| Monoamine oxidase A |
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Ribbon diagram of an MAO-A monomer, with FAD and clorgiline bound, oriented as if attached to the outer membrane of a mitochondrion.[1]
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| Available structures |
| PDB |
Ortholog search: PDBe, RCSB |
| List of PDB id codes |
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1H8Q, 2BXR, 2BXS, 2Z5X, 2Z5Y
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| Identifiers |
| Symbols |
MAOA ; MAO-A |
| External IDs |
OMIM: 309850 MGI: 96915 HomoloGene: 203 ChEMBL: 1951 GeneCards: MAOA Gene |
| EC number |
1.4.3.4 |
| Gene ontology |
| Molecular function |
• primary amine oxidase activity
• flavin adenine dinucleotide binding
• serotonin binding
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| Cellular component |
• mitochondrion
• mitochondrial outer membrane
• integral component of membrane
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| Biological process |
• cellular biogenic amine metabolic process
• xenobiotic metabolic process
• synaptic transmission
• neurotransmitter secretion
• neurotransmitter catabolic process
• neurotransmitter biosynthetic process
• dopamine catabolic process
• serotonin metabolic process
• phenylethylamine metabolic process
• small molecule metabolic process
• oxidation-reduction process
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| Sources: Amigo / QuickGO |
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| RNA expression pattern |
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| More reference expression data |
| Orthologs |
| Species |
Human |
Mouse |
| Entrez |
4128 |
17161 |
| Ensembl |
ENSG00000189221 |
ENSMUSG00000025037 |
| UniProt |
P21397 |
Q64133 |
| RefSeq (mRNA) |
NM_000240 |
NM_173740 |
| RefSeq (protein) |
NP_000231 |
NP_776101 |
| Location (UCSC) |
Chr X:
43.65 – 43.75 Mb |
Chr X:
16.62 – 16.69 Mb |
| PubMed search |
[1] |
[2] |
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Monoamine oxidase A, also known as MAO-A, is an enzyme that in humans is encoded by the MAOA gene.[2][3] Monoamine oxidase A is an isozyme of monoamine oxidase. It preferentially deaminates norepinephrine (noradrenaline), epinephrine (adrenaline), serotonin, and dopamine (which is equally deaminated by MAO-A and MAO-B).
It is inhibited by clorgyline and befloxatone. Inhibition of both MAO-A and MAO-B using a monoamine oxidase inhibitor (MAO inhibitor) is used in the treatment of clinical depression, erectile dysfunction and anxiety.
Contents
- 1 Function
- 2 Clinical significance
- 3 Aggression and the "Warrior gene"
- 3.1 Animal studies
- 3.2 Epigenetics
- 3.3 Legal implications
- 3.4 Cancer research
- 4 MAO-A inhibitors
- 5 MAO-A inducers
- 6 References
- 7 Further reading
Function
Monoamine oxidase A is an enzyme that degrades amine neurotransmitters, such as dopamine, norepinephrine, and serotonin. The protein localizes to the outer mitochondrial membrane. Its encoding gene is adjacent to a related gene (MAOB) on the opposite strand of the X chromosome.
Clinical significance
In humans, there is a 30-base repeat sequence repeated in one of several different numbers of times in the promoter region of the gene coding for MAO-A. There are 2R (two repeats), 3R, 3.5R, 4R, and 5R variants of the repeat sequence, with the 3R and 4R variants most common in Caucasians. The 3.5R and 4R variants have been found to be more highly active than 3R or 5R, in a study which did not examine the 2R variant.[4] An association between the 2R allele of the VNTR region of the gene and an increase in the likelihood of committing serious crime or violence has been found.[4][5][6]
MAO-A levels in the brain as measured using positron emission tomography are elevated by an average of 34% in patients with major depressive disorder.[7] Genetic association studies examining the relationship between high-activity MAOA variants and depression have produced mixed results, with some studies linking the high-activity variants to major depression in females,[8] depressed suicide in males,[9] major depression and sleep disturbance in males[10] and major depressive disorder in both males and females.[11]
Other studies failed to find a significant relationship between high-activity variants of the MAOA gene and major depressive disorder.[12][13] In patients with major depressive disorder, those with MAOA G/T polymorphisms (rs6323) coding for the highest-activity form of the enzyme have a significantly lower magnitude of placebo response than those with other genotypes.[14]
There is a link between low activities forms of the MAOA gene and autism.[15]
Mutation in the MAOA gene results in monoamine oxidase deficiency, or Brunner syndrome.[16]
Aggression and the "Warrior gene"
A version of the monoamine oxidase-A gene has been popularly referred to as the warrior gene.[17] Several different versions of the gene are found in different individuals, although a functional gene is present in most humans (with the exception of a few individuals with Brunner syndrome).[18] In the variant, the allele associated with behavioural traits is shorter (30 bases) and may produce less MAO-A enzyme.[19] This gene variation is in a regulatory promoter region about 1000 bases from the start of the region that encodes the MAO-A enzyme.
