ライフサイエンスコーパス: FAD

1 FAD APP mutations displayed a relative increase in 3- an

2 FAD degradation to riboflavin occurs via still poorly ch

3 FAD docked to the ATP site with ribityl 4'-OH in a possi

4 FADs with promiscuous and unique activities have been id

5 onset of degeneration ( approximately 46.1% FAD and approximately 45% FMN).

6 we therefore investigated the effects of 11 FAD mutations on the aggregation kinetics of Abeta, as w

7 erminal tail (CTT) helix that binds beside a FAD cofactor and is essential for light signaling.

8 all as a single amino acid substitution in a FAD enzyme might result in the acquisition of new SP com

9 NQO1 is a FAD-dependent, two-domain multifunctional stress protein

10 n NAD(P)H quinone oxidoreductase 1 (NQO1), a FAD-dependent enzyme which activates cancer pro-drugs an

11 ps in the cryptochrome interior, can yield a FAD-Trp radical pair state with the FAD and Trp partners

12 electron transfer route including the FAD (a-FAD), the [2Fe-2S] cluster of NfnA and the FAD (b-FAD),

13 NAD(H) binds to a-FAD and NADP(H) consequently to b-FAD, which is position

14 gy transfer efficiencies (E%) vs NAD(P)H-a2%/FAD-a1% as sensitive parameters in predicting drug respo

15 nd (a1%) fraction was decreased, NAD(P)H-a2%/FAD-a1% FLIM-based redox ratio and ROS increased, follow

16 Cysteine-to-alanine substitution abrogated FAD-I's ability to induce hBD-2.

17 Upon blue light absorption, FAD is converted to the neutral radical state, the likel

18 directional synaptic plasticity accompanying FAD-linked mutations.

19 percentage of AD cases, called familial AD (FAD), are associated with mutations in presenilin 1, pre

20 overexpress proteins linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and

21 eta that contains longer Abeta; familial AD (FAD)-associated mutations in PSEN2 increased the levels

22 eletion of Prnp rescued several familial AD (FAD)-associated phenotypes after disease onset in a mous

23 rious mouse models that express familial AD (FAD)-linked mutations, often in combinations.

24 46V knockin (KI) mouse model of familial AD (FAD).

25 (ASM(+/-)) in a mouse model of familial AD (FAD; amyloid precursor protein [APP]/presenilin 1 [PS1])

26 ; n = 5), Pick disease (n = 4), familial AD (FAD; n = 2; PSEN1 p.G206A and p.S170P), and frontotempor

27 Here we identify high affinity FAD and iron biding sites and characterize a single b-ty

28 EtfAf contains one FAD (alpha-FAD) in subunit alpha and a second FAD (beta-FAD) in sub

29 As a result of a domain movement, alpha-FAD is able to approach beta-FADH(-) by about 4 A and to

30 yielding a stable anionic semiquinone, alpha-FAD, which donates this electron further to Dh-FAD of Bc

31 hondrial apoptosis-inducing factor (AIF), an FAD-containing and NADH-specific oxidoreductase critical

32 [NiFe] center, four [4Fe4S] clusters and an FAD) is clearly visible along with a well-defined substr

33 d acylase and its subsequent oxidation by an FAD-dependent L-amino acid oxidase (L-AAO).

34 ned with an additional transgene encoding an FAD-linked APP "Swedish" variant that is synthesized bro

35 ha-helix and to the active-site entrance; an FAD isoalloxazine ring exposed to solvent; and a large a

36 968 is an FAD-dependent enzyme responsible for catalyzing the disu

37 vert D-2HG to alpha-ketoglutarate, namely an FAD-dependent transhydrogenase activity using pyruvate a

38 of prephenalenone to phenalenone requires an FAD-dependent monooxygenase (FMO) PhnB, which catalyzes

39 Photolyases are proteins with an FAD chromophore that repair UV-induced pyrimidine dimers

40 ino acid residues near the dicarboxylate and FAD binding site, which facilitates formation of the cov

41 NAD (nicotinamide adenine dinucleotide), and FAD (flavin adenine dinucleotide).

42 ated several differences in terms of DNA and FAD binding and electron transfer pathways.

