ライフサイエンスコーパス: adenosine triphosphate

1 host crucial metabolic pathways and produce adenosine triphosphate.

2 ies on oxidative phosphorylation to generate adenosine triphosphate.

3 an ectonucleotidase that generates PPi from adenosine triphosphate.

4 phase accompanied by a drop in intracellular adenosine triphosphate.

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

6 ted by the intracytoplasmatic application of adenosine triphosphate.

7 ranes, and energy transfer molecules such as adenosine triphosphate.

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

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

10 regeneration entails: increased synthesis of adenosine triphosphate, a reduced inflammatory response,

11 Extracellular adenosine triphosphate accelerated interleukin-12-driven

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 air of substrates TMP and a non-hydrolyzable adenosine triphosphate analog, and in complex with a pai

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

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

17 the carboxyl terminus of the peptide through adenosine triphosphate and amino acyl-tRNA-dependent che

18 o a significant increase in the synthesis of adenosine triphosphate and growth factors resulting in n

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

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

21 ion of these cell-like compartments required adenosine triphosphate and microtubule polymerization bu

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

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

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

25 that generate cellular energy in the form of adenosine triphosphate and phosphocreatine (PCr).

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

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

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

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

30 olecules, including toxin-antitoxin modules, adenosine triphosphate, and guanosine (penta) tetraphosp

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

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

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

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

35 ever, aged primates have a >70% reduction in adenosine triphosphate (ATP) and a decrease in cytochrom

36 sphate, inorganic tripolyphosphate (3polyP), adenosine triphosphate (ATP) and adenosine monophosphate

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

38 that the G protein-coupled receptor agonists adenosine triphosphate (ATP) and histamine promoted rapi

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

40 t transporter from Aquifex aeolicus bound to adenosine triphosphate (ATP) and in a lipid environment,

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

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

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

44 Measurements of adenosine triphosphate (ATP) and metabarcoding of enviro

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

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

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

48 ifically, we employed sequences specific for adenosine triphosphate (ATP) and tobramycin as test-bed

49 They utilize cycles of adenosine triphosphate (ATP) binding and hydrolysis to t

50 vity" and "alkyl-induced" pockets within the adenosine triphosphate (ATP) binding site of PI3Kgamma.

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

52 try to investigate the impact of variants on adenosine triphosphate (ATP) binding.

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

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

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

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

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

58 le unit, shortening because of hydrolysis of adenosine triphosphate (ATP) by myosin molecular motors.

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

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

61 Only under cellular adenosine triphosphate (ATP) concentrations, these chang

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

63 We assessed the adenosine triphosphate (ATP) content decay of mouse live

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

65 CofB also shows activation by adenosine triphosphate (ATP) despite the reaction requir

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

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

68 the eukaryotic DNA ligases are known to use adenosine triphosphate (ATP) for DNA ligation.

69 tween the genomes is essential for efficient adenosine triphosphate (ATP) generation.

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

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

72 DNA compaction by cohesin requires adenosine triphosphate (ATP) hydrolysis and is force sen

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

74 action-diffusion numerical simulations of 1) adenosine triphosphate (ATP) hydrolysis into adenosine m

75 DEAH helicases couple adenosine triphosphate (ATP) hydrolysis to conformationa

76 Based on ensemble measurements, Mot1 can use adenosine triphosphate (ATP) hydrolysis to displace TBP

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

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

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

80 ses direct ciliary and flagellar beating via adenosine triphosphate (ATP) hydrolysis.

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

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

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

84 Adenosine triphosphate (ATP) induces pain via activation

85 ensely packed adjacent to myofibrils because adenosine triphosphate (ATP) is needed to fuel sarcomere

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

87 In tissue infections, adenosine triphosphate (ATP) is released into extracellu

88 Adenosine triphosphate (ATP) is released into the extrac

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

90 bnormal mitochondrial fragmentation, reduced adenosine triphosphate (ATP) levels and a higher fatigab

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

92 hondrial functionality with reduced cellular adenosine triphosphate (ATP) levels, altered mitochondri

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

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

95 ial, reduced calcium levels, and also higher adenosine triphosphate (ATP) production capacity than th

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

97 a wide range of cellular functions including adenosine triphosphate (ATP) production, lipid synthesis

98 ucial for iron-sulfur cluster biogenesis and adenosine triphosphate (ATP) production.

