ライフサイエンスコーパス: NADH

1 NADH (NAD(+)) is an essential metabolite involved in var

2 NADH and NAD(+) are a ubiquitous cellular redox couple.

3 NADH ED-FRAP parameters were optimized to deliver 23.8 m

4 NADH-dependent electron transfer via the redox component

5 NADH-free forms of CtBPs cooperated with the p53-binding

6 Cytochrome bc1-aa3 oxidase and type-2 NADH dehydrogenase (NDH-2) are respiratory chain compone

7 g(2+)) and its ternary complex (KARI:2Mg(2+):NADH:inhibitor) are temperature-dependent in correlation

8 Here, we identify Aifm2, a NADH oxidoreductase domain containing flavoprotein, as a

9 llelic variation at OsNR2, a gene encoding a NADH/NADPH-dependent NO(3)(-) reductase (NR).

10 ed with protein folding, cell-cell adhesion, NADH dehydrogenase activity, ATP-binding, proteasome com

11 An AfFabI.NADH crystal structure at 1.86 angstrom resolution revea

12 hibit oxidative phosphorylation by affecting NADH oxidation in the plant pathogens Zymoseptoria triti

13 Altering NADH and NADPH metabolism using drug strategies and IDH1

14 isethionate (2-hydroxyethanesulfonate) by an NADH-dependent reductase.

15 NAD(P)H quinone dehydrogenase 1 (NQO1) in an NADH-dependent manner.

16 ing site for the stable immobilisation of an NADH-dependent dehydrogenase (i.e. lactate dehydrogenase

17 photocurrent of the nanostructures shows an NADH-dependent magnitude.

18 Moreover, complex 1 and NADH synergistically photoreduce cytochrome c under hypo

19 eal pai stacking in adducts of complex 1 and NADH, facilitating photoinduced single-electron transfer

20 The produced NH(3) and NADH were reacted in situ with leucine dehydrogenase (Le

21 ess were reflected by low amounts of ATP and NADH and an increased abundance of oxidized lipids deriv

22 regulation of pathways that generate ATP and NADH, and promote the proton gradient.

23 lls due to its ability to regenerate ATP and NADH/NADPH.

24 mice have increased acetyl-CoA (14-fold) and NADH (2-fold), indicating metabolic shifts yield suffici

25 al for supplementing NAD+ for glycolysis and NADH for oxidative phosphorylation.

26 tion of reduced methyl viologen (MV(*+)) and NADH for the nitrogenase and l-alanine dehydrogenase.

27 and Neu5Ac, as well as to co-factors NAD and NADH.

28 and ATP), pyridine dinucleotides (NAD(+) and NADH), and short-chain acyl-CoAs (acetyl, malonyl, succi

29 beta-hydroxybutyrate or cofactors NAD(+) and NADH.

30 ated by Nrf2 and involved in GSH, NADPH, and NADH generation were significantly lower including PRX1

31 ntioxidant cofactors glutathione, NADPH, and NADH were significantly reduced.

32 ivalents to support the NH(3) production and NADH recycling catalyzed by nitrogenase and diaphorase.

33 Decreased ATP production and NADH recycling, associated with mitochondrial uncoupling

34 he interim glycolytic products (pyruvate and NADH) are held in cytosolic equilibrium with the product

35 oxygen species, extracellular pyruvate, and NADH levels, consistent with impaired complex I activity

36 ights analysis (CCSWA) to the riboflavin and NADH data tables since better differentiation was achiev

37 component analysis (PCA), the riboflavin and NADH spectra allowed clear differentiation between sturg

38 olic tracing, histone mass spectrometry, and NADH fluorescence lifetime imaging microscopy in these c

39 including those for ATP6, ATP8 synthase, and NADH dehydrogenase subunits, supporting electron microsc

40 ion, especially for ATP6, ATP8 synthase, and NADH dehydrogenase subunits.

41 hat of the genetically unrelated bifurcating NADH-dependent ferredoxin NADP(+) oxidoreductase (NfnI).

42 cally compromised proteins that fail to bind NADH.

43 de) to achieve effective bioelectrocatalytic NADH regeneration.