43 role for this molecule in modulating FMN and FAD levels in the treponemal periplasm.

44 Free FMN and FAD were not detectable and only trace amounts of FMN we

45 avin and the cognate flavocoenzymes, FMN and FAD, by in vitro biotransformation with better than 90%

46 boflavin and its two cofactor forms, FMN and FAD.

47 creased accumulation of riboflavin, FMN, and FAD.

48 by increasing the amount of oxidized NAD and FAD cofactors.

49 cence from the metabolic co-factors NADH and FAD with quantitation from Fluorescence Lifetime Imaging

50 orescence intensity and lifetime of NADH and FAD, coenzymes of metabolism.

51 eA2 genes and strictly dependent on NADH and FAD.

52 ment involving the NTD, C-terminal NADH, and FAD domains, and the flexible linker between them is ess

53 ssible orientations of the reacting sLys and FAD subunits (called "downward" and "upward").

54 Moreover, anti-FAD-I antibodies blocked F. nucleatum induction of hBD-2

55 wild-type APPTM (AAPTM WT) and mutant APPTM (FAD mutants V44M) with solution NMR.

56 f pixel-wise optical redox ratio, defined as FAD/(FAD + NAD(P)H), revealed three distinct redox distr

57 and good estimates of the numbers of fish at FADs, our method could provide fisheries-independent est

58 arate and succinate at a covalently attached FAD within the FrdA subunit.

59 gen-bonded to N5 and O4 of the bifurcating b-FAD and might play a key role in adjusting a low redox p

60 the [2Fe-2S] cluster of NfnA and the FAD (b-FAD), and the two [4Fe-4S] clusters of NfnB.

61 binds to a-FAD and NADP(H) consequently to b-FAD, which is positioned in the center of the NfnAB comp

62 nB close to the [4Fe-4S] cluster distal to b-FAD.

63 FAD) in subunit alpha and a second FAD (beta-FAD) in subunit beta.

64 EtfAf-NAD(+) complex structure revealed beta-FAD as acceptor of the hydride of NADH.

65 Bifunctional FAD synthetases (FADSs) fold in two independent modules;

66 proteins, the complex was also found to bind FAD, hinting that these cofactors may be involved in sen

67 Beside Moco, eukaryotic NR also binds FAD and heme as additional redox active cofactors, and t

68 es of known structures, mammalian CRY2 binds FAD dynamically with an open cofactor pocket.

69 Both FAD and FMN flavin groups mediate the transfer of NADPH

70 Unlike mammalian NOS that contain both FAD and FMN binding domains within a single polypeptide

71 in was found to contain a bicovalently bound FAD cofactor.

72 complex II enzymes harbor a covalently bound FAD co-factor that is essential for their ability to oxi

73 (-1) protein, which was mainly protein-bound FAD.

74 ent monooxygenases, contains a tightly bound FAD prosthetic group, and is required for the stereosele

75 d resonance energy transfer to the catalytic FAD cofactor are key roles for the antenna chromophores

76 How PSEN1 mutations cause FAD is unclear, and pathogenic mechanisms based on gain

77 he mechanisms by which FADS ensures cellular FAD homeostasis.

78 structurally and biochemically characterized FAD pyrophosphate enzyme in bacteria.

79 ction" of gamma-secretase that characterizes FAD-associated PSEN.

80 NAD+, another adenosine-containing cofactor FAD and highly abundant uridine-containing cell wall pre

81 electron transfer between a flavin cofactor (FAD) and a triad of tryptophan residues.

82 BLUF, despite their sharing highly conserved FAD binding architectures.

83 he flavin-binding site in the more conserved FAD domain.

84 urified from Escherichia coli, YUC6 contains FAD as a cofactor, which has peaks at 448 nm and 376 nm

85 However, direct biochemical data correlating FAD redox chemistry with CheA kinase activity have been

86 Light reduces the dCRY FAD to an anionic semiquinone (ASQ) radical and increase

87 FADX group enzymes had no detectable Delta12 FAD activity but instead catalyzed cis-Delta13 desaturat

88 es placed five Santalaceae FADs with Delta12 FADs, which include Arabidopsis thaliana FAD2.