99 Adenosine triphosphate (ATP) promoted the reaction but w

100 Adenosine triphosphate (ATP) release and autocrine purin

101 The plasma membrane adenosine triphosphate (ATP) release channel pannexin 1

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

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

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

105 Adenosine triphosphate (ATP) resynthesis during oxygenat

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

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

108 tructure of the F(1)-catalytic domain of the adenosine triphosphate (ATP) synthase has been determine

109 The adenosine triphosphate (ATP) synthase in human mitochond

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

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

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 of oligomycin, an inhibitor of mitochondrial adenosine triphosphate (ATP) synthesis.

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

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

117 observed in cell systems, administration of adenosine triphosphate (ATP) to mice enhanced lipopolysa

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

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

120 tion, stressed or infected cells can release adenosine triphosphate (ATP) to the extracellular medium

121 ciated with P(i) liberation in real-time for adenosine triphosphate (ATP) turnover by myosin, the act

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

123 sed to detect the low weight target molecule adenosine triphosphate (ATP), a common biomarker, which

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

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

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

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

128 d cycle (TCA) intermediates and synthesis of adenosine triphosphate (ATP), but the reason for glutama

129 2+, and mitochondria, an important source of adenosine triphosphate (ATP), has been the subject of mu

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

131 ious biomolecules including small molecules (adenosine triphosphate (ATP), limit of detection (LOD) o

132 incubated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP), or 4OH-tamoxifen, respecti

133 icles also utilize the excessive presence of adenosine triphosphate (ATP), riboflavin, and Zn(2+) in

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

135 Adenosine triphosphate (ATP), the chemical energy curren

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

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

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

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

140 We focused on adenosine triphosphate (ATP)-binding cassette (ABC) tran

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

142 omplexes in adenosine diphosphate (ADP)- and adenosine triphosphate (ATP)-bound conformations, highli

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

144 larger lesions in rat molars shows that the adenosine triphosphate (ATP)-competitive GSK-3 inhibitor

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

146 id core to be HSP70 family chaperones, whose adenosine triphosphate (ATP)-dependent activity maintain

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

148 We show that Uls1, an adenosine triphosphate (ATP)-dependent chromatin remodel

149 gase (NgrRnl) exemplifies the Rnl5 family of adenosine triphosphate (ATP)-dependent polynucleotide li

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

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

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

153 First, we build an adenosine triphosphate (ATP)-driven DNA nanogatekeeper.

154 ngage specific protein substrates before the adenosine triphosphate (ATP)-fueled mechanical unfolding

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

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

157 er-soluble cationic porphyrin that undergoes adenosine triphosphate (ATP)-templated self-assembly int

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

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

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

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

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

163 loyed to form the biological energy currency adenosine triphosphate (ATP).

164 to the hydrolysis of fuel molecules such as adenosine triphosphate (ATP).

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

166 erved gamma-rotation angle dependence of the adenosine triphosphate (ATP)/adenosine diphosphate (ADP)

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

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

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

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

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

172 This mutation impairs adenosine triphosphate binding and reduces catalytic act

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

174 A member 2 [SLC10A2]) and six known loci (in adenosine triphosphate binding cassette subfamily G memb

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

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

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

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

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

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

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

182 Multidrug resistance-associated protein 1 (adenosine triphosphate-binding cassette subfamily C memb

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

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

185 The adenosine triphosphate-binding cassette transporters P-g

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

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

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

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

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

191 Because adenosine triphosphate-citrate lyase and adenosine monop

192 cular outcome studies are bempedoic acid, an adenosine triphosphate-citrate lyase inhibitor that redu

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

194 tervention in targeting cancers resistant to adenosine triphosphate competitive drugs.

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

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

197 02, compared to NE), whereas skeletal muscle adenosine triphosphate concentrations were increased.