44 to be also accepted by human FMO1, and both NADH and NADPH cofactors could act as electron donors, a

45 Catalysis of both NADH oxidation and lipophilic quinone reduction by membr

46 roscopy (FLIM) to distinguish free and bound NADH in mitochondria, nuclei and cytoplasm.

47 idus necator H16 both with and without bound NADH.

48 ting the energy from ubiquinone reduction by NADH to drive protons across the energy-transducing inne

49 ate the recycling of reduced redox carriers (NADH and ferredoxin) in response to environmental H(2) c

50 The cellular NADH/NAD(+) ratio is fundamental to biochemistry, but th

51 y expression of the Saccharomyces cerevisiae NADH:ubiquinone oxidoreductase in L6 cells.

52 applied here, included besides its classical NADH oxidation reaction the generation of cytosolic pyru

53 simulations, here we show that the cofactor NADH is a key player in the GDH regulation process. Our

54 ntrinsically fluorescent metabolic cofactors NADH and NADPH with subcellular spatial resolution.

55 erophilum The EtfABCX enzyme complex couples NADH oxidation to the endergonic reduction of ferredoxin

56 e, and the resultant increase in cytoplasmic NADH/NAD(+) ratio diverts glucose precursors away from g

57 ase-1; but not by a more reduced cytoplasmic NADH/NAD redox state.

58 s of directly lowering the hepatic cytosolic NADH/NAD(+) ratio in mice.

59 bust marker of an elevated hepatic cytosolic NADH/NAD(+) ratio, also known as reductive stress.

60 se conditions is related to Mg(2+)-dependent NADH generation by malic enzyme.

61 The sodium-dependent NADH dehydrogenase (Na(+)-NQR) is a key component of the

62 s Blue modified SPCE (MB-SPCE) by depositing NADH and the enzyme 3alpha-hydroxysteroid dehydrogenase

63 ed form of nicotinamide adenine dinucleotid (NADH) ratio and the NAD(+)-dependent deacetylase activit

64 n between nicotinamide adenine dinucleotide (NADH) and a protein-bound flavin (FMN) cofactor.

65 residues, nicotinamide adenine dinucleotide (NADH) and vitamin A were scanned on sturgeon samples kep

66 , reduced nicotinamide adenine dinucleotide (NADH), and flavin denine dinucleotide (FAD) in fresh bra

67 ,4-dihydronicotinamide adenine dinucleotide (NADH)-an important coenzyme in living cells-generating N

68 DPH), and nicotinamide adenine dinucleotide (NADH).

69 ating the nicotinamide adenine dinucleotide (NADH/NAD(+)) ratio and decreasing expression of the O(2)

70 upted the nicotinamide adenine dinucleotide (NADH/NAD(+)) ratio, and decreased intracellular glutathi

71 reduced nicotinamide adenine dinucleotides (NADH) from 91 potential energy substrates simultaneously

72 it synthesis, but that assembly of RCI (i.e. NADH dehydrogenase) is far less efficient, with dramatic

73 zymatic reduction of GSNO can involve either NADH or NADPH.

74 fluorescence microscopy of their endogenous NADH.

75 cidated recently for the flavin-based enzyme NADH-dependent ferredoxin NADP(+) oxidoreductase I (NfnI

76 transduction activity towards the co-enzyme NADH, delivering a wide linear range of 20-960 muM and a

77 LDH in apo state and ternary complex (enzyme-NADH-oxamate) solved at 2.79 and 1.89 angstrom.

78 beta-oxidation into the reducing equivalents NADH and FADH(2) Although mitochondrial matrix uptake of

79 ell and subcellular resolution by evaluating NADH autofluorescence kinetics during the mitochondrial

80 ell and subcellular resolution by evaluating NADH autofluorescence kinetics during the mitochondrial

81 in mitochondria but did not enhance external NADH oxidation significantly unless AtAOX1A was concomit

82 e BAT-specific first mammalian NDE (external NADH dehydrogenase)-like enzyme, Aifm2 oxidizes NADH to

83 insertion led to a 90% decrease of external NADH oxidation in isolated mitochondria.

84 lude that AtNDB2 is the predominant external NADH dehydrogenase in mitochondria and together with AtA

85 vels could be the lack of reduction factors (NADH or NADPH).

