ライフサイエンスコーパス: AOS

1 AOS and epoxyalcohol synthase activities are mechanistic

2 AOS catalyses the production of an unstable epoxide (an

3 AOS converts 8R-hydroperoxyeicosatetraenoic acid to the

4 AOS demonstrated higher stability and less reduction in

5 AOS of A. terreus appears to have evolved independently

6 AOS patients in participating centers underwent extensiv

7 AOS predisposes patients to aggressive and widespread ca

8 AOS was only observed in nfvPPA.

9 AOS, caused by pathogenic SMAD3 variants, is a recently

10 ced the jasmonate-responsive lipoxygenase 2, AOS, and AtVSP gene transcripts and induction was strong

11 We included 44 AOS patients from 7 families with pathogenic SMAD3 varia

12 tution in the P450 domain (C1073S) abolished AOS activity.

13 The roles of the main (MOS) and accessory (AOS) olfactory systems of garter snakes in response to a

14 ion that appear to be highly conserved among AOS sequences from other plants but are not conserved am

15 ene oxides, indicating that the enzyme is an AOS.

16 sing statistics of the present climate or an AOS model approximation are developed here; these formul

17 ence of etiologic continuity between COS and AOS.

18 is of etiological continuity between COS and AOS.

19 n the presence of left parietal features and AOS, and amnestic AD could be differentiated from bvFTD,

20 e SAXS data also support a model for LOX and AOS domain orientation in the fusion protein inferred fr

21 n functional distinction between the MOS and AOS is the type of sensory information processing perfor

22 ssion of pathogenesis-related genes PR1a and AOS.

23 ic aphasia' (PAA) in the opposite case, and 'AOS + PAA' when mixed motor speech and language symptoms

24 tructures of guayule (Parthenium argentatum) AOS (CYP74A2) and its complex with the substrate analog

25 Both AOS CoMFA and CoMSIA analyses were used to construct std

26 ting that the optimal concentration for both AOS and SDS surfactants is 1.5 times the CMC.

27 different concentrations and may be used by AOS neural circuitry to discriminate among naturally occ

28 both necessary and sufficient for converting AOS into a GLV biosynthetic enzyme.

29 Coral AOS achieves specificity for the allene oxide formed by

30 The data indicate that cytoplasmic AOS responds to wounding by increasing the levels of the

31 the JA-isoleucine biosynthesis enzymes DDE2/AOS and JAR1 are functional.

32 is necessary for at least two very different AOS-mediated processes: basal resistance to Peronospora

33 ients have more salient genetic risk than do AOS.

34 re an additional cause of autosomal-dominant AOS or isolated ACC and provide further evidence for a k

35 RBPJ, and NOTCH1 lead to autosomal-dominant AOS.

36 , excitatory synaptic puncta, and downstream AOS activation.

37 ve genes (ATEG), which may code for a 9R-DOX-AOS fusion protein.

38 acalis feeding group: LOX1, ASN1, eIF3, DXS, AOS, TIM, LOX5, BBTI2, BBTI11, BBTI12, BBTI13, Cl-1B, TP

39 argeting of tomato (Lycopersicon esculentum) AOS (LeAOS) and HPL (LeHPL) to isolated chloroplasts.

40 how that Sema6A is required for establishing AOS connections in multiple locations.

41 transgenic plants constitutively expressing AOS, wound-induced JA levels were 50-100% higher compare

42 agnetic circular dichroism spectra of ferric AOS and of its cyanide and azide complexes, and the elec

43 t region for all three derivatives of ferric AOS are almost the mirror image of those in catalase.

44 transgenic tobacco plants containing a flax AOS cDNA without a chloroplast transit sequence under th

45 er, in wounded tissues overexpressing a flax AOS, levels of JA and the transcript of a pathogenesis-r

46 Induction of the flax AOS gene in transgenic plants with chlor-tetracycline (T

47 Overexpression of the flax AOS in induced transgenic plants did not increase JA lev

48 cline (Tc) led to the expression of the flax AOS mRNA and protein, which resulted in high level of me

49 lar fractionation demonstrated that the flax AOS protein and activity were associated with the cytoso

50 en compared to those not expressing the flax AOS.

51 formations is widely implicated although for AOS reactions, without direct experimental support.

52 ve genes have been identified as a cause for AOS prior to this report.

53 to find suitable ferromagnetic materials for AOS.

54 iological significance requires a functional AOS.

55 In the past, however, AOS devices required higher activation energies, and hen

56 In AOS, aspirin acetylates three serine residues near the C

57 y, ferromagnetic material is demonstrated in AOS under multiple pulses.

58 in the context of cardiovascular features in AOS-affected individuals.

