ライフサイエンスコーパス: MAO

1 MAO A is a key enzyme that degrades a number of monoamin

2 MAO B messenger RNA also correlated with viral loads in

3 MAO B messenger RNA was highest in macaques with the mos

4 MAO subjects also had increased plasma concentrations of

5 MAO-A density (by Western blot) and activity (by [(14)C]

6 MAO-A KD decreased basal reactive oxygen species levels

7 MAO-A KD specifically increased the activity of complex

8 MAO-A VT (an index of MAO-A density) was measured using

9 MAO-A VT was significantly greater in the PFC (37%, inde

10 T-cell populations in 9 lean, 12 MNO, and 13 MAO subjects.

11 A)) = 260 nM; IC(50)(MAO-B) = 200 nM; IC(50)(MAO-A) = 10 muM) and dose dependently counteracts halope

12 AO-B inhibitor (K(i)(A(2A)) = 260 nM; IC(50)(MAO-B) = 200 nM; IC(50)(MAO-A) = 10 muM) and dose depend

13 t study, we compared the protein levels of a MAO A-transcriptional activator, Kruppel-like factor 11

14 Together, these results suggest that a MAO-dependent long-lasting alteration in the proliferati

15 ing evidence shows that monoamine oxidase A (MAO A), the key enzyme catalyzing serotonin (5-hydroxytr

16 has been reported that monoamine oxidase A (MAO A, a major neurotransmitter-degrading enzyme) is sig

17 ucocorticoids and brain monoamine oxidase A (MAO A, which degrades monoamine neurotransmitters).

18 selective inhibitors of monoamine oxidase A (MAO-A) and B (MAO-B) holds a therapeutic relevance in th

19 Monoamine oxidase A (MAO-A) is an important brain enzyme that creates oxidati

20 Monoamine oxidase A (MAO-A) is an important enzyme on the outer mitochondrial

21 of the 40% increase in monoamine oxidase A (MAO-A) levels that occurs during PPB, a dietary suppleme

22 abnormality is elevated monoamine oxidase A (MAO-A) levels, which occurs in the prefrontal and anteri

23 f the gene encoding the monoamine oxidase A (MAO-A) to reduce serotonin levels in the brain.

24 se in the expression of monoamine oxidase-A (MAO-A) and MAO-B in the lateral OFC and by a decrease in

25 Monoamine oxidase-A (MAO-A) is a treatment target in neurodegenerative illnes

26 Monoamine oxidase-A (MAO-A), a key brain enzyme which metabolizes monoamines,

27 he mitochondrial enzyme monoamine oxidase-A (MAO-A), which produces hydrogen peroxide as a catalytic

28 nt rat cerebral cortex monoamine oxidases A (MAO A) and B (MAO B) determined.

29 nd by a decrease in the expression of MAO-A, MAO-B, and tryptophan hydroxylase in the dorsal raphe nu

30 targets, the first potent, dual-acting A2AAR/MAO-B inhibitors with a nonxanthine structure were devel

31 may be useful tools for validating the A2AAR/MAO-B dual target approach in PD.

32 BPD was associated with greater PFC and ACC MAO-A VT compared with moderate BPD, MDE, and healthy co

33 In BPD, PFC and ACC MAO-A VT were positively correlated with mood symptoms (

34 Eight drug molecules, including COX, ACE, MAO, and PDE inhibitors, have been successfully [(18)F]-

35 al stress, which transcriptionally activates MAO A.

36 In contrast, the properties affecting MAO B affinity were the polarity and bulk of the para-su

37 reveals for the first time that KLF11 is an MAO A regulator and is produced in response to neuronal

38 derate (~6%) weight gain in MNO (n = 12) and MAO (n = 8) subjects with a mean BMI of 36 +/- 4 kg/m2 w

39 ng the monoamine metabolic enzymes MAO A and MAO B (MAO AB-deficient mice) exhibit diminished prolife

40 oamines, because of the absence of MAO A and MAO B, cause functional alterations that are accompanied

41 f the structures and mechanisms of MAO A and MAO B, which are pharmacological targets for specific in