89 previously uncharacterized Mg(2+)-dependent FAD pyrophosphatase within the ApbE superfamily.

90 ant integral membrane fatty acid desaturase (FAD) family, FAD2, FAD3, FAD6, FAD7, and FAD8, self-asso

91 eromone-biosynthetic fatty acid desaturases (FADs) MsexD3, MsexD5, and MsexD6 abundantly expressed in

92 D, which donates this electron further to Dh-FAD of BcdAf after a second domain movement.

93 (RF) cofactors, flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), are two key cofact

94 f the cofactors flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), the physiologicall

95 e adsorption of flavin adenine dinucleotide (FAD) and glucose oxidase (GOx) onto carbon nanotube (CNT

96 toactivation of flavin adenine dinucleotide (FAD) bound near a triad of Trp residues, but mutation of

97 ral part of the flavin adenine dinucleotide (FAD) cofactor of the dehydrogenase domain of CDH.

98 ng the oxidized flavin adenine dinucleotide (FAD) cofactor, and a cryptochrome C-terminal extension (

99 Flavin-adenine dinucleotide (FAD) dependent glucose dehydrogenase (GDH) is a thermost

100 respect to the flavin adenine dinucleotide (FAD) domain that precludes binding of the nicotinamide c

101 Flavin adenine dinucleotide (FAD) is involved in important metabolic reactions where

102 llular level of flavin adenine dinucleotide (FAD), a metabolic cofactor of LSD1, causing HIF-1alpha d

103 enzyme cofactor flavin adenine dinucleotide (FAD), which was not the part of active enzyme.

104 f the catalytic flavin adenine dinucleotide (FAD)- and heme-binding domains of Cylindrospermum stagna

105 ransfer between flavin adenine dinucleotide (FAD)-dependent glucose dehydrogenase and electrodes.

106 ) (NAD(P)H) and flavin adenine dinucleotide (FAD).

107 tide (NADH), and flavin denine dinucleotide (FAD) in fresh brain samples of a mouse model of Alzheime

108 and its cofactor flavin adenine dinucleotide(FAD), and prompts VVD switching from Dark state to Light

109 2 is enhanced by familial Alzheimer disease (FAD) causing mutations in APP and is believed to play a

110 Initially, a USDA Foreign Animal Disease (FAD) investigation confirmed the presence of Senecavirus

111 inant forms of familial Alzheimer's disease (FAD) are caused by mutations in genes encoding beta-amyl

112 posed that the familial Alzheimer's disease (FAD) causing presenilin (PSEN) mutations PSEN1-L435F and

113 Familial Alzheimer's disease (FAD) is characterized by autosomal dominant heritability

114 e carrying the familial Alzheimer's disease (FAD) mutation L435F or C410Y recapitulate the phenotypes

115 se models with familial Alzheimer's disease (FAD) mutations exhibit amyloid-beta-induced synaptic and

116 Familial Alzheimer's disease (FAD)-causing mutant presenilins (PS) interact with inosi

117 lls expressing familial Alzheimer's disease (FAD)-causing mutant presenilins (PSs).

118 major cause of familial Alzheimer's disease (FAD).

119 of early-onset familial Alzheimer's disease (FAD).

120 ng domain (RBD) and the F activation domain (FAD).

121 nt studies showed that electrons flow during FAD photoreduction proceeds via two Trp triads.

122 ur method to different association dynamics, FAD numbers, population sizes and heterogeneities of the

123 ly relevant variants in FLAD1, which encodes FAD synthase (FADS), as the cause of MADD and respirator

124 H80R mutation reactivates P187S by enhancing FAD binding affinity through local and dynamic stabiliza

125 ysis revealed 10 novel private CNVs in 10 EO-FAD families overlapping a set of genes that includes: A

126 ysis for the presence of rare CNVs in 261 EO-FAD and early/mixed-onset pedigrees.