59 ands showed a higher rate than that found in AOS probands (P<0.0001).

60 support a common tyrosinate-ligated heme in AOS as in catalase, significant differences exist in the

61 tide (NT-proBNP) was significantly higher in AOS patients compared with matched controls (p < 0.001).

62 oxygen bond with formation of compound II in AOS and compound I in 5,8-LDS are influenced by Asn and

63 in this pathway might also be implicated in AOS pathogenesis.

64 ide H synthase, the three serine residues in AOS are not thought to line the putative substrate chann

65 ations in the four genes with known roles in AOS pathology (ARHGAP31, RBPJ, DOCK6, and EOGT), we foun

66 zymes that was hitherto not known to include AOSs.

67 tudies provide both structural insights into AOS and related P450s and a structural basis to understa

68 to overexpression of the cytoplasm-localized AOS, while (Z)-3-hexenal and (Z)-3-hexenyl acetate appea

69 lt in large/abnormal offspring syndrome (LOS/AOS) which is characterized by macrosomia.

70 The systemic induction of LOX2, AOS, and vegetative storage protein was lower in the PLD

71 Many AOS neurons respond selectively to bile acids that are v

72 sulfated steroids, recently discovered mouse AOS ligands, caused widespread activity among vomeronasa

73 ron paramagnetic resonance spectra of native AOS (high-spin, g = 6.56, 5.22, 2.00) and of its cyanide

74 In addition, the cyanide affinity of native AOS (K(d) = 10 mM at pH 7) is about 3 orders of magnitud

75 nd identify bile acids as a class of natural AOS ligands.

76 ular cloning and characterization of a novel AOS-encoding cDNA (LeAOS3) from Lycopersicon esculentum

77 time-dependent inhibition and acetylation of AOS, which leads the irreversible inactivation of this e

78 ecular mechanisms underlying the assembly of AOS circuits critical for moving image perception.

79 in the understanding of the genetic basis of AOS, for the majority of affected subjects, the underlyi

80 tions in NOTCH1 are the most common cause of AOS and add to a growing list of human diseases that hav

81 e report the cloning and characterization of AOS (LeAOS) and HPL (LeHPL) cDNAs from tomato (Lycopersi

82 ed to identify novel genetic determinants of AOS.

83 probands, each with a clinical diagnosis of AOS.

84 e protein components operating downstream of AOS that mediate any of these processes.

85 for tyrosinate ligation to the heme iron of AOS as has been established for catalases.

86 ities of CNS are an unusual manifestation of AOS.

87 Partitioning of AOS and HPL to different envelope membranes suggests dif

88 ocognitive impairments found in relatives of AOS probands.

89 ort that mouse faeces are a robust source of AOS chemosignals and identify bile acids as a class of n

90 sults identify faeces as a natural source of AOS information, and suggest that bile acids may be mamm

91 vival and reproduction, but understanding of AOS function is limited by a lack of identified natural

92 fabrication of parallel, laterally oriented AOS nanoribbons based on lift-off and nano-imprinting.

93 lthy siblings and with adult-onset patients (AOS), carry significantly more rare chromosomal copy num

94 lthy siblings and with adult-onset patients (AOS), carry significantly more rare chromosomal copy num

95 rmation of compound II in analogy with plant AOS (CYP74) and prostacyclin synthase (CYP8A1).

96 may be a downstream target which potentiates AOS production by altering NAD(H)/NADP(H) homeostasis.

97 ce [(i) severity-agrammatism; (ii) prominent AOS; and (iii) prominent dysarthria].

98 ally studied both single- and multiple-pulse AOS under different coupling strength between spins and

99 An information metric to quantify AOS model errors in the climate is proposed here which i

100 in EOGT and DOCK6 cause autosomal-recessive AOS, whereas mutations in ARHGAP31, RBPJ, and NOTCH1 lea

101 d N964D mutants both showed markedly reduced AOS activity, suggesting that Asn(964) may facilitate ho

102 teps by a non-polar residue markedly reduces AOS activity and, unexpectedly, is both necessary and su

103 EY1 and HES1, indicating that NOTCH1-related AOS arises through dysregulation of the Notch signaling

104 o be due to a vasculopathy in NOTCH1-related AOS.

105 e selectively expressed in mammalian retinal AOS components and refine oDSGC circuitry to constrain O

106 ase in plant growth-promoting rhizobacteria, AOS in coral, and epoxyalcohol synthase in amphioxus.

