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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 Kits (31) and Monoamine Oxidase A Proteins (10) and many more products for this protein.
Showing 10 out of 88 products:
Human Polyclonal Monoamine Oxidase A Primary Antibody for IHC (p), IHC - ABIN446982
Maeda, Morikawa, Takadate, Suzuki, Minowa, Hanagata, Onogawa, Motoi, Nishimura, Unno: Mass spectrometry-based proteomic analysis of formalin-fixed paraffin-embedded extrahepatic cholangiocarcinoma. in Journal of hepato-biliary-pancreatic sciences 2015
Show all 2 references for ABIN446982
Cow (Bovine) Polyclonal Monoamine Oxidase A Primary Antibody for WB - ABIN2786499
Shiels, Huang, Hoffman, Shugart, Bolton, Platz, Helzlsouer, Alberg: A community-based study of cigarette smoking behavior in relation to variation in three genes involved in dopamine metabolism: Catechol-O-methyltransferase (COMT), dopamine beta-hydroxylase (DBH) and monoamine oxidase-A (MAO-A). in Preventive medicine 2008
Human Polyclonal Monoamine Oxidase A Primary Antibody for ELISA, WB - ABIN250814
Domschke, Sheehan, Lowe, Kirley, Mullins, Osullivan, Freitag, Becker, Conroy, Fitzgerald, Gill, Hawi et al.: Association analysis of the monoamine oxidase A and B genes with attention deficit hyperactivity disorder (ADHD) in an Irish sample: preferential transmission of the MAO-A 941G allele to affected ... in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 2005
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 Antibodies) allele modifies the effects of maternal temperament on offspring's personality development.
the association of SLC6A4 (show SLC6A4 Antibodies) and MAOA genes with measures of obesity
evidence of a moderating effect of the MAOA gene on antisocial outcomes in a population-based sample of young males; higher risks for antisocial outcomes were observed in males carrying the MAOA low-frequency alleles in comparison with high-frequency allele carriers for most outcomes when exposed to violence
Results emphasize the importance of childhood as a sensitive period in which accumulating adversity might increase the vulnerability to externalizing psychopathology in MAOA-L males and MAOA-H females
These results indicate a possible impact of the MAOA-promotor polymorphism on the neurobiological modulation of aggressive behavior
Huntington disease (show HTT Antibodies) 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 Antibodies) 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 Antibodies) or MAO-A polymorphism is associated with sedentary behavior.
5HTTLPR (show SLC6A4 Antibodies) and uMAOA polymorphisms were not risk factors for depression.
Report isolation of MOA (show MAOB Antibodies)-A inhibitors from Vernonia cinerea.
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 Antibodies) 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.
These findings demonstrate that regulation of monoamine levels by Mao (show MAO Antibodies) activity in beta cells is pivotal for physiological insulin (show INS Antibodies) secretion and that loss of MaoB (show MAOB Antibodies) expression may contribute to the beta cell dysfunction in type 2 diabetes.
Results suggest a role for KLF11 (show KLF11 Antibodies) 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 Antibodies) 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 Antibodies) 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 (show HTR6 Antibodies).
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