The frequency distribution of variants of the MAO-A gene differs between ethnic groups.[19][20] 59% of Black men, 54% of Chinese men, 56% of Maori men, and 34% of Caucasian men carry the 3R allele. 5.5% of Black men, 0.1% of Caucasian men, and 0.00067% of Asian men carry the 2R allele.[6][19][20][21][22][23][24][25][26][27]
A connection between a version of the monoamine oxidase A gene (3R) and several types of antisocial behavior has been found. Maltreated children with genes causing high levels of MAO-A were less likely to develop antisocial behavior.[28] Low MAO-A activity in combination with abuse experienced during childhood results in an increased risk of aggressive behaviour as an adult.[29] High testosterone, maternal tobacco smoking during pregnancy, poor material living standards, dropping out of school, and low IQ can also trigger violent behavior in men with the low-activity alleles (which are overwhelmingly the 3R allele).[30][31] Even in the absence of such interaction factors, the 3R allele has a small main effect on aggression and antisocial behavior, according to a large meta-analysis, which found no significant publication bias.[32]
In individuals with the low activity MAO-A gene, when faced with social exclusion or ostracism showed higher levels of aggression than individuals with the high activity MAO-A gene.[33] Low activity MAO-A could significantly predict aggressive behaviour in a high provocation situation, but was less associated with aggression in a low provocation situation. Individuals with the low activity variant of the MAO-A gene were just as likely as participants with the high activity variant to retaliate when the loss was small. However, they were more likely to retaliate and with greater force when the loss was large.[34]
“Monoamine oxidases (MAOs) are enzymes that are involved in the breakdown of neurotransmitters such as serotonin and dopamine and are, therefore, capable of influencing feelings, mood, and behaviour of individuals”.[35] According to this, if there was a mutation to the gene that is involved in the process of promoting or inhibiting MAO enzymes, it could affect a person’s personality or behaviour and could therefore make them more prone to aggression. A deficiency in the MAO-A gene has shown higher levels of aggression in males, which could further stimulate more research into this controversial topic. “A deficiency in monoamine oxidase A (MAO-A) has been shown to be associated with aggressive behaviour in men of a Dutch family”.[36]
Animal studies
A dysfunctional MAO-A gene has been correlated with increased aggression levels in mice,[37][38] and has been correlated with heightened levels of aggression in humans.[39] In mice, a dysfunctional MAO-A gene is created through insertional mutagenesis (called ‘Tg8’).[37] Tg8 is a transgenic mouse strain that lacks functional MAO-A enzymatic activity. Mice that lacked a functional MAO-A gene exhibited increased aggression towards intruder mice.[37][40]
Some types of aggression exhibited by these mice were territorial aggression, predatory aggression, and isolation-induced aggression.[38] The MAO-A deficient mice that exhibited increased isolation-induced aggression reveals that an MAO-A deficiency may also contribute to a disruption in social interactions.[41] There is research in both humans and mice to support that a nonsense point mutation in the eighth exon of the MAO-A gene is responsible for impulsive aggressiveness due to a complete MAO-A deficiency.[37][39]
Epigenetics
Epigenetics likely plays an important role in the expression of the MAO-A gene through methylation in women.[42] Studies have linked methylation of the MAO-A gene with nicotine and alcohol dependence in women.[43] A second MAO-A VNTR promoter, P2, influences epigenetic methylation in women only and interacts with having experienced child abuse to influence antisocial personality disorder symptoms, also only in women.[44] Epigenetic methylation of MAO-A in men is very low and with little variability compared to women. It also has a much higher heritability in men than women.[45]