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

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

200 ine, which may be generated by extracellular adenosine triphosphate degradation, impairs the parenchy

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

202 Adenosine triphosphate-dependent chromatin remodeling ma

203 ognition of a replication error it undergoes adenosine triphosphate-dependent conformational changes

204 or is a novel therapeutic strategy to dampen adenosine triphosphate-dependent IL-1beta signaling.

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

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

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

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

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

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

211 hiamin pyrophosphate transporter, leading to adenosine triphosphate depletion.

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

213 Sensing of extracellular adenosine triphosphate (eATP) by the purinergic receptor

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

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

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

217 The P2X7 receptor (P2X7R) is an adenosine triphosphate-gated ion channel that is predomi

218 The P2X7 receptor is an adenosine triphosphate-gated ion channel, which is abund

219 y accelerated rates of mineral oxidation and adenosine triphosphate generation relative to sterile di

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

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

222 e disassembled, as by Sec17, Sec18, and ATP (adenosine triphosphate), HOPS is required, and GST-PX do

223 Moreover, the IDRs also regulate the adenosine triphosphate hydrolysis and nuclease activitie

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

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

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

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

228 asmid segregation events by stimulating ParF adenosine triphosphate hydrolysis.

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

230 ug-binding site controls the dynamics of the adenosine triphosphate-hydrolyzing NBDs.

231 mononucleotide) and tissues (eg, succinate, adenosine triphosphate, hypoxia-inducible factor-1alpha,

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

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

234 IL1beta production by lipopolysaccharide and adenosine triphosphate in PBMCs.

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

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

237 Intratracheal replenishment of adenosine triphosphate in Trpv4 mice abrogated the prote

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

239 ond between the gamma and beta phosphates of adenosine triphosphate into mechanical work, which resul

240 Adenosine triphosphate is a well-defined intracellular e

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

242 The adenosine triphosphate level of the cell is predictive o

243 changes in pH value, conductivity/impedance, adenosine triphosphate level, concentration of dissolved

244 with increased intracellular charge, higher adenosine triphosphate level, quicker substrate consumpt

245 Increased intracellular adenosine triphosphate levels activate the purinergic re

246 he BACS group exhibited significantly higher adenosine triphosphate levels and lower expression of ph

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

248 acted with Panx3 by modulating intracellular adenosine triphosphate levels and thereby enhanced HaCaT

249 reased tricarboxylic acid cycle activity and adenosine triphosphate levels as a consequence of enhanc

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

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

252 Adenosine triphosphate levels significantly improved dur

253 Adenosine triphosphate levels under UW preservation fall

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

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

256 h a dramatic drop in glycolysis and cellular adenosine triphosphate levels while oxidative phosphoryl

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

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

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

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

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

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

263 Adenosine triphosphate molecule has been implicated in v

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

265 e we show that liposomes containing calcium, adenosine triphosphate, or carboxyfluorescein are tether

266 c or specific inhibitors targeting the TRPV4/adenosine triphosphate/P2X signaling axis, may represent

267 etion of cellular guanosine triphosphate and adenosine triphosphate pools, and is counteracted by its

268 nflammasome model of lipopolysaccharide plus adenosine triphosphate, PRL inhibited the priming (expre

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

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

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

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

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

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

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

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

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

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

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

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

281 tly shown that the absence of ABCC6-mediated adenosine triphosphate release from the liver and, conse

282 Extracellular adenosine triphosphate rises in blood and bile after PH

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

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

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

286 ted p27 (phosp27) to CDK4 altered the kinase adenosine triphosphate site to promote phosphorylation o

287 25% when values were greater than 450 ng/mL adenosine triphosphate (strong immune cell response).

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

289 enes in HFpEF were enriched in mitochondrial adenosine triphosphate synthesis/electron transport, pat

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

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

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

293 ATPase (enzymatic hydrolysis of adenosine triphosphate to inorganic phosphate) levels we

294 their central role in energetics, producing adenosine triphosphate to power most cellular processes.

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

296 his species is crucial for the regulation of adenosine triphosphate turnover in the first nucleotide-

297 Adenosine triphosphate was kept constant at physiologica

298 Adenosine triphosphate was selected as the target life m

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.