127 early-onset familial Alzheimer's disease (EO-FAD).

128 st study reporting rare gene-rich CNVs in EO-FAD and early/mixed-onset AD that are likely to underlie

129 Of these, 21 cases of EO-FAD families carrying unique APP locus duplications rema

130 ansfer from Y8 to the electronically excited FAD.

131 ich expression of an ubiquitously expressed, FAD-linked mutant PSEN1 gene was selectively inactivated

132 3D-differentiated neuronal cells expressing FAD mutations exhibited high levels of detergent-resista

133 ontaneous Ca(2+) signals in cells expressing FAD-causing mutant PS.

134 routing observed in knock-in mice expressing FAD-linked PS1 mutation.

135 We report that neurons expressing FAD-linked PS1 variants or functionally deficient PS1 ex

136 el-wise optical redox ratio, defined as FAD/(FAD + NAD(P)H), revealed three distinct redox distributi

137 justing a low redox potential of the FADH(*)/FAD pair required for ferredoxin reduction.

138 re consistent with involvement of the FADox, FAD(*-) and FADH(-) redox forms of flavin.

139 Finally, FAD-I activation of hBD-2 expression was mediated via bo

140 rate that CryA is capable of binding flavin (FAD) and methenyltetrahydrofolate (MTHF), fully compleme

141 PNDRs are flavoproteins (FAD-binding) and catalyze pyridine-nucleotide-dependent

142 e, whereas the low activity and affinity for FAD in p.P187S is caused by increased fluctuations at th

143 r SDH assembly factor 2 that is required for FAD insertion into SDH1.

144 quinone-binding site and the requirement for FAD as cofactor.

145 ability, indicating a rate-limiting role for FAD in LSD1-mediated HIF-1alpha regulation.

146 oscopy detected a strong hydrogen bond, from FAD N5-H to the carbonyl group of the Asn378 side chain,

147 tophagic dysfunction in neurons derived from FAD patient induced pluripotent stem cells (iPSCs) was r

148 s able to transfer reducing equivalents from FAD to a redox-active disulfide bridge, which further re

149 ion at both CNT and N-CNT electrodes is from FAD that either specifically adsorbs from solution or ad

150 In this study, a novel fungus FAD dependent glucose dehydrogenase, derived from Asperg

151 cells by tracking auto-fluorescent NAD(P)H, FAD and tryptophan (Trp) lifetimes and their enzyme-boun

152 t of specific intermediates (C4a-hydroperoxy-FAD and C4a-hydroxy-FAD) in the reaction, define rate co

153 ediates (C4a-hydroperoxy-FAD and C4a-hydroxy-FAD) in the reaction, define rate constants and the orde

154 upancy of the low-activity (L) mode, IP3R in FAD-causing mutant PS-expressing cells exhibits signific

155 Interestingly, significant reductions in FAD and FMN levels were observed before the onset of deg

156 esenilin activity plays an important role in FAD pathogenesis.

157 F and AMID containing naturally incorporated FAD displayed no NADH oxidase activities.

158 ) and enzyme-bound (a2%) fraction increased, FAD enzyme-bound (a1%) fraction was decreased, NAD(P)H-a

159 lysis, NADPH-derived electrons transfer into FAD and then distribute into the FMN domain for further

160 l epithelial cells (HOECs) and designated it FAD-I (Fusobacterium-associated defensin inducer).

161 heme at the expense of NADH oxidized at its FAD site, was electrochemically studied at graphite (Gr)

162 ycle is initiated by light absorption by its FAD chromophore, which is most likely fully oxidized (FA

163 aptures CRY2 by simultaneously occupying its FAD-binding pocket with a conserved carboxy-terminal tai

164 ansport chain through the redox state of its FAD cofactor.

165 trons from NADPH to cytochromes P450 via its FAD and FMN.

166 X-ray crystallography showed two juxtaposed FAD molecules per monomer in redox communication with an

167 Kynurenine-3-monooxygenase (KMO) is a key FAD-dependent enzyme of tryptophan metabolism.

168 Microbial molecules like FAD-I may be utilized in novel therapeutic ways to bolst

169 is suggested that for some enzyme molecules FAD leaks out from the active site, adsorbs onto graphit

170 We found that most FAD mutations increased the rate of aggregation of Abeta

171 and characterization of the multifunctional FAD-dependent enzyme LgnC is now described.