Legal implications
In a 2009 criminal trial in the United States, an argument based on a combination of "warrior gene" and history of child abuse was successfully used to avoid a conviction of first-degree murder and the death penalty; however, the convicted murderer was sentenced to 32 years in prison.[46][47]
Cancer research
MAO-A produces an amine oxidase, which is a class of enzyme known to affect carcinogenesis. Clorgyline, an MAO-A enzyme inhibitor, prevents apoptosis in melanoma cells, in vitro.[48] Cholangiocarcinoma suppresses MAO-A expression, and those patients with higher MAO-A expression had less adjacent organ invasion and better prognosis and survival.[49]
MAO-A inhibitors
Main articles: Reversible inhibitor of monoamine oxidase A and Monoamine oxidase inhibitor
- Synthetic compounds
- Befloxatone (MD370503)
- Brofaromine (Consonar)
- Cimoxatone
- Clorgyline (irreversible)
- Methylene Blue
- Minaprine (Cantor)
- Moclobemide (Aurorix, Manerix)
- Pirlindole (Pirazidol)
- Toloxatone (Humoryl)
- Tyrima (CX 157)
- Tranylcypromine (nonselective and irreversible)
- Herbal sources
- Curcumin (Turmeric)
- Harmala Alkaloids (Syrian Rue, Passion Flower, Ayahuasca)
MAO-A inducers
- Synthetic compounds
- Valproic Acid (Depakote)[50]
References
- ^ PDB: 2BXS; De Colibus L, Li M, Binda C, Lustig A, Edmondson DE, Mattevi A (September 2005). "Three-dimensional structure of human monoamine oxidase A (MAO A): relation to the structures of rat MAO A and human MAO B". Proc. Natl. Acad. Sci. U.S.A. 102 (36): 12684–9. doi:10.1073/pnas.0505975102. PMC 1200291. PMID 16129825.
- ^ Hotamisligil GS, Breakefield XO (Aug 1991). "Human monoamine oxidase A gene determines levels of enzyme activity". American Journal of Human Genetics 49 (2): 383–92. PMC 1683299. PMID 1678250.
- ^ Grimsby J, Chen K, Wang LJ, Lan NC, Shih JC (May 1991). "Human monoamine oxidase A and B genes exhibit identical exon-intron organization". Proceedings of the National Academy of Sciences of the United States of America 88 (9): 3637–41. doi:10.1073/pnas.88.9.3637. PMC 51507. PMID 2023912.
- ^ a b Guo G, Ou XM, Roettger M, Shih JC (May 2008). "The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity". European Journal of Human Genetics 16 (5): 626–34. doi:10.1038/sj.ejhg.5201999. PMC 2922855. PMID 18212819.
- ^ Guo G, Roettger M, Shih JC (August 2008). "The integration of genetic propensities into social-control models of delinquency and violence among male youths" (PDF). American Sociological Review 73 (4): 543–568. doi:10.1177/000312240807300402. [dead link]
- ^ a b Beaver KM, et al. (2012). "Exploring the association between the 2-repeat allele of the MAOA gene promoter polymorphism and psychopathic personality traits, arrests, incarceration, and lifetime antisocial behavior". Personality and Individual Differences. doi:10.1016/j.paid.2012.08.014. "We examine the effect of the 2R allele of MAOA on a range of antisocial outcomes. ► The 2R was related to arrest, incarceration, and lifetime antisocial behavior. ► These associations were only observable for African-American males. ► Only 0.1% of Caucasian males carried the 2-repeat allele."
- ^ Meyer JH, Ginovart N, Boovariwala A, Sagrati S, Hussey D, Garcia A, et al. (Nov 2006). "Elevated monoamine oxidase a levels in the brain: an explanation for the monoamine imbalance of major depression". Archives of General Psychiatry 63 (11): 1209–16. doi:10.1001/archpsyc.63.11.1209. PMID 17088501.
- ^ Schulze TG, Müller DJ, Krauss H, Scherk H, Ohlraun S, Syagailo YV, et al. (Dec 2000). "Association between a functional polymorphism in the monoamine oxidase A gene promoter and major depressive disorder". American Journal of Medical Genetics 96 (6): 801–3. doi:10.1002/1096-8628(20001204)96:6<801::AID-AJMG21>3.0.CO;2-4. PMID 11121185.