86 erved among Black women and genes coding for NADH dehydrogenase and cytochrome c oxidase subunits.

87 50-fold decrease in catalytic efficiency for NADH production and a significantly reduced rate of glut

88 e chemically modified platinum electrode for NADH electrocatalysis.

89 Firstly, NiO-FET was tested for NADH detection showing a linear concentration range 1aM

90 brevis (Lb)NOX(1), a bacterial water-forming NADH oxidase, to assess the metabolic consequences of di

91 adenine dinucleotide reduced/oxidized forms (NADH/NAD(+)) are critical for maintaining redox homeosta

92 Four NADH dehydrogenases are encoded in the genome, suggestin

93 which changes in the extramitochondrial-free NADH:NAD(+) ratio signaled through the CtBP family of NA

94 ive state rejuvenated the mitochondrial free NADH levels of old NTg neurons by 71% and old 3xTg-AD ne

95 capacity for maintaining mitochondrial free NADH levels was found in old compared to young neurons a

96 uctive treatment to reverse the loss of free NADH in old and Alzheimer's neurons.

97 is is coupled with an increased pool of free NADH, increased mitochondrial biogenesis, triggering of

98 e flexibility of mitochondrial-specific free NADH in live neurons from non-transgenic (NTg) or triple

99 the reversibility of aging subcellular free NADH levels in live neurons.

100 s that mimic cytosolic conditions where free NADH concentration is negligible and the GAPDH-NADH comp

101 s studies showed that LDH activity with free NADH and GAPDH-NADH complex always take place in paralle

102 glycolysis and uncoupling biosynthesis from NADH generation.

103 ssed along the electron transport chain from NADH to O(2) generates a membrane potential and pH gradi

104 omplex of the chain, harvests electrons from NADH to reduce quinone, while pumping protons across the

105 iments indicated that the two electrons from NADH were allocated to the plant-type [2Fe-2S] cluster a

106 n-sulfur clusters, reduced by electrons from NADH.

107 hysical barriers that isolate complex I from NADH, disrupt complex I activity, or destabilize cristae

108 The Bf-FAD accepts electrons pairwise from NADH, directs one to a lower-reduction midpoint potentia

109 d that LDH activity with free NADH and GAPDH-NADH complex always take place in parallel.

110 lap between the off-rates for the LDH-(GAPDH-NADH) complex and the GAPDH-NADH complex.

111 In the case of a transient LDH-(GAPDH-NADH) complex, the relative contribution from the channe

112 DH concentration is negligible and the GAPDH-NADH complex is dominant.

113 r the LDH-(GAPDH-NADH) complex and the GAPDH-NADH complex.

114 ry substrates in the Krebs cycle to generate NADH and flavin adenine dinucleotide, which are further

115 regeneration of NAD(+) from GAPDH-generated NADH because an increased NADH:NAD(+) ratio inhibits GAP

116 equence of ALDH7A1 activity, which generates NADH (nicotinamide adenine dinucleotide, reduced form) f

117 bly isotopically-labelled cofactor ([4-(2)H]-NADH).

118 By coupling [4-(2)H]-NADH-recycling to an array of C=O, C=N, and C=C bond red

119 ((2)H(2)O) to generate and recycle [4-(2)H]-NADH.

120 Our work identifies an elevated hepatic NADH/NAD(+) ratio as a latent metabolic parameter that i

121 High NADH/NAD(+) ratios were associated with succinate accumu

122 ly higher concentration of NADH and a higher NADH/NAD(+) ratio than E. coli cells lacking XaFDH.

123 However, NADH binding significantly reduced the electron density

124 marked decrease in mitochondrial complex I (NADH dehydrogenase) activity, coupled to decreased ATP s

125 Complex I (NADH dehydrogenase, NDU) and complex IV (cytochrome-c-ox

126 Respiratory complex I (NADH:ubiquinone oxidoreductase) captures the free energy

127 Energy-transducing respiratory complex I (NADH:ubiquinone oxidoreductase) is one of the largest an

128 Type II NADH:quinone oxidoreductase (NDH-2) plays a crucial role

129 rroborated that WSUCF1 biofilms uses type-II NADH dehydrogenase and demethylmenaquinone methyltransfe

130 In myotubes, however, impaired NADH oxidation following ETC inhibition neither depletes

131 In myoblasts, we find that impaired NADH oxidation upon electron transport chain (ETC) inhib

132 in blood lactate:pyruvate ratio and improved NADH:NAD(+) balance in the heart and brain.

