Recombinant Mouse Amine oxidase [flavin-containing] A (Maoa), partial

1. Study provides experimental evidence showing that sleep deprivation induces an increase in monoamine oxidase A levels in certain brain regions, such as the amygdala and hippocampus of mice that might mediate depressive-like behaviors. PMID: 28365314
2. This study unravels a new link between MAO-dependent H2O2 production and lysosomal dysfunction. Altogether, our findings demonstrate that the MAO-A/H2O2 axis has a negative impact on the elimination and recycling of mitochondria through the autophagy-lysosome pathway, which participates in cardiomyocyte death and heart failure PMID: 26959532
3. Results demonstrate that C17H11IOSe, a selective inhibitor of cortical MAO-A, elicited an antidepressant-like action in mice by interacting with the serotonergic system PMID: 28012831
4. data lead us to conclude that elevation of AP-1 or NF-kB indirectly decreases MAO-A protein levels which, in turn, diminishes MAO-A ability in the VTA of the mesolimbic dopaminergic pathway PMID: 26841904
5. Huntington disease neural cells exhibit increased Monoamine oxidase-A and Monoamine oxidases-B expression and activity PMID: 25398695
6. acute stress induces anxiety-like responses by affecting rapid dendritic remodeling in the pyramidal cells of orbitofrontal cortex and basolateral amygdala; furthermore, our data show that MAO-A and monoamine metabolism are required for these phenomena. PMID: 25857821
7. These findings demonstrate that regulation of monoamine levels by Mao activity in beta cells is pivotal for physiological insulin secretion and that loss of MaoB expression may contribute to the beta cell dysfunction in type 2 diabetes. PMID: 26546820
8. Results suggest a role for KLF11 in upregulating MAO-A in depressive disorder and chronic social stress, suggesting that inhibition of the pathways regulated by this transcription factor may aid in the therapeutics of neuropsychiatric illnesses PMID: 25502632
9. The results of this study suggest that heightened dACC and amygdala activation and their connectivity are neuroaffective mechanisms underlying anger control in participants with the low-functioning allele of the MAOA gene. PMID: 24564461
10. These results suggest that early developmental enhancements in 5-HT levels have long-term effects on the modulation of behavioral flexibility associated with MAO-A deficiency. PMID: 23871843
11. Under conditions of chronic hemodynamic stress, enhanced MAO-B activity is a major determinant of cardiac structural and functional disarrangement. PMID: 23581564
12. Knockdown of MAO-A expression in embryos induces high serotonin levels and abnormal brain development, which can be rescued by inactivation of serotonin receptor-6. PMID: 24497636
13. Both monoamine oxidase A (and B) knockout mice displayed neuropathological alterations typical of autism-spectrum disorders. PMID: 22850464
14. chronic elevations of monoamines, because of the absence of MAO A and MAO B, cause functional alterations that are accompanied with changes in the cellular mechanisms underlying learning and memory. PMID: 23858446
15. MAO-A is expressed in the mouse aorta, induced by in vivo lipopolysaccharide and angiotensin II treatment and contribute via the generation of H(2)O(2) to endothelial dysfunction in vascular disease models. PMID: 23670301
16. Our current findings suggest that congenitally low MAO-A activity leads to abnormal development of the cerebellum. PMID: 22971542
17. MAO-A(Neo) hypomorphic mice show significant increases in dendritic length in the pyramidal neurons of orbitofrontal cortex, but not basolateral amygdala, in comparison with wild type littermates. PMID: 21832987
18. Direct influence of presenilin-1 variants on MAO-A function provides an explanation for the changes in monoaminergic tone observed in several neurodegenerative processes, including Alzheimer disease. PMID: 21373759
19. Differentiation to neural cells in MAO neoembryonic stem cells is reduced compared to wild-type mice, suggesting MAO A plays a regulatory role in neural stem cell differentiation. PMID: 21607742
20. MAO-A as a vital regulator of embryonic brain development. PMID: 21697081
21. SIRT1 deacetylates the brain-specific helix-loop-helix transcription factor NHLH2 on lysine 49 to increase its activation of the MAO-A promoter. PMID: 22169038
