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MAOA is one of two neighboring gene family members that encode mitochondrial enzymes which catalyze the oxidative deamination of amines, such as dopamine, norepinephrine, and serotonin. Additionally we are shipping Monoamine Oxidase A Antibodies (81) and Monoamine Oxidase A Proteins (10) and many more products for this protein.
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study found the ability to consolidate sleep during the dark cycle was disrupted by prenatal iron deprivation, specifically in monkeys with the low-MAOA genotype
The effects of iron deficiency are dependent on MAOA genotype in terms of both direction and size of the effect.
rhMAOA-LPR (show FAS ELISA Kits) allele modifies the effects of maternal temperament on offspring's personality development.
These results indicate a possible impact of the MAOA-promotor polymorphism on the neurobiological modulation of aggressive behavior
Huntington disease (show HTT ELISA Kits) neural cells exhibit increased Monoamine oxidase-A and Monoamine oxidases-B expression and activity
Our study substantiates the involvement of the monoamine oxidase A and 5,10-methylenetetrahydrofolate reductase (show MTHFR ELISA Kits) polymorphisms in climacteric depression.
Study demonstrated lower brain MAO-A levels in antisocial personality disorder, support an important extension of preclinical models of impulsive aggression into a human disorder marked by pathological aggression and impulsivity
These data support part of our hypothesis that NHLH2 (show NHLH2 ELISA Kits) or MAO-A polymorphism is associated with sedentary behavior.
5HTTLPR (show SLC6A4 ELISA Kits) and uMAOA polymorphisms were not risk factors for depression.
Report isolation of MOA (show MAOB ELISA Kits)-A inhibitors from Vernonia cinerea.
The 3/3 genotype of the 30-bp VNTR polymorphism in the monoamine oxidase A promoter region does not contribute to the development of depressive symptoms in late-reproductive-age women.
Lower spontaneous brain activity in the pons of the MAOA-L male adolescents may provide a neural mechanism by which boys with the MAOA-L genotype confers risk for impulsivity and aggression.
These findings demonstrate that regulation of monoamine levels by Mao (show MAO ELISA Kits) activity in beta cells is pivotal for physiological insulin (show INS ELISA Kits) secretion and that loss of MaoB (show MAOB ELISA Kits) expression may contribute to the beta cell dysfunction in type 2 diabetes.
cloning and characterization of monoamine oxidase A and B genes in pig
Two pools of ten bovine embryos, comprised of the 4-, 8- to 16-cell, morula, blastocyst, and expanded blastocyst stages, were collected. Total RNA was isolated, and the RT-PCR-RFLP technique was used to observe expression of the MAOA gene.
MAOA was seriously demethylated or showed aberrant methylation patterns in four aborted clones.
data lead us to conclude that elevation of AP-1 (show JUN ELISA Kits) or NF-kB indirectly decreases MAO-A protein levels which, in turn, diminishes MAO-A ability in the VTA of the mesolimbic dopaminergic pathway
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.
Results suggest a role for KLF11 (show KLF11 ELISA Kits) 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
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.
These results suggest that early developmental enhancements in 5-HT (show DDC ELISA Kits) levels have long-term effects on the modulation of behavioral flexibility associated with MAO-A deficiency.
Under conditions of chronic hemodynamic stress, enhanced MAO-B (show MAOB ELISA Kits) activity is a major determinant of cardiac structural and functional disarrangement.
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.
Both monoamine oxidase A (and B) knockout mice displayed neuropathological alterations typical of autism-spectrum disorders.
This gene is one of two neighboring gene family members that encode mitochondrial enzymes which catalyze the oxidative deamination of amines, such as dopamine, norepinephrine, and serotonin. Mutation of this gene results in Brunner syndrome. This gene has also been associated with a variety of other psychiatric disorders, including antisocial behavior. Alternatively spliced transcript variants encoding multiple isoforms have been observed.
monoamine oxidase A
, amine oxidase [flavin-containing] A-like
, amine oxidase [flavin-containing] A
, monoamine oxidase type A
, putative monoamine oxidase A