133 esulting in an immediate, linear increase in NADH fluorescence proportional to the steady-state NADH

134 solated islets, glucose-induced increases in NADH and ATP are impaired and both oxidative and glycoly

135 d that Leu(46) and Phe(123) were involved in NADH binding, whereas Trp(70) and Ser(45) were the key r

136 ), not previously observed to participate in NADH-mediated reduction of the FdsABG holoenzyme.

137 of NADH oxidation, as further increases in [NADH] elevate ubiquinol-related complex III reduction be

138 of a protective p53 response by an increased NADH:NAD(+) ratio enables cells to avoid cellular damage

139 om GAPDH-generated NADH because an increased NADH:NAD(+) ratio inhibits GAPDH.

140 ochondrial coupling efficiency and increased NADH production, suggesting an impairment on ATP product

141 We observed decreased OAA, increased NADH/NAD(+), and increased succinate-supported mitochond

142 On light irradiation, complex 1 induces NADH depletion, intracellular redox imbalance and immuno

143 activity, or destabilize cristae and inhibit NADH-dependent respiration.

144 ucleotide NADP(+) into NAD(+) and NADPH into NADH.

145 An elevated intracellular NADH:NAD(+) ratio, or 'reductive stress', has been assoc

146 TP production and an increased intracellular NADH/NAD(+) ratio compared with BMDMs from WT mice.

147 DMs with lactate increased the intracellular NADH/NAD(+) ratio and upregulated NF-kappaB activation a

148 As the intracellular NADH:NAD(+) ratio can be in near equilibrium with the ci

149 pyruvate ratio, normalized the intracellular NADH:NAD(+) ratio, upregulated glycolytic ATP production

150 se model of mitochondrial disease that lacks NADH:ubiquinone oxidoreductase subunit S4 (NDUFS4), a su

151 Photoexcited dihydronicotinamides like NADH and analogues have been found to generate alkyl rad

152 eaky channeling complex only at the limiting NADH concentrations.

153 l subunits at high levels, and mitochondrial NADH and reactive oxygen species (ROS) accumulation duri

154 Complex I (mitochondrial NADH:ubiquinone oxidoreductase), a membrane-bound redox-

155 The ensuing reduction in mitochondrial NADH utilization, measured with two-photon NAD(P)H fluor

156 cription factor Nrf2 increased mitochondrial NADH levels and restored mitochondrial membrane potentia

157 Measures of mitochondrial NADH flux by mitoRACE are sensitive to physiological and

158 providing a direct measure of mitochondrial NADH flux.

159 mol/mg) caused a more oxidized mitochondrial NADH/NAD state and an increase in lactate/pyruvate ratio

160 nmol/mg) caused a more reduced mitochondrial NADH/NAD state similar to Complex 1 inhibition by roteno

161 flux through the steady-state mitochondrial NADH pool by rapidly inhibiting mitochondrial energetic

162 ting evolutionary links to the mitochondrial NADH dehydrogenase (Complex I).

163 n has a biphasic effect on the mitochondrial NADH/NAD redox state in mouse hepatocytes.

164 NO reductase (GSNOR, Adh5) accounts for most NADH-dependent GSNOR activity, whereas NADPH-dependent G

165 ondrial oxidative capacity, increased muscle NADH content, and higher muscle free radical release mea

166 al changes, including the drop in myocardial NADH levels, the release of lipofuscin-like pigments, an

167 igger this cascade by decreasing the NAD(+) /NADH ratio and NHEJ-repair in vitro and in diabetes mous

168 oA-S-S-G along with redox coenzymes (NAD(+), NADH, NADP(+), NADPH), energy coenzymes (ATP, ADP, AMP),

169 rately by biosensors that detect pH, NAD(+), NADH, NADPH, histidine, and glutathione redox potential.

170 s mito-Ca(2+) loading lowers cellular NAD(+)/NADH redox and downregulates ribbon size.