42 CSE significantly reduced MAO-A and MAO-B activities in vitro, whereas nicotine did not.

43 docking experiments carried out on MAO-A and MAO-B structures proved new information about the enzyme

44 Monoamine oxidases A and B (MAO-A and MAO-B) are enzymes of the outer mitochondrial membrane t

45 xpression of monoamine oxidase-A (MAO-A) and MAO-B in the lateral OFC and by a decrease in the expres

46 al function, notably complex I activity, and MAO-A may be a target for protection against neurodegene

47 Recombinant human MAO-B and MAO-A enzyme preparations were used to determine inhibit

48 Expression of 5-HT(B) and MAO-A was suppressed in the AMY of female pigs; 5-HT(B)

49 orter stress or glucocorticoid exposures and MAO-A levels/activity is not well established.

50 With ethylene as the feed and MAO as cocatalyst/activator, SNS-based complexes Ti-C0-C

51 energy of interaction between inhibitor and MAO B residues during inhibitor egress is an effective i

52 eir affinity for dopamine D(2) receptors and MAO A.

53 T(B), 5-HT(A), 5-HT(B), and D receptors, and MAO-A was determined by Q-RT-PCR and data subjected to m

54 9 nM; selective versus other AR subtypes and MAO-A), which inhibited A2AAR-induced cAMP accumulation

55 which acts as a dual human A(2a) antagonist/MAO-B inhibitor (K(i)(A(2A)) = 260 nM; IC(50)(MAO-B) = 2

56 mpound is the best balanced A(2A) antagonist/MAO-B inhibitor reported to date, and it could be consid

57 itors, whereas small molecule antidepressant MAO acetylenic inhibitors like pargyline do not inhibit

58 As MAO-A creates oxidative stress, facilitates apoptosis, a

59 ns 2-12 showed good inhibitory activities at MAO-B, AChE, and BChE but low selectivity.

60 On average, MAO-A VT in perimenopausal age was elevated by 34% compa

61 creased levels of monoamine oxidase A and B (MAO A and B) leading to increased dopamine turnover in t

62 l cortex monoamine oxidases A (MAO A) and B (MAO B) determined.

63 Monoamine oxidases A and B (MAO-A and MAO-B) are enzymes of the outer mitochondrial

64 bitors of monoamine oxidase A (MAO-A) and B (MAO-B) holds a therapeutic relevance in the treatment of

65 monoamine metabolic enzymes MAO A and MAO B (MAO AB-deficient mice) exhibit diminished proliferation

66 otopic membrane protein monoamine oxidase B (MAO B) is an important drug target for Parkinson's disea

67 olinesterase (AChE) and monoamine oxidase B (MAO B), a series of multitarget ligands was properly des

68 was further studied in monoamine oxidase B (MAO-B) and cyclooxygenase-1 (COX-1) enzyme through molec

69 reversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is

70 AARs) and inhibition of monoamine oxidase B (MAO-B) in the brain are considered attractive strategies

71 nson's disease in which monoamine oxidase B (MAO-B) is overexpressed and which emulates several featu

72 eversible inhibitors of monoamine oxidase B (MAO-B).

73 linesterase (AChE), and monoamine oxidase B (MAO-B).

74 mine agonists, and monoamine oxidase type B (MAO-B) inhibitors.

75 r determinants for high affinity toward both MAO isoforms.

76 sma levels of selegiline are elevated, brain MAO-A might also be inhibited.

77 direct evidence that it also inhibits brain MAO-A in humans.

78 ositron emission tomography to measure brain MAO-A V(T) on two different days: One under acute psycho

79 We measured brain MAO-A in 18 healthy men after a 28-day treatment with Zy

80 s provide the first direct evidence of brain MAO-A inhibition in humans by formulations of selegiline

81 nhibitory potency of ciproxifan on rat brain MAO, these findings should be considered, when using hig

82 postulated but not verified to target brain MAO-A in addition to MAO-B.

83 erved a significant reduction in whole-brain MAO-A binding as reflected by reductions in 10 of 11 bra

84 ed complexes of Hf and Zr, when activated by MAO at 50-80 degrees C, generate high molecular weight p

85 h increased resistance toward degradation by MAO-A.