172 cursors is carried out by MccB THIF-type NAD/FAD adenylyltransferases.

173 e concentrations of l-arginine (Arg), NADPH, FAD, FMN, tetrahydrobiopterin (BH4), and calmodulin, ind

174 A linear arrangement of cofactors (NADPH, FAD, and two membrane-embedded heme moieties) injects el

175 h the FMN domain rotated away from the NADPH-FAD center, toward the oxygenase dimer.

176 ted NO synthases (NOSs), which contain NADPH/FAD- and FMN-binding domains.

177 229) forming a salt bridge between the NADPH/FAD and FMN domains in the conformationally closed struc

178 release in HOECs similar to those of native FAD-I (nFAD-I) isolated from F. nucleatum ATCC 25586.

179 ar to that of WT FrdA, contained noncovalent FAD, and displayed a reduced capacity to interact with S

180 ve behavior of tuna around floating objects (FADs).

181 ngs to the glutathione reductase family 2 of FAD-dependent oxidoreductases according to the structura

182 one of the variant proteins, the addition of FAD significantly improved protein stability, arguing fo

183 characterization and in vivo application of FAD substrates indicated that MsexD3 and MsexD5 biosynth

184 anisms underlying the covalent attachment of FAD remain to be fully elucidated.

185 ) are found in approximately 80% of cases of FAD, with some of these patients presenting cerebellar d

186 he C-terminal domain, while a combination of FAD and the inhibitor dicoumarol overcome these alterati

187 s possible that this phenotypic diversity of FAD associated with mutations within the Abeta sequence

188 ely argue for a noncell autonomous effect of FAD-linked PS1 mutants on EE-mediated adult hippocampal

189 by mutant Abeta peptides, but the effects of FAD mutations on aggregation kinetics and conformational

190 LSD1 target genes as well as the enzymes of FAD biosynthetic pathway in triple-negative breast cance

191 Although expression of FAD-linked PS1 mutations enhances toxic Abeta production

192 dehydrogenase (MCD) belongs to the family of FAD-dependent acyl-CoA dehydrogenase (ACD) and is a key

193 lying normal Abeta production, the impact of FAD mutations on this process and how anti-amyloidogenic

194 A mechanism of FAD-coupled electron bifurcation by NfnAB is proposed.

195 ypes after disease onset in a mouse model of FAD.

196 se conditions, ET from the adenine moiety of FAD becomes a competitive relaxation pathway.

197 h more extensive and long-term monitoring of FAD-associated tunas and good estimates of the numbers o

198 ver nuclei contain approximately 300 pmol of FAD.mg(-1) protein, which was mainly protein-bound FAD.

199 o stimulate IP3R channels in the presence of FAD-causing mutant PS to the same level of activity as c

200 of AHAS correlated with the slow process of FAD re-reduction.

201 ctive and (ii) a characteristic slow rate of FAD reduction by the pyruvate oxidase side reaction of t

202 Reconstruction of FAD gene phylogeny indicates that MsexD3 was recruited f

203 as positioned over the isoalloxazine ring of FAD, whereas that of HETDZ had the opposite orientation,

204 east cancers, reflecting the significance of FAD-dependent LSD1 activity in cancer progression.

205 ain, that is modulated by the redox state of FAD.

206 Moreover, a subset of FAD mutants in PSEN1, normally more broadly distributed

207 as FADS is essential for cellular supply of FAD cofactors, the finding of biallelic frameshift varia

208 lobin (HMP), which contains one heme and one FAD as prosthetic groups and is capable of reducing O(2)

209 EtfAf contains one FAD (alpha-FAD) in subunit alpha and a second FAD (beta-

210 L), and Asp(556) (hydrogen bonding of ATP or FAD ribose to L domain).

211 iously for berberine bridge enzyme and other FAD-dependent oxidoreductases.