171 ociated with increased total cellular NAD(+)/NADH.

172 This change in NAD(+)/NADH is caused by increased mitochondrial membrane poten

173 Dysregulation in NAD(+)/NADH levels is associated with increased cell division a

174 NRH substantially increases NAD(+)/NADH ratio in cultured cells and in liver and no inducti

175 teroplasmy also affects mitochondrial NAD(+)/NADH ratio, which correlates with nuclear histone acetyl

176 ysical behavior to that of the native NAD(+)/NADH.

177 histone acetylation, whereas nuclear NAD(+)/NADH ratio correlates with changes in nDNA and mtDNA tra

178 or increasing ATP hydrolysis restores NAD(+)/NADH homeostasis and proliferation even when glucose oxi

179 ch as shifting equilibria like in the NAD(+)/NADH or GSH/GSSG couples), on non-natural molecules such

180 of UDP-glucuronic acid can alter the NAD(+)/NADH ratio via the enzyme UDP-glucose dehydrogenase, whi

181 glutarate (alphaKG) abundance and the NAD(+)/NADH ratio, indicating that constitutive endoplasmic ret

182 rs cell proliferation by reducing the NAD(+)/NADH ratio.

183 onsistent with a rapid decline in the NAD(+)/NADH ratio.

184 sociation of citrin with glycolysis and NAD+/NADH ratio led us to hypothesize that it may play a role

185 rial proteins associated with decreased NAD+/NADH ratio in the TTNtv hearts.

186 -aspartate shuttle, which regulates the NAD+/NADH ratio between the cytosol and mitochondria.

187 Cell viability, ROS, NADPH, NADH, and ATP levels were fully rescued by TRPM2 and par

188 and backbone carbonyl group of M1 of NDUFA1 (NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subun

189 nother Fe-S center within Complex I (Ndufs1, NADH [nicotinamide adenine dinucleotide] dehydrogenase [

190 FeS chain and modulates the binding of a new NADH molecule.

191 tamine, leading to cytosolic accumulation of NADH and increased oxidative status.

192 develop a blue-light (365 nm) activation of NADH coupled to electron paramagnetic resonance (EPR) me

193 ires an electron transport chain composed of NADH (or NADPH), cytochrome b(5) reductase (b(5)R), and

194 have a significantly higher concentration of NADH and a higher NADH/NAD(+) ratio than E. coli cells l

195 w-potential fouling-free anodic detection of NADH.

196 rotein S12 (RPS12), the 5' editing domain of NADH dehydrogenase subunit 7 (ND7 5'), and C-rich region

197 occus fermentans bifurcates the electrons of NADH, sending one to the low-potential ferredoxin and th

198 effects are inhibited by forced elevation of NADH, reduced expression of CtBP, or transfection with a

199 integral components and assembly factors of NADH:ubiquinone oxidoreductase, Mtln does not alter its

200 +) ratio signaled through the CtBP family of NADH-sensitive transcriptional regulators to control the

201 etabolism by fluorescence lifetime (FLIM) of NADH and signaling by kinases Akt and ERK revealed that

202 ility of reducing equivalents in the form of NADH as an important mechanism by which metabolic activi

203 of NADP(+) from NAD(+) (the oxidized form of NADH), on three serine residues (Ser(44), Ser(46), and S

204 piericidin, demonstrating the importance of NADH-related ubiquinone reduction for ROS production und

205 x I mitochondrial respiration due to lack of NADH for the electron transport chain.

206 ith essential roles in influencing levels of NADH and NADPH, in all analyzed organs of conventional m

207 We analyzed the mechanism of NADH-channeling from D-glyceraldehyde-3-phosphate dehydr

208 donor, it recognizes putative metabolites of NADH, such as N-methyl- and N-ribosyl-dihydronicotinamid

209 mann-fold motifs that bind the ADP moiety of NADH, NADPH, FADH and ATP.