86 The characteristics exhibited by MAO A/B KO mice highlight the potential of these animals

87 dative/pro-apoptotic processes implicated by MAO-A overexpression.

88 lying defective brain development induced by MAO-A knockdown during in vitro embryogenesis.

89 in the modulation of aggression mediated by MAO A.

90 glucocorticoid administration and decreased MAO-A binding, activity and protein levels.

91 onal and glial cells significantly decreased MAO-A activity and protein levels.

92 over, most of the tested compounds displayed MAO inhibitory effect when tested in vivo.

93 croRNA (miRNA) was used to stably knock down MAO-A mRNA, protein, and catalytic activity by 60-70% in

94 Moreover, dysfunctional MAO-A expression led to elevated levels of embryonic ser

95 with valuable tools for designing effective MAO B inhibitors as well as outline a method that can be

96 nt designed to counter functions of elevated MAO-A activity eliminates vulnerability to depressed moo

97 These results suggest that elevated MAO-A VT is associated with multiple indicators of BPD s

98 nistration typically associate with elevated MAO-A levels/activity.

99 ative symptoms were associated with elevated MAO-A VT in the PFC and ACC (MANOVA, severity: F(2,38)=5

100 In summary, endogenous MAO-A levels influence mitochondrial function, notably c

101 These engineered MAO-N biocatalysts have been applied in deracemization r

102 mice lacking the monoamine metabolic enzymes MAO A and MAO B (MAO AB-deficient mice) exhibit diminish

103 We re-explored MAO antidepressant agent phenelzine (phenethylhydrazine)

104 % inhibitory concentration of compound 6 for MAO-B was 227 +/- 36.8 nM.

105 on was demonstrated between the affinity for MAO A, but not MAO B, and the levels of 3,4-dihydroxyphe

106 esults suggest that FoxO1 is a repressor for MAO A transcription, and its phosphorylation is involved

107 line at high doses loses its selectivity for MAO-B, there is no direct evidence that it also inhibits

108 Our findings reveal novel roles for MAOs and serotonin in the regulation of IPC proliferatio

109 Adipose tissue from MAO individuals contains increased numbers of Th17 and T

110 Adipose tissue from MAO subjects had 3- to 10-fold increases in numbers of C

111 Furthermore, MAO-A KD protected against inhibitors of complex I, III,

112 n KLF11 levels and those of its target gene, MAO A, both in association with MDD.

113 inhibitory activity (IC50 = 30 nM) and good MAO B/A selectivity (selectivity index, SI = 94) along w

114 Hence, greater MAO-A VT during perimenopause may represent a new target

115 D and a microarray analysis reported greater MAO-A messenger RNA in the PFC of rodents exposed to alc

116 drinking correlated positively with greater MAO-A VT in the PFC (r = .67, p = .005) and all brain re

117 isplayed good inhibitory activities and high MAO-B selectivity.

118 c substituents producing compounds with high MAO B affinity.

119 ; ACC: r = .38, p = .046), while hippocampus MAO-A VT was negatively correlated with verbal memory (r

120 dole-5-carboxamide (53, PSB-1410, IC50 human MAO-B 0.227 nM, >5700-fold selective versus MAO-A).

121 ole-5-carboxamide (38a, PSB-1491, IC50 human MAO-B 0.386 nM, >25000-fold selective versus MAO-A) and

122 t and selective MAO-B inhibitors (IC50 human MAO-B 0.612 nM, >16000-fold selective versus MAO-A).

123 zole-5-carboxamide (30, PSB-1434, IC50 human MAO-B 1.59 nM, selectivity versus MAO-A>6000-fold), high

124 amide (17, Ki human A2A, 39.5 nM; IC50 human MAO-B, 34.9 nM; selective versus other AR subtypes and M

125 class of potent MAO-B inhibitors (IC50 human MAO-B: 1.63 nM).