212 the dark, these photoreceptors bind oxidized FAD in the photolyase homology region (PHR).

213 As purified, Aer contains fully oxidized FAD, which can be chemically reduced to the anionic semi

214 ally relevant photoreduction of the oxidized FAD cofactor to the semi-reduced FADH(.) radical in isol

215 Reduction of the oxidizing FAD cofactor (E'0 of -153 mV) is followed by the strongl

216 When PAS-FAD is reduced, PAS interaction with HAMP is relaxed and

217 enzymes form quasi-stable C4a-(hydro)peroxyl FAD intermediates.

218 gesting that clinical PSEN mutations produce FAD through a loss-of-function mechanism.

219 5 representing an alternative 3UFA-producing FAD has been acquired via activation of a presumably ina

220 When ATP is present and D396 protonated, FAD remains in close contact with W400, thereby enhancin

221 Exogenously provided FAD restores HIF-1alpha stability, indicating a rate-lim

222 ostasis and mitochondrial dysfunction in PS1-FAD PCs reduces their activity and contributes to motor

223 mutation is the largest known cohort of PS1-FAD patients.

224 In a murine model of PS1-FAD, animals exhibited mild ataxia and reduced PC simple

225 agrees with previous work showing that PSEN1 FAD causing mutations generate invariably long Abeta and

226 e at least one of the two interfaces-the RBD-FAD interface and/or the RBD-RBD interface.

227 ensemble of RBD globally, including the RBD-FAD interface, suggesting the latter's role in G stimula

228 In the reductive half-reaction, FAD is reduced and a C4a-hydroperoxyflavin intermediate

229 Recombinant FAD-I (rFAD-I) expressed in Escherichia coli triggered l

230 Mutations that disrupt ATP binding reduce FAD binding and reduce enzyme activity.

231 ic to AHAS: (i) the requirement of a reduced FAD cofactor for the enzyme to be active and (ii) a char

232 ound that both oxidized (FADox) and reduced (FAD) forms of dCRY undergo light-induced conformational

233 amino acid sequences placed five Santalaceae FADs with Delta12 FADs, which include Arabidopsis thalia

234 AD (alpha-FAD) in subunit alpha and a second FAD (beta-FAD) in subunit beta.

235 Human FMN cyclase, which splits FAD and other ribonucleoside diphosphate-X compounds to

236 In this study, FAD dependent glucose dehydrogenase was fused to a natur

237 Taken together, these results indicate that FAD mutations falling within the Abeta sequence lead to

238 the highly inducing strains, indicating that FAD-I is the principal F. nucleatum agent for hBD-2 indu

239 Here we report that FAD mutations in beta-amyloid precursor protein and pres

240 Collectively, our findings reveal that FAD mutations can cause complete loss of Presenilin-1 fu

241 TIMS-MS experiments showed that FAD can exist in the gas phase as deprotonated (M = C27H

242 anges in the fluorescence decay suggest that FAD can exist in four conformations in solution, where t

243 The FAD binding domain of CRY1, two C-terminal BMAL1 domains

244 The FAD cofactor of the enzyme is buried within the proteina

245 The FAD mutations also led to the adoption of alternative am

246 The FAD-dependent oxidoreductase-containing domain 1 (FOXRED

247 tes far from the mutated site, affecting the FAD binding site located at the N-terminal domain (NTD)

248 a-FAD), the [2Fe-2S] cluster of NfnA and the FAD (b-FAD), and the two [4Fe-4S] clusters of NfnB.

249 o Delta(1)-pyrroline-5-carboxlylate, and the FAD cofactor is reduced.

250 S is caused by increased fluctuations at the FAD binding site.

251 nerated Psen1 knockin (KI) mice carrying the FAD mutation L435F or C410Y.

252 hypoxia response regulation by coupling the FAD dependence of LSD1 activity to the regulation of HIF

253 ting with electrochemical responses from the FAD and heme domains, respectively.

254 at 500 ns shows major contributions from the FAD anion radical, which is demonstrated to then be prot

255 oreductases, in a second shell away from the FAD cofactor acting to polarize the peptide bond through

256 nding domain in shuttling electrons from the FAD-binding domain to the heme oxygenase domain.