210 Here, we established live monitoring of NADH/NAD(+) in plants using the genetically encoded fluo

211 inding of quinone-like compounds (but not of NADH) leads to a related global conformational change, a

212 on of NAD(P)(+), Fdx2-dependent oxidation of NADH and Fdx4- and Fdx11-dependent reduction of NAD(+) M

213 a redox enzyme that may promote oxidation of NADH to facilitate enhanced glycolysis in the cytosol an

214 teps of photorespiration versus oxidation of NADH to generate ATP by oxidative phosphorylation.

215 luated using SECM imaging in the presence of NADH, demonstrating the uniformity of the reactive layer

216 MitoRACE measures the rate of NADH flux through the steady-state mitochondrial NADH po

217 For maximal ROS production, the rate of NADH generation has to be equal or below that of NADH ox

218 een well characterized, however, the role of NADH dehydrogenases in feeding electrons to Mtr has been

219 Understanding the role of NADH in extracellular electron transfer may help improve

220 of the quinone binding pocket to the site of NADH reduction.

221 electron transfer from the excited state of NADH to the oxidized, Rieske-type, [2Fe-2S](2+) cluster

222 generation has to be equal or below that of NADH oxidation, as further increases in [NADH] elevate u

223 However, utilisation of NADH-dependent enzymes for (2)H-labelling is not straigh

224 re compared with the alpha-2 degrees KIEs on NADH/NAD(+) and the Hammett correlations in closely rela

225 and STD-NMR experiments did not show NAD or NADH exchange on the NMR timescale.

226 Direct application of NAD(+) or NADH increases or decreases ribbon size respectively, po

227 bolism yields a "surplus" of either NADPH or NADH.

228 are closer to the FMN than they are in other NADH dehydrogenases.

229 ase) captures the free energy from oxidising NADH and reducing ubiquinone to drive protons across the

230 I function, retaining the ability to oxidize NADH within the electron transport chain.

231 H dehydrogenase)-like enzyme, Aifm2 oxidizes NADH to maintain high cytosolic NAD levels in supporting

232 ogically active redox cofactor that oxidizes NADH bound by M. smegmatis carveol dehydrogenase (MsCDH)

233 gnificant metabolic flexibility in oxidizing NADH under a variety of conditions.

234 pyruvate dehydrogenase activity in producing NADH during anerobic lactate metabolism.

235 well-known formate dehydrogenase to promote NADH-dependent reactions, we here propose employing form

236 -bond flipping upon NAD(+) binding in proper NADH dehydrogenases.

237 derivatives, without being able to recognize NADH, the reference hydrure donor compound, in contrast

238 t p30 by measurement of mitochondrial redox (NADH/FAD) state by 3D optical cryo-imaging, electroretin

239 luorescence lifetime of enzyme-bound reduced NADH and its phosphorylated form, NADPH (NAD(P)H; 2.77 +

240 t was found that HPR1-T335D exhibits reduced NADH-dependent hydroxypyruvate reductase activity while

241 xisomes could not compensate for the reduced NADH-dependent HPR1 activity.

242 e-modified biocathode was used to regenerate NADH to support the conversion from ethyl 4-chloroacetoa

243 ry sites in proximity of the antenna region, NADH acts as a positive allosteric modulator by enhancin

244 ggesting that quinone availability regulates NADH-coupled respiration activity.

245 es, we report that MDM2 negatively regulates NADH:ubiquinone oxidoreductase 75 kDa Fe-S protein 1 (ND

246 DK1 inhibition on mitochondrial respiration, NADH turnover, ATP/ADP, and calcium influx.

247 Related to the respiratory NADH dehydrogenase complex (complex I), NDH transfers el

248 CI* contains CI's NADH-binding and CoQ-binding modules, the proximal-pumpi

249 Our study reveals that the same NADH dehydrogenase complexes are utilized under oxic con

250 with genetic tools for compartment-specific NADH oxidation to trace mechanisms linking different for

251 luorescence proportional to the steady-state NADH flux rate, thereby providing a direct measure of mi

252 t the 49-kDa mitochondrial complex I subunit NADH dehydrogenase (ubiquinone) Fe-S protein 2 (NDUFS2)

253 Using LbNOX, we demonstrate that NADH reductive stress mediates the effects of GCKR varia

254 Protein I (COPI) complex, we elucidate that NADH generated by ALDH7A1 targets Brefeldin-A ADP-Ribosy

255 We also found that NADH production rate remained significantly impaired aft

256 the presence of alpha-FAD, we observed that NADH transferred a hydride to beta-FAD at a rate of 920

257 as well as uncovering an unexpected way that NADH acts in cellular energetics.

