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1 R antagonist or after incubation with MAO-A (monoamine oxidase-A).
2 e include potent and selective inhibitors of monoamine oxidase A.
5 NIRKO mice also exhibit increased levels of monoamine oxidase A and B (MAO A and B) leading to incre
10 eas was similarly modulated by inhibition of monoamine oxidase-A and was reduced in animals with indu
12 dent amine oxidizing enzymes including human monoamine oxidases A and B (MAO A and MAO B) show aromat
16 cture (which also has inhibitory activity at monoamine oxidases A and B and at the serotonin and nore
17 d binding to the norepinephrine transporter, monoamine oxidase A, and alpha2-adrenoceptors were measu
18 ty towards acetyl/butyrylcholinesterases and monoamine oxidases A/B as well as the histamine H3 recep
20 ors, the sequences of three Sp1 sites in the monoamine oxidase A core promoter were used in the yeast
21 ryptophan hydroxylase 1 and a suppression of monoamine oxidase A expression (enzymes responsible for
22 gnificant association between high levels of monoamine oxidase A expression and poorly differentiated
25 his study shows that glucocorticoid enhances monoamine oxidase A gene expression by 1) regulation of
28 e evidence indicates that the low-expressing monoamine oxidase A genotype specifically predisposes to
30 ve of either serotonin uptake transporter or monoamine oxidase-A inhibition, as well as slight increa
31 tor), SERT RNA-interference, and iproniazid (monoamine oxidase-A inhibitor), blocked 5-HT-induced S10
32 the current study, we used a genetic model (monoamine oxidase-A knockout mouse) in which brain 5-HT
33 , high serotonin transporter levels, and low monoamine oxidase A levels, suggesting that low intersti
35 quencies of a microsatellite and RFLP at the monoamine oxidase A locus in bipolar affective disorder
36 near the covalent 8alpha-S-cysteinyl FAD in monoamine oxidase A (MAO A) and to test the suggestion t
40 ly shown that the serotonin-degrading enzyme monoamine oxidase A (MAO A) is an important source of hy
47 The interaction of recombinant human liver monoamine oxidase A (MAO A) with a series of phenethylam
52 by increased blood glucocorticoids and brain monoamine oxidase A (MAO A, which degrades monoamine neu
56 compared to linezolid but suffer from potent monoamine oxidase A (MAO-A) inhibition and low solubilit
63 o counter the effects of the 40% increase in monoamine oxidase A (MAO-A) levels that occurs during PP
64 One such biological abnormality is elevated monoamine oxidase A (MAO-A) levels, which occurs in the
65 hydroxyphenylglycolaldehyde (DOPEGAL) is the monoamine oxidase A (MAO-A) metabolite of norepinephrine
66 ylglycolaldehyde (DOPEGAL) is the neurotoxic monoamine oxidase A (MAO-A) metabolite of norepinephrine
67 ating transcription of the gene encoding the monoamine oxidase A (MAO-A) to reduce serotonin levels i
69 As PI-2014 displayed off-target binding to monoamine oxidase A (MAO-A), a new lead with improved bi
70 SIRT1 did so by increasing expression of monoamine oxidase A (MAO-A), a SIRT1 target that reduces
71 zolid (marketed as Zyvox), are inhibitors of monoamine oxidase A (MAO-A), which presents an undesired
72 ompanied by an increase in the expression of monoamine oxidase-A (MAO-A) and MAO-B in the lateral OFC
76 cluding catechol-O-methyltransferase (COMT), monoamine oxidase-A (MAO-A), vesicular monoamine transpo
77 study examined how the mitochondrial enzyme monoamine oxidase-A (MAO-A), which produces hydrogen per
78 affinity to recombinant rat cerebral cortex monoamine oxidases A (MAO A) and B (MAO B) determined.
80 region contains, among others, the genes for monoamine oxidase A (MAOA) and B (MAOB), which are invol
83 r adipose NE levels that stem from decreased monoamine oxidase A (MAOA) expression and NE clearance b
84 A functional promoter polymorphism in the monoamine oxidase A (MAOA) gene has been implicated as a
85 g RNA (lncRNA), acting as a regulator of the monoamine oxidase A (MAOA) gene in the brain, and named
86 examining allelic variation in the X-linked monoamine oxidase A (MAOA) gene, previously associated w
87 esonance imaging and genetic analysis of the monoamine oxidase A (MAOA) gene, we investigated how str
88 olymorphisms in dopamine receptor (DRD4) and monoamine oxidase A (MAOA) genes showed significant asso
89 (5HT) and the monoamine-metabolizing enzyme monoamine oxidase A (MAOA) have been repeatedly implicat
95 ic mouse line in which the gene that encodes monoamine oxidase A (MAOA) is disrupted, resulting in ex
96 ohorts of Finnish prisoners, revealed that a monoamine oxidase A (MAOA) low-activity genotype (contri
98 g growth differentiation factor-3 (GDF3) and monoamine oxidase A (MAOA) that is known to degrade nora
99 ing the neurotransmitter-metabolizing enzyme monoamine oxidase A (MAOA) was found to moderate the eff
103 cancer (PCa) exhibit increased expression of monoamine oxidase A (MAOA), a mitochondrial enzyme that
105 polymorphisms affecting transcription level: monoamine oxidase A (MAOA), neuropeptide Y (NPY), endoth
107 hydroxyphenylglycolaldehyde (DOPEGAL) is the monoamine oxidase A metabolite of norepinephrine (NE) an
108 hydroxyphenylglycolaldehyde (DOPEGAL) is the monoamine oxidase A metabolite of norepinephrine and epi
109 3,4-Dihydroxyphenylglycolaldehyde is the monoamine oxidase-A metabolite of two catecholamine neur
110 luded those involved in cellular metabolism: monoamine oxidase-A, mitochondrial-A synthase complex, a
111 (p < 0.05) increases in adenosine deaminase, monoamine oxidase-A, nucleotides tri-phosphatase, 5'-nuc
113 tistically significant effects on binding to monoamine oxidase A or to the norepinephrine transporter
115 toma cell line, SK-N-BE (2)-C, inhibited the monoamine oxidase A promoter and enzymatic activity.
117 ith clorgyline, an irreversible inhibitor of monoamine oxidase A, restored hippocampal noradrenaline
119 rine secretion; P < 0.01), with no effect on monoamine oxidase A (serotonin catabolism), serotonin re
121 -serotonin and increased after inhibition of monoamine oxidase-A, the main enzyme responsible for ser