribonucleotides.

258 e respiratory deficiency lowed mitochondrial adenosine triphosphate production and increased the prod

259 Significant reductions of mitochondrial adenosine triphosphate production and oxygen consumption

260 showed a 1.5-fold increase in mitochondrial adenosine triphosphate production and were less prone to

261 nelles responsible for energy conversion and adenosine triphosphate production in eukaryotic cells.

262 ergy deficiency due to reduced mitochondrial adenosine triphosphate production is currently the leadi

263 Although diminished mitochondrial adenosine triphosphate production is recognized as a sou

264 rates and, as a consequence, respiration and adenosine triphosphate production without the need to re

265 adenine dinucleotide (NAD(+)) biosynthesis, adenosine triphosphate production, and mitochondrial res

266 he loss of mitochondrial membrane potential, adenosine triphosphate production, and reactive oxygen s

267 g across the thylakoid membrane and elevated adenosine triphosphate production.

268 IL1beta production by lipopolysaccharide and adenosine triphosphate (R(2) = .88).

269 diac energetic status (phosphocreatine/gamma-adenosine triphosphate ratio, 1.3+/-0.1 versus 1.9+/-0.1

270 lation between T1 values and phosphocreatine/adenosine triphosphate ratios (r=-0.59, P<0.0001).

271 olite, exposing the worms to light increased adenosine triphosphate, reduced oxidative damage, and in

272 age-associated impairments in red blood cell adenosine triphosphate release and stimulation of endoth

273 ly discovered that absence of ABCC6-mediated adenosine triphosphate release from the liver and conseq

274 Extracellular adenosine triphosphate rises in blood and bile after PH

275 gnificantly impairs platelet aggregation and adenosine triphosphate secretion induced by numerous ago

276 ll platelets have defects in aggregation and adenosine triphosphate secretion induced by thrombin, co

277 Activation of mitochondrial adenosine triphosphate-sensitive potassium (KATP) channe

278 d ex vivo for rubidium efflux as a marker of adenosine triphosphate-sensitive potassium channel activ

279 n, at least in part, the reduced efficacy of adenosine triphosphate-sensitive potassium channel block

280 Excessive opening of the adenosine triphosphate-sensitive potassium channel in va

281 to norepinephrine and PNU-37883A (a vascular adenosine triphosphate-sensitive potassium channel inhib

282 thus investigated the hemodynamic effects of adenosine triphosphate-sensitive potassium channel pore

283 ensitive potassium channel activity, and for adenosine triphosphate-sensitive potassium channel subun

284 ivation of protease activated receptor-2 and adenosine triphosphate signaling.

285 usting nicotinamide adenine dinucleotide and adenosine triphosphate stores, exacerbating mitochondria

286 25% when values were greater than 450 ng/mL adenosine triphosphate (strong immune cell response).

287 sensitive conferring protein at lysine-70 in adenosine triphosphate synthase complex promoted its int

288 de-3-phosphate dehydrogenase, beta actin and adenosine triphosphate synthase subunit to be the most s

289 ent with a mitochondrial uncoupling agent or adenosine triphosphate synthesis inhibitor reduced lamel

290 wild-type allotopic ND4 prevented defective adenosine triphosphate synthesis, suppressed visual loss

291 ons related to T cell receptor signaling and adenosine triphosphate synthesis.

292 rome has long been attributed to energy (ie, adenosine triphosphate synthetic) failure such as that c

293 similarly high positivity rate of adenosine/adenosine triphosphate testing was found in both groups.

294 ons such as mRNA capping, the cyclization of adenosine triphosphate, the hydrolysis of thiamine triph

295 An integrated circuit is powered by adenosine triphosphate through the action of Na(+)/K(+)

296 and IL18; cells were incubated with LPS and adenosine triphosphate to activate the NLRP3 complex.

297 that DDX3X, like Ded1p, utilizes exclusively adenosine triphosphates to unwind helices, oligomerizes

298 Adenosine triphosphate was kept constant at physiologica

299 es (interleukin-1beta and interleukin-6) and adenosine triphosphate were also measured.

300 gy, with the potential to replenish cellular adenosine triphosphate without oxygen.