107 ination associated with Athabasca oil sands (AOS) mining operations has on the surrounding boreal for

108 activities in Canada's Athabasca oil sands (AOS) region has led to concerns about emissions of conta

109 ) is a variant of adult-onset schizophrenia (AOS) by determining if first-degree relatives of COS pro

110 ) is a variant of adult-onset schizophrenia (AOS) by determining whether parents of COS probands show

111 cumented risk for adult onset schizophrenia (AOS), autism, epilepsy and/or ID.

112 suite of imperfect Atmosphere Ocean Science (AOS) computer models is a central issue in climate chang

113 conventional CoMFA, all orientation search (AOS) CoMFA, and CoMSIA were applied to the training sets

114 Inorganic amorphous oxide semiconductor (AOS) materials such as amorphous InGaZnO (a-IGZO) posses

115 ng dermis, resembling defects seen in severe AOS.

116 The American Ophthalmological Society (AOS) is 1 of the 3 founding organizations of the America

117 th development of the active oxygen species (AOS) burst.

118 Active oxygen species (AOS) generated in response to stimuli and during develop

119 erest were: limb apraxia, apraxia of speech (AOS), and left parietal symptoms of dyslexia, dysgraphia

120 icative of dysarthria and apraxia of speech (AOS).

121 XG) as a polymer and alpha-olefin sulfonate (AOS) as a surfactant.

122 All-optical switching (AOS) of magnetization induced by ultrafast laser pulses

123 wo affected sibs with Adams Oliver syndrome (AOS) (OMIM 100300).

124 Adams-Oliver syndrome (AOS) is a rare developmental disorder characterized by t

125 Adams-Oliver syndrome (AOS) is a rare disorder characterized by congenital limb

126 ated individuals with Adams-Oliver syndrome (AOS), a rare disease with major features of aplasia cuti

127 families affected by Adams-Oliver syndrome (AOS), a rare multiple-malformation disorder consisting p

128 1 are associated with Adams-Oliver syndrome (AOS), a syndrome characterized by congenital scalp defec

129 velopmental disorder, Adams-Oliver syndrome (AOS), characterized by the combination of aplasia cutis

130 pe of the aneurysms-osteoarthritis syndrome (AOS) and to provide clinical recommendations.

131 xygenase (9R-DOX) and allene oxide synthase (AOS) activities in membrane fractions.

132 We identified novel allene oxide synthase (AOS) activity and a by-product that provides evidence of

133 Allene oxide synthase (AOS) and fatty acid hydroperoxide lyase (HPL) are plant-

134 Allene oxide synthase (AOS) and hydroperoxide lyase (HPL) are related cytochrom

135 response pathway, the allene oxide synthase (AOS) and hydroperoxide lyase (HPL) branches, which are r

136 Although allene oxide synthase (AOS) and hydroperoxide lyase are atypical cytochrome P45

137 8R-Lipoxygenase and allene oxide synthase (AOS) are parts of a naturally occurring fusion protein f

138 t a cytosol-localized allene oxide synthase (AOS) can promote JA biosynthesis, transgenic tobacco pla

139 e, and the N-terminal allene oxide synthase (AOS) domain promotes the conversion of the hydroperoxide

140 rate lipoxygenase and allene oxide synthase (AOS) domains of the coral protein in Escherichia coli (B

141 Allene oxide synthase (AOS) is a cytochrome P-450 (CYP74A) that catalyzes the f

142 Allene oxide synthase (AOS) is a P450 enzyme that plays a key role in the biosy

143 but had no effect on allene oxide synthase (AOS) or hydroperoxide lyase in wounded leaves.

144 Coral allene oxide synthase (AOS), a hemoprotein with weak sequence homology to catal

145 etitive inhibitors of allene oxide synthase (AOS), the cytochrome P450 that initiates plant oxylipin

146 ynthetic gene CYP74A (allene oxide synthase, AOS) using reverse genetics screening methods.

147 ss, mutation of the ALLENE OXIDE SYNTHETASE (AOS) jasmonate biosynthesis gene did not rescue the stre

148 This action observation system (AOS) is thought to encode neutral voluntary actions, and

149 system (MOS) and accessory olfactory system (AOS) detect and process pheromonal stimuli, yet the func

150 The accessory olfactory system (AOS) guides behaviours that are important for survival a

151 TEMENT The mouse accessory olfactory system (AOS) interprets social chemosignals, but we poorly under

152 The accessory olfactory system (AOS) is critical for the development and expression of s

153 analyzed by the accessory olfactory system (AOS).

154 mediated via the accessory olfactory system (AOS).

155 mary role of the accessory olfactory system (AOS).

156 that project to the accessory optic system (AOS) and contribute to gaze-stabilizing reflexes.

157 The accessory optic system (AOS) detects retinal image slip and reports it to the oc

158 n and connect to the accessory optic system (AOS) in the brain, which generates compensatory eye move

159 tic tract (NOT)--the accessory optic system (AOS) target controlling horizontal image stabilization.