258 The NADH photo-activation coupled with EPR is broadly applic

259 of the electron transport chain such as the NADH dehydrogenases (NDH-2 and NdhA) and the terminal re

260 tional change to participate in covering the NADH-binding pocket and establishing the water channels

261 rial pyruvate carrier (UK5099) decreased the NADH/NAD(+) ratio and reduced NF-kappaB activation.

262 propose a putative mechanistic model for the NADH-driven proton/electron-transfer reaction in complex

263 nt formate dehydrogenase and a member of the NADH dehydrogenase superfamily.

264 neurons, is the regulatory component of the NADH malate-aspartate shuttle.

265 nesis by preventing the incorporation of the NADH module rather than decreasing its stability.

266 but can regenerate NAD+ by expression of the NADH oxidase from Lactobacillus brevis (LbNOX)(13) targe

267 ents of rapid freeze-quenched samples of the NADH reduction of FdsBG identified a neutral flavin semi

268 to probe the energetics and dynamics of the NADH-driven PCET reaction in complex I.

269 Reduced glucose availability reduces the NADH:NAD(+) ratio, NF-kappaB transcriptional activity, a

270 dox ratio becomes progressively smaller, the NADH lifetime becomes progressively shorter, and the mit

271 Here, we report that the NADH-oxidizing N-module of CI is turned over at a higher

272 further show that the binding of GTP to the NADH-bound GDH activates a triangular allosteric network

273 According to the NADH-bound structure, the nicotinamide ring stacks onto

274 ifunctional protein (TFP) interacts with the NADH-binding domain of complex I of the ETC, whereas the

275 production of GalOA in combination with the NADH-yielding sorbitol metabolism.

276 -annotated 28 C-terminal residues within the NADH dehydrogenase subunit 4.

277 LDHA binds to NADH and promotes reactive oxygen species (ROS) to induc

278 unusual in being a dodecamer, bispecific to NADH and NADPH, and losing activity above pH 7.8.

279 e overall structure and affinity of BmLDH to NADH but dramatically altered the closure of the enzyme'

280 F/dihydroethidium staining, perturbed NAD-to-NADH and glutathione-to-glutathione disulfide ratios, in

281 the uniformity of the reactive layer towards NADH oxidation.

282 their cofactor preference from NADPH towards NADH and demonstrated their functionality by the product

283 lycolysis for energy generation and uncouple NADH generation from biosynthesis.

284 oxybutyrate dehydrogenase (BDH) depends upon NADH availability.

285 flavodoxin):NADP(+) oxidoreductase could use NADH to reduce Fd and thus facilitate ADO-mediated alkan

286 FabI) displays cooperative kinetics and uses NADH as a cofactor, and its crystal structure at 1.72 an

287 fully reduced FMNH(-), initially formed via NADH-mediated reduction, to the Fe(2)S(2) cluster.

288 chondria and disrupts electron transport via NADH photocatalysis.

289 anine dehydrogenase to generate alanine with NADH as a coenzyme.

290 ndrial DNA (mtDNA) mutations associated with NADH dehydrogenase subunits and nuclear gene mutations t

291 he analyte or biosensors by combination with NADH producing enzymes.

292 ably using visible light in combination with NADH, the ubiquitous reductant of life.

293 es of T. thermophilus enzyme in complex with NADH or quinone-like compounds.

294 M structures of two Sso-KARI complexes, with NADH+inhibitor and NADPH+inhibitor at pH 7.5, which indi

295 NAD(+) cycling with NADH requires complex I electron flow and is needed to f

296 es were created that are more efficient with NADH.

297 lpha-FAD(*-), the reduction of beta-FAD with NADH was 1500 times slower.

298 Interaction of Mtln with NADH-dependent cytochrome b5 reductase stimulates comple

299 erichia coli initiates synthesis of RNA with NADH (the reduced form of nicotinamide adenine dinucleot

300 absorption, EPR, and optical titrations with NADH or inorganic reductants with and without NAD(+), we