126 Recombinant human MAO-B and MAO-A enzyme preparations were used to determi

127 dence shows a relationship between the human MAO-B (hMAO-B) enzyme and neuropsychiatric/degenerative

128 ctively countered the enhanced aggression in MAO A KO mice, at doses that did not inherently affect m

129 nd glia cells indicate that these changes in MAO A and B are a direct consequence of loss of insulin

130 endogenous alpha-synuclein via elevations in MAO-B levels could be abrogated by the addition of depre

131 our findings suggest that excessive 5-HT in MAO-A-deficient mouse embryos triggers cellular signalin

132 III and IV resulted in a similar increase in MAO-A expression, while up-regulation of MAO-A was lower

133 centrations and secretion rates increased in MAO, but not MNO, subjects.

134 eover, we found that elevated 5-HT levels in MAO-A knockdown embryos coincided with an enhanced activ

135 lates proliferation in wild-type, but not in MAO AB-deficient, NSC.

136 not in the ventricular zone, are reduced in MAO AB-deficient mice.

137 esence of a functional FoxO1-binding site in MAO A core promoter.

138 40 promoter factor 1 (Sp1) binding sites in MAO B promoter.

139 Increased MAO-A level, when greater severity and reversed neuroveg

140 Increased MAO-A levels in prefrontal cortex (PFC) and anterior cin

141 in the rat brain, which results in increased MAO A mRNA and enzymatic activity.

142 y regulatory mechanisms leading to increased MAO A catalytic activity and mRNA levels because of dire

143 F11 knockdown reduces glucocorticoid-induced MAO A expression in cultured neurons; 3) induction of KL

144 ates the relationship between stress-induced MAO A and the transcription factor Kruppel-like factor 1

145 lly repressed both the basal and VPA-induced MAO A catalytic and promoter activities to 30 to 60%.

146 nalogues of 17f, namely 18b and 19a, inhibit MAO-B with IC(50) of 68 and 48 nM, respectively, being 5

147 hen variability in constituents that inhibit MAO-A could impact smoking.

148 st cigarette smoke constituents that inhibit MAO-A, in the range seen in chronic smokers, are likely

149 t, and therapeutic use of drugs that inhibit MAO-B are major challenges for future therapy.

150 but not DAT; and while Emsam also inhibited MAO-A (33.2+/-28.9 (range 9-68%) the difference did not

151 ydis selegiline dose significantly inhibited MAO-A (36.9+/-19.7%, range 11-70%, p<0.007)) but not DAT

152 unds acting as monoamine oxidase inhibitors (MAO-Is) and bearing a 6'-substituted (E)-2-(benzofuran-3

153 ic antidepressant imipramine, which inhibits MAO activity and reduces oxidative stress.

154 levodopa (IPX066), safinamide which inhibits MAO-B, dopamine uptake and glutamate and pardoprunox whi

155 The monoamine oxidase isoenzymes (MAOs) A and B play important roles in the homeostasis of

156 The novel glucocorticoid-KLF11-MAO A pathway may play a crucial role in modulating dist

157 show that (1) tranylcypromine (TCP), a known MAO inhibitor, increases sensitivity to the primary rein

158 ats received pre-session injections of known MAO inhibitors.

159 -fluorodeprenyl-D2 was consistent with known MAO-B expression in the human brain.

160 After declines in estrogen level, MAO-A density may be elevated for a month or longer, and

161 comparison with male wild-type littermates, MAO A/B KO mice exhibited abnormally high and overgenera

162 Accordingly, male MAO A-deficient humans and mice exhibit an extreme predi

163 armine positron emission tomography measured MAO-A total distribution volume (MAO-A VT), an index of

164 using different amounts of methylalumoxane (MAO), giving in each case a very active catalytic mixtur

165 In comparison with WT male mice, MAO A KO counterparts exhibited increases in 5-HT and NE

166 Furthermore, it better models MAO inhibition and is more sensitive to stress-induced r

167 In contrast, the small molecule MAO cyclopropylamine inhibitor tranylcypromine is a time

168 r occupancy by Sp1 were shown at the natural MAO B core promoter.

169 ine oxidase variants from Aspergillus niger (MAO-N) which display remarkable substrate scope and tole

170 ated between the affinity for MAO A, but not MAO B, and the levels of 3,4-dihydroxyphenylacetic acid

171 tissue lipogenesis increased in MNO, but not MAO, subjects.