160 r information to the accessory optic system (AOS) to inform oculomotor outputs.

161 e transmitted to the accessory optic system (AOS) where they initiate the optokinetic response.

162 n and project to the accessory optic system (AOS), oscillated with the same frequency as their eyes.

163 nuclei termed the "accessory optic system" (AOS) generate slip-compensating eye movements that stabi

164 s summation of synaptic potentials at target AOS cells and thus provides a secondary mechanism by whi

165 e crystal structures of Arabidopsis thaliana AOS, free and in complex with substrate or intermediate

166 ncy in the aos mutant, our results show that AOS is critical for the biosynthesis of all biologically

167 lb neurons in ex vivo preparations show that AOS neurons are strongly and selectively activated by pe

168 Our results also suggest that AOS expression is limiting JA levels in wounded plants,

169 The AOS comprising the peripheral sensory vomeronasal organ

170 GFP, in which the RGCs projecting to all the AOS nuclei are fluorescently labeled.

171 Although the AOS domain has homology to catalase in primary structure

172 ves the noncovalent interactions between the AOS and LOX domains and suggests that the C2-like domain

173 e heme environment is largely conserved, the AOS heme is planar and the distal histidine is flanked b

174 mit manipulation of specific circuits in the AOS and show that Sema6A is required for establishing AO

175 r-considered anthropogenic PAH source in the AOS region.

176 first view of information processing in the AOS with respect to individual chemical cues.

177 The first dedicated circuit in the AOS, the accessory olfactory bulb (AOB), exhibits cellul

178 is and an ionic reaction intermediate in the AOS-catalyzed transformation.

179 entration-dependent neuronal activity in the AOS.

180 fic proteolysis of the linker that joins the AOS and LOX domains.

181 For ferrimagnetic material, the AOS is attributed to magnetic circular dichroism and ang

182 The early history of the AOS and its role in the founding of the ABO are addresse

183 Here, we report the structure of the AOS domain and its striking structural homology to catal

184 Metabolism of the preferred substrate of the AOS domain, 8R-HPETE, is inhibited by the enantiomer 8S-

185 entation with constitutive expression of the AOS gene.

186 pothesize that the sustained activity of the AOS induces a new sensory state in the animal, reflectin

187 ective motor repertoire, but the role of the AOS' areas in processing affective kinematic information

188 y to the other major terminal nucleus of the AOS, the nucleus of the optic tract (NOT).

189 to the medial terminal nucleus (MTN) of the AOS.

190 is required for the functional output of the AOS.

191 ate the medial terminal nucleus (MTN) of the AOS.

192 Here, we numerically study the AOS process and provide new insights into the long-stand

193 ng JA levels in wounded plants, but that the AOS hydroperoxide substrate levels, controlled by upstre

194 Here we investigated whether the AOS plays a role in representing dynamic emotional bodil

195 While the AOS CoMFA models gave the best internal predictions (cro

196 ygenase well suited for partnership with the AOS domain, which shows maximum rates of approximately 1

197 two Cre lines that permit genetic access to AOS circuits responding to vertical motion.

198 SGCs labeled in Hoxd10-GFP mice projected to AOS nuclei controlling horizontal but not vertical image

199 ibit other P450s that have motifs similar to AOS and consequently serve as potential biochemical targ

200 ocial chemosignals, but we poorly understand AOS information processing.

201 al sources in this region (i.e., unprocessed AOS bitumen, upgrader residual coke, forest fires, coal,

202 ssively shifting to the value of unprocessed AOS bitumen.

203 Screening a cohort of 52 unrelated AOS subjects, we detected 8 additional unique NOTCH1 mut

204 water oxidation system; the mixed valencies (AOS = 3.7); and the lowest charge transfer resistances (

205 types of RGCs project to each of the various AOS nuclei remain unresolved.

206 Despite the importance of signalling via AOS in eukaryotes, little is known about the protein com

207 and c.6049_6050delTC) in 2 kindreds in which AOS was segregating as an autosomal dominant trait.

208 eviously reported clinical profiles (75 with AOS and agrammatism, 12 PPAOS and six PAA).

209 rebellar cortical dysplasia in a family with AOS.

210 tional regulator for the Notch pathway, with AOS, a human genetic disorder.

211 earch to detect impairments in patients with AOS and ADHD and in the relatives of patients with AOS.

212 d ADHD and in the relatives of patients with AOS.

213 ressed plants than in wild-type plants, with AOS exhibiting a distinct pattern.

214 s (MAPKs) MPK3 and MPK6 after treatment with AOS or elicitor and is necessary for at least two very d