Monoaminoxidase A

Deckert J et al. (1999) Excess of high activity monoamine oxidase A gene promoter alleles in female patients with panic disorder.

Shih JC et al. (1999) Monoamine oxidase: from genes to behavior.

Gilad Y et al. (2002) Evidence for positive selection and population structure at the human MAO-A gene.

Desautels A et al. (2002) Evidence for a genetic association between monoamine oxidase A and restless legs syndrome.

Caspi A et al. (2002) Role of genotype in the cycle of violence in maltreated children.

Fossella J et al. (2002) Assessing the molecular genetics of attention networks.

Fan J et al. (2003) Mapping the genetic variation of executive attention onto brain activity.

Cohen IL et al. (2003) Association of autism severity with a monoamine oxidase A functional polymorphism.

Chen ZY et al. (1992) Organization of the human monoamine oxidase genes and long-range physical mapping around them.

Chen K et al. (2004) A spontaneous point mutation produces monoamine oxidase A/B knock-out mice with greatly elevated monoamines and anxiety-like behavior.

Newman TK et al. (2005) Monoamine oxidase A gene promoter variation and rearing experience influences aggressive behavior in rhesus monkeys.

Passamonti L et al. (2006) Monoamine oxidase-a genetic variations influence brain activity associated with inhibitory control: new insight into the neural correlates of impulsivity.

Meyer-Lindenberg A et al. (2006) Neural mechanisms of genetic risk for impulsivity and violence in humans.

Hotamisligil GS et al. (1991) Human monoamine oxidase A gene determines levels of enzyme activity.

Ou XM et al. (2006) Monoamine oxidase A and repressor R1 are involved in apoptotic signaling pathway.

Guo G et al. (2008) The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity.

McDermott R et al. (2009) Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation.

Grimsby J et al. (1991) Human monoamine oxidase A and B genes exhibit identical exon-intron organization.

Whibley A et al. (2010) Deletion of MAOA and MAOB in a male patient causes severe developmental delay, intermittent hypotonia and stereotypical hand movements.

Cohen IL et al. (2011) Autism severity is associated with child and maternal MAOA genotypes.

Sims KB et al. (1989) Monoamine oxidase deficiency in males with an X chromosome deletion.

Lan NC et al. (1989) Human monoamine oxidase A and B genes map to Xp 11.23 and are deleted in a patient with Norrie disease.

Levy ER et al. (1989) Localization of human monoamine oxidase-A gene to Xp11.23-11.4 by in situ hybridization: implications for Norrie disease.

Ozelius L et al. (1988) Human monoamine oxidase gene (MAOA): chromosome position (Xp21-p11) and DNA polymorphism.

de la Chapelle A et al. (1985) Norrie disease caused by a gene deletion allowing carrier detection and prenatal diagnosis.

Kochersperger LM et al. (1986) Assignment of genes for human monoamine oxidases A and B to the X chromosome.

Denney RM et al. (1982) Human liver MAO-A and MAO-B separated by immunoaffinity chromatography with MAO-B-specific monoclonal antibody.

Pintar JE et al. (1981) Gene for monoamine oxidase type A assigned to the human X chromosome.

Castro Costa MR et al. (1980) Properties of monoamine oxidase in control and Lesch-Nyhan fibroblasts.

Nöthen MM et al. (1995) Association analysis of the monoamine oxidase A gene in bipolar affective disorder by using family-based internal controls.

Cases O et al. (1995) Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA.

Kawada Y et al. (1995) Possible association between monoamine oxidase A gene and bipolar affective disorder.

Lim LC et al. (1994) Monoamine oxidase A gene and bipolar affective disorder.

Brunner HG et al. (1993) Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A.

Brunner HG et al. (1993) X-linked borderline mental retardation with prominent behavioral disturbance: phenotype, genetic localization, and evidence for disturbed monoamine metabolism.

Lenders JW et al. (1996) Specific genetic deficiencies of the A and B isoenzymes of monoamine oxidase are characterized by distinct neurochemical and clinical phenotypes.

Sabol SZ et al. (1998) A functional polymorphism in the monoamine oxidase A gene promoter.