172 o the left, (2) inhibition of MAO-A, but not MAO-B, increases low-dose nicotine self-administration,

173 We also report a novel MAO-N mediated asymmetric oxidative Pictet-Spengler appr

174 These novel MAO-Is may represent promising hits for the development

175 abolically abnormal insulin-resistant obese (MAO) subjects, metabolically normal insulin-sensitive ob

176 e defined as "metabolically abnormal obese" (MAO), are protected from the adverse metabolic effects o

177 ons of monoamines, because of the absence of MAO A and MAO B, cause functional alterations that are a

178 ve form of FoxO1 abolished the activation of MAO A by VPA and Akt.

179 phorylation is involved in VPA activation of MAO A.

180 ase inhibitor) reduced the VPA activation of MAO A.

181 mechanisms for glucocorticoid activation of MAO B gene and provides new insights into the hormonal r

182 d Sp1-activated glucocorticoid activation of MAO B promoter.

183 The combined deficiency of MAO A and B results in significantly elevated levels of

184 The effects of MAO-A knockdown (KD) on ATP, oxidative stress, electron

185 Expression of MAO isoforms has been detected in the developing embryo.

186 l OFC and by a decrease in the expression of MAO-A, MAO-B, and tryptophan hydroxylase in the dorsal r

187 The functions of MAO-A influence oxidative stress and apoptosis, 2 proces

188 ts was to further characterize the impact of MAO inhibition on the primary reinforcing and reinforcem

189 MAO-A VT (an index of MAO-A density) was measured using [(11)C]harmine positro

190 of acute stress upon MAO-A V(T,) an index of MAO-A density, in human brain and acute glucocorticoid e

191 distribution volume (MAO-A VT), an index of MAO-A density, in severe BPD subjects (n = 14), moderate

192 We hypothesized that MAO-A VT, an index of MAO-A level, is elevated in the prefrontal cortex (PFC)

193 D1 demonstrated moderate inhibition of MAO-A (IC50 = 48.848 +/- 1.935 muM), potency (pEC50 = 6.

194 Although CSE inhibition of MAO-A activity in vitro was found to be partially irreve

195 for nicotine to the left, (2) inhibition of MAO-A, but not MAO-B, increases low-dose nicotine self-a

196 ty can be strongly enhanced by inhibition of MAO-A.

197 dose of l-deprenyl yielded 70% inhibition of MAO-B in all regions.

198 In contrast, inhibitors of MAO or Nox had no effect on dopamine release, suggesting

199 but is unlikely to reflect an involvement of MAO inhibition.

200 ntrast, targeted inhibition and knockdown of MAO-A expression (E7.5-E10.5) caused structural abnormal

201 2) overexpressing KLF11 increases levels of MAO A mRNA and enzymatic activity, which is further enha

202 nowledge of the structures and mechanisms of MAO A and MAO B, which are pharmacological targets for s

203 Notably, the prefrontal cortex (PFC) of MAO A KO mice exhibited higher expression of NR2A and NR

204 olin-2-iminato ligand (L) in the presence of MAO and/or TTPB as cocatalysts have been explored.

205 nd reduced ATP, followed by up-regulation of MAO-A mRNA, protein, and enzyme activity levels.

206 in MAO-A expression, while up-regulation of MAO-A was lower following complex II inhibition.

207 new insights into the hormonal regulation of MAO.

208 fied two novel transcriptional repressors of MAO B, E2F-associated phosphoprotein (EAPP) and R1 (RAM2

209 Our findings suggest that the role of MAO A in pathological aggression may be mediated by chan

210 Here, we investigated the role of MAO-A in maladaptive hypertrophy and heart failure.

211 en possible to expand the substrate scope of MAO-N to accommodate amine substrates containing bulky a

212 Atomistic molecular dynamics simulations of MAO B either embedded in a lipid bilayer or free in solu

213 Additional MD simulations of MAO B in complex with seven different reversible inhibit

214 n the present study, the cognitive status of MAO A/B knockout (KO) mice was examined with a wide arra

215 However, suppression of MAO-B does not induce developmental alterations.

216 e the impetus for increased transcription of MAO B and that MAO, and more broadly, oxidative stress,

217 Use of MAO-SLC7A1 knockdown in conceptuses decreased arginine t

218 Values of MAO-A VT in the prefrontal cortex, anterior cingulate co

219 uitable PET radioligand for visualization of MAO-B activity in the human brain.