257 (IFC), reduced perceptual sensitivity in the FAD task.

258 als an electron transfer route including the FAD (a-FAD), the [2Fe-2S] cluster of NfnA and the FAD (b

259 by several classes of enzymes, including the FAD-dependent amine oxidases KDM1A/B.

260 uditory cortex was assessed by measuring the FAD+/NADH ratio using fluorescence imaging.

261 Moreover, the FAD mutation impairs synaptic function, learning and mem

262 y and stress tolerance, whereas mutating the FAD- and NADPH-binding sites, that are common to TR and

263 The putative resting state of the FAD cofactor in these proteins is its fully oxidized for

264 of inhibition involves the oxidation of the FAD cofactor, leading to a time-dependent inhibition of

265 at is associated with tighter binding of the FAD cofactor.

266 r mechanism and concomitant reduction of the FAD cofactor.

267 leading into the sulfur-reducing side of the FAD isoalloxazine ring, suggesting how this enzyme class

268 of blue/UVA light leads to formation of the FAD neutral radical as the likely signaling state, and u

269 population sizes and heterogeneities of the FAD-array.

270 er that will enhance solvent exposure of the FAD.

271 at the observed effects of ATP and pH on the FAD photoreduction find their roots in the earliest stag

272 iated by TORC1 signaling through reading the FAD-dependent ATP level.

273 changes are required for NADPH to reduce the FAD.

274 says show that NADPH efficiently reduces the FAD only when RIF is present, implying that RIF binds be

275 We show here that the FAD-dependent monooxygenase Coq6, which is known to hydr

276 lating electron flow from NADPH, through the FAD and FMN cofactors, to the heme oxygenase domain, the

277 e access to HMP orientated on Gr through the FAD-domain and/or partial denaturation of HMP.

278 rt electrons from the protein surface to the FAD cofactor for activation and/or signaling-state forma

279 The RIF naphthoquinone blocks access to the FAD N5 atom, implying that large conformational changes

280 analysis shows that RIFMO dimerizes via the FAD-binding domain to form a bell-shaped homodimer in so

281 d E2 generate acetyl-coenzyme A, whereas the FAD/NAD(+)-dependent E3 performs redox recycling.

282 il-based chemotherapy regimens, of which the FAD binding protein NQO1 was subsequently validated by i

283 membrane domain that are associated with the FAD and metal binding sites are not only present in Stea

284 yield a FAD-Trp radical pair state with the FAD and Trp partners separated beyond a critical distanc

285 confirmed the enzyme adopts a fold common to FAD-dependent monooxygenases, contains a tightly bound F

286 e protonation state of D396 (proton donor to FAD degrees (-)).

287 rtic acid D396, the putative proton donor to FAD.(-), from ~7.4 to >9, and favours a reaction pathway

288 the transfer of a hydride ion equivalent to FAD, leading to an imine intermediate.

289 s and Abeta precursor processing, leading to FAD and neurodegeneration.

290 flexibility to the photoactive site prior to FAD excitation, with the consequence of increased ISO-W4

291 uate their role in the etiology of AD in two FAD mouse models.

292 YUC6 contains a previously unrecognized FAD- and NADPH-dependent thiol-reductase activity (TR) t

293 The flavin chromophore in blue-light-using FAD (BLUF) photoreceptors is surrounded by a hydrogen bo

294 tors cellular oxygen and redox potential via FAD bound to a cytosolic PAS domain.

295 Macrophages were FAD(HI) and demonstrated a glycolytic-like NADH-FLIM sig

296 We propose a structural model in which FAD mutations (V44M and V44A) can open the T48 site gamm

297 ases determines substrate specificity, while FAD-causing mutations strongly enhance accumulation of a

298 d Ca(2+) signaling, which is associated with FAD PS, is mediated by InsP3R and contributes to disease

299 action is Mg(2+)-dependent and proceeds with FAD but not FMN.

300 In the present work, FAD conformational changes were studied in solution and