22. Data from studies in knockout mice suggest that MAOA deficiency leads to a general inability to appropriately assess contextual risk and attune defensive and emotional responses to environmental cues. PMID: 21156093
23. Genetic knockout of MAO A, one of the key enzymes in catecholamine and serotonin metabolism in the brain, weakened the startle reaction and tail suspension test-induced hyperthermia PMID: 20490692
24. Expression of Maoa in the mouse striatum is modulated by a sequence variant (B2 SINE indel) in the 3' UTR of Comt (catechol-O-methyltransferase). PMID: 20808911
25. The findings of this study revealed novel roles for MAO-a and serotonin in the regulation of intermediate progenitor cells proliferation in the developing brain. PMID: 20702706
26. enhanced MAO-A activity coupled with increased intramyocardial norepinephrine availability results in augmented reactive oxygen species generation, contributing to maladaptive remodeling and left ventricular dysfunction PMID: 19910579
27. Knockout of the monoamine oxidase type A gene had no effect on movement activity,anxiety, predisposition to catalepsy, sex behavior but increased aggression PMID: 11766896
28. Knock-out of this gene disrupts formation of barrel domains in the somatosensory cortex PMID: 12351728
29. Transgenic mice lacking this protein demonstrate a higher resistance to acute ethanol exposure compared to mice of the C3H strain. Long-term exposure changed the resistance to hypnotic action of ethanol. PMID: 12447479
30. MAOA expression was restricted to the sympathetic ganglia and to the meningeal and capillary blood vessels. PMID: 12900932
31. Observed chase/escape and anxiety-like behavior in the MAO A/B KO mice, different from MAO A or B single KO mice, suggest that varying monoamine levels result in both a unique biochemical and behavioral phenotype. PMID: 15272015
32. Effect of monoamine oxidease A knockout on the expression of 5-HTlA receptors. PMID: 16121945
33. demonstrates the functions of MAO A and its repressor R1(RAM2/CDCA7L/JPO2) in apoptotic signaling pathways PMID: 16829576
34. a constitutive deficiency of MAOA reduces the rewarding effects of nicotine without altering behavioral responses to novel stimuli PMID: 16893910
35. monoamine oxidase A has a role in regulating neurotransmitter levels, brain structure, and aggressive behavior PMID: 17090537
36. Upregulation of ceramide/sphingosine 1-phosphate ratio is a critical event in MAO-A-mediated cardiac cell apoptosis. PMID: 17158340
37. These findings consolidate evidence linking MAO A to aggression and highlight subtle yet distinctive phenotypical characteristics. PMID: 18418249
38. A mutation in the clock gene Per2 in mice leads to reduced expression and activity of MAOA in the mesolimbic dopaminergic system. PMID: 18439826
39. Data show that serotonin immunoreactivity cell bodies are observed in auditory brainstem neurons of the postnatal monoamine oxidase-A knockout mouse. PMID: 18634763
40. data suggest that genetic deficiency in MAOA enzyme is associated with changes in cholinergic activity, which may account for some of the behavioral alterations observed in mice and humans lacking MAOA PMID: 19111597
41. Regulation of peripheral serotonin by MAO-A plays a role in ventricular remodeling via activation of 5-HT(2A) receptors. PMID: 19162038
42. knockout of enzyme in serotonin and catecholamines metabolism, MAO A, decreased the startle response and TST-induced hyperthermia but had no effect on TST-induced immobility in Tg8 mice indicating the differences in regulation of these responses. PMID: 19445388
43. Decreased cell size and increased intracellular serotonin level were observed in the case of monoamine oxidase A deficiency, while excessive cell size and decreased intracellular serotonin level were observed in the case of autoreceptor deficiency. PMID: 19705758
44. Sequence variation within serotonin system genes, for example, a repeat polymorphism in the transcriptional control region of the monoamine oxidase gene (MAOA-LPR), increases the propensity for adolescent males to consume alcohol. PMID: 15251892

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KEGG: mmu:17161

STRING: 10090.ENSMUSP00000026013

UniGene: Mm.21108