220 oid hormone, stimulates MAO B (an isoform of MAOs) promoter and catalytic activities via both the fou

221 ta and gamma) increased the transcription of MAOs A and B; the effects were abolished by parkin, but

222 which parkin suppresses the transcription of MAOs to control oxidative stress induced by dopamine oxi

223 n vivo morpholino antisense oligonucleotide (MAO)-mediated knockdown of SLC7A1 mRNA, the arginine tra

224 The docking experiments carried out on MAO-A and MAO-B structures proved new information about

225 ity and reversed neurovegetative symptoms on MAO-A VT in the PFC and ACC was analyzed using a multiva

226 attenuated the stimulating effect of VPA on MAO A.

227 arkers of DA and 5-HT function in the DMS or MAO expression in the ventral tegmental area of low- vs

228 , and evaluated for their monoamine oxidase (MAO) A and B inhibiting effect.

229 t time that VPA activates monoamine oxidase (MAO) A catalytic activity, mRNA level, and promoter acti

230 nd selective inhibitor of monoamine oxidase (MAO) A.

231 ect evidence of increased monoamine oxidase (MAO) activity in the brain of a simian immunodeficiency

232 or antagonist) as well as monoamine oxidase (MAO) and functional binding assays were conducted to inv

233 to visualize and quantify monoamine oxidase (MAO) B activity in vivo.

234 Monoamine oxidase (MAO) B deaminates a number of biogenic and dietary amine

235 ine levels partly through monoamine oxidase (MAO) inhibition.

236 rats pretreated with the monoamine oxidase (MAO) inhibitor clorgyline.

237 line ligand agmatine, the monoamine oxidase (MAO) inhibitor harmane, the alpha(2)-adrenoceptor agonis

238 constituents that inhibit monoamine oxidase (MAO) may increase the reinforcing value of low doses of

239 The flavoenzyme monoamine oxidase (MAO) regulates mammalian behavioral patterns by modulati

240 monoamine metabolized by monoamine oxidase (MAO), exists widely in plants, animals, fermented foods,

241 d dopamine receptors, and monoamine oxidase (MAO)-A in brains of sub-adult pigs were evaluated.

242 t omega-transaminase (TA)/monoamine oxidase (MAO-N) cascade process for the synthesis of chiral 2,5-d

243 gous to the mitochondrial monoamine oxidases MAO-A/B and produces hydrogen peroxide in the nucleus as

244 miting the expression of monoamine oxidases (MAO)--mitochondrial enzymes responsible for the oxidativ

245 prepared, and tested as monoamine oxidases (MAOs) and acetyl- and butyryl-cholinesterase (AChE and B

246 (CREDs), hydrolases and monoamine oxidases (MAOs), providing a comprehensive overview of their uses,

247 ducing the activities of monoamine oxidases (MAOs), which degrade monoamine neurotransmitters includi

248 se nicotine self-administration, (3) partial MAO-A inhibition, to the degree observed in chronic ciga

249 The most potent MAO-B inhibitors were N-(3'-chlorophenyl)-4-oxo-4H-chrom

250 , were identified as a novel class of potent MAO-B inhibitors (IC50 human MAO-B: 1.63 nM).

251 nding 6'-benzyloxy derivatives showed potent MAO-B inhibition and inverted selectivity profile.

252 ch higher than moclobemide) and a pronounced MAO-A/B selectivity.

253 g 5-7-fold more potent than the prototypical MAO-B inhibitor deprenyl (IC(50) = 334 nM).

254 state (M2)-specific genes (Mannose receptor, MAO-A, and CD36) and therefore conclude that Hck acts as

255 g sites; 4) KLF11 knockout mice show reduced MAO A mRNA and catalytic activity in the brain cortex co

256 CSE significantly reduced MAO-A and MAO-B activities in vitro, whereas nicotine di

257 nd R1 (RAM2/CDCA7L/JPO2), that down-regulate MAO B via MAO B core promoter, which contains Sp1 sites.

258 irreversibility than did previously reported MAO-B radioligands.

259 umulation and showed competitive, reversible MAO-B inhibition.

260 ments for development of specific reversible MAO B inhibitors is in a fairly mature status.

261 r novel class of highly potent and selective MAO-B inhibitors (IC50 human MAO-B 0.612 nM, >16000-fold

262 Since MAO-A metabolizes monoamines, this phenomenon may explai

263 ated by the addition of deprenyl, a specific MAO-B inhibitor.

264 synthetic glucocorticoid hormone, stimulates MAO B (an isoform of MAOs) promoter and catalytic activi

265 Furthermore, in humans, striatal MAO activity was elevated in individuals with HIV enceph

266 In the adult central nervous system, MAOs have important functions for neurotransmitter homeo

267 arge dietary intake of tyramine while taking MAO inhibitors has been reported; therefore, the measure

268 or increased transcription of MAO B and that MAO, and more broadly, oxidative stress, have significan

269 ken together, these results demonstrate that MAO A is a novel target for VPA via Akt/FoxO1 signaling

270 We hypothesized that MAO-A levels in PFC and ACC would be highest in severe B

271 We hypothesized that MAO-A levels in the PFC and ACC are most elevated in MDE

272 We hypothesized that MAO-A VT, an index of MAO-A level, is elevated in the pr

273 ) using positron emission tomography and the MAO-A radiotracer [(11)C]clorgyline.

274 A levels because of direct activation of the MAO A promoter via Sp/KLF-binding sites; 4) KLF11 knocko

275 brain cortex in vitro in the presence of the MAO inhibitor pargyline.

276 lysine 49 to increase its activation of the MAO-A promoter.

277 ic inhibition of 5-Htr6 activity rescued the MAO-A knockdown phenotype and restored apoptotic activit

278 Thus, MAO-B represents an attractive target for the treatment

279 erified to target brain MAO-A in addition to MAO-B.

280 ivatives exhibited outstanding affinities to MAO-A (7.0 nM < IC50 < 49 nM, much higher than moclobemi

281 low dipole moment increased the affinity to MAO A, whereas groups with high dipole moment yielded co

282 evelopment and abnormal function compared to MAO control.

283 cal features with a preferential response to MAO inhibitors, which is especially well-evidenced for r

284 n vitro high affinity and selectivity toward MAO-A isoenzyme, compared to clorgyline and moclobemide,

285 brain and acute glucocorticoid exposure upon MAO-A levels in human neuronal and glial cell lines.

286 s are to assess effects of acute stress upon MAO-A V(T,) an index of MAO-A density, in human brain an

287 n an important role of KLF11 in upregulating MAO A in MDD and chronic social stress, suggesting that

288 MAO-B 0.386 nM, >25000-fold selective versus MAO-A) and N-(3,4-dichlorophenyl)-1H-indole-5-carboxamid

289 MAO-B 0.612 nM, >16000-fold selective versus MAO-A).

290 MAO-B 0.227 nM, >5700-fold selective versus MAO-A).

291 4d, 14e, and 14g) showing selectivity versus MAO A and remarkably inhibiting colony formation in THP-

292 IC50 human MAO-B 1.59 nM, selectivity versus MAO-A>6000-fold), high potency and selectivity are optim

293 2/CDCA7L/JPO2), that down-regulate MAO B via MAO B core promoter, which contains Sp1 sites.

294 hy measured MAO-A total distribution volume (MAO-A VT), an index of MAO-A density, in severe BPD subj

295 trate that MNO people are resistant, whereas MAO people are predisposed, to the adverse metabolic eff

296 It is unknown whether MAO-A levels are abnormal in AD.

297 Indeed, treating animals with MAO-A inhibitors or selective serotonin reuptake inhibit

298 strual cycle length, was not associated with MAO-A VT (F8,18 = 0.548; P = .81) but tendency to cry wa

299 ndency to cry was positively correlated with MAO-A VT in the prefrontal cortex (r = 0.54; P = .008).

300 viors that can be reversed by treatment with MAO inhibitors, as well as the tricyclic antidepressant