- ^ Du L, Faludi G, Palkovits M, Sotonyi P, Bakish D, Hrdina PD (Jul 2002). "High activity-related allele of MAO-A gene associated with depressed suicide in males". Neuroreport 13 (9): 1195–8. doi:10.1097/00001756-200207020-00025. PMID 12151768.
- ^ Du L, Bakish D, Ravindran A, Hrdina PD (Sep 2004). "MAO-A gene polymorphisms are associated with major depression and sleep disturbance in males". Neuroreport 15 (13): 2097–101. doi:10.1097/00001756-200409150-00020. PMID 15486489.
- ^ Yu YW, Tsai SJ, Hong CJ, Chen TJ, Chen MC, Yang CW (Sep 2005). "Association study of a monoamine oxidase a gene promoter polymorphism with major depressive disorder and antidepressant response". Neuropsychopharmacology 30 (9): 1719–23. doi:10.1038/sj.npp.1300785. PMID 15956990.
- ^ Serretti A, Cristina S, Lilli R, Cusin C, Lattuada E, Lorenzi C, et al. (May 2002). "Family-based association study of 5-HTTLPR, TPH, MAO-A, and DRD4 polymorphisms in mood disorders". American Journal of Medical Genetics 114 (4): 361–9. doi:10.1002/ajmg.10356. PMID 11992558.
- ^ Huang SY, Lin MT, Lin WW, Huang CC, Shy MJ, Lu RB (2009). "Association of monoamine oxidase A (MAOA) polymorphisms and clinical subgroups of major depressive disorders in the Han Chinese population". The World Journal of Biological Psychiatry 10 (4 Pt 2): 544–51. doi:10.1080/15622970701816506. PMID 19224413.
- ^ Leuchter AF, McCracken JT, Hunter AM, Cook IA, Alpert JE (Aug 2009). "Monoamine oxidase a and catechol-o-methyltransferase functional polymorphisms and the placebo response in major depressive disorder". Journal of Clinical Psychopharmacology 29 (4): 372–7. doi:10.1097/JCP.0b013e3181ac4aaf. PMID 19593178.
- ^ Cohen IL, Liu X, Lewis ME, Chudley A, Forster-Gibson C, Gonzalez M, et al. (Apr 2011). "Autism severity is associated with child and maternal MAOA genotypes". Clinical Genetics 79 (4): 355–62. doi:10.1111/j.1399-0004.2010.01471.x. PMID 20573161.
- ^ "Entrez Gene: MAOA monoamine oxidase A".
- ^ Hogenboom M (28 October 2014). "Share this pageEmail Print Share this page". BBC News. Retrieved 2014-11-01.
- ^ Online 'Mendelian Inheritance in Man' (OMIM) MONOAMINE OXIDASE A; MAOA. -309850
- ^ a b c Sabol SZ, Hu S, Hamer D (Sep 1998). "A functional polymorphism in the monoamine oxidase A gene promoter". Human Genetics 103 (3): 273–9. doi:10.1007/s004390050816. PMID 9799080.
- ^ a b Lea R, Chambers G (2007). "Monoamine oxidase, addiction, and the "warrior" gene hypothesis". The New Zealand Medical Journal 120 (1250): U2441. PMID 17339897.
- ^ Lu RB, Lin WW, Lee JF, Ko HC, Shih JC (Jun 2003). "Neither antisocial personality disorder nor antisocial alcoholism is associated with the MAO-A gene in Han Chinese males". Alcoholism, Clinical and Experimental Research 27 (6): 889–93. doi:10.1097/01.ALC.0000071927.64880.0E. PMID 12824808.
- ^ Zhang M, Chen X, Way N, Yoshikawa H, Deng H, Ke X, et al. (Sep 2011). "The association between infants' self-regulatory behavior and MAOA gene polymorphism". Developmental Science 14 (5): 1059–65. doi:10.1111/j.1467-7687.2011.01047.x. PMID 21884321.
- ^ Zhou Q, Hofer C, Eisenberg N, Reiser M, Spinrad TL, Fabes RA (Mar 2007). "The developmental trajectories of attention focusing, attentional and behavioral persistence, and externalizing problems during school-age years". Developmental Psychology 43 (2): 369–85. doi:10.1037/0012-1649.43.2.369. PMC 1832154. PMID 17352545.
- ^ Chen S, Wang J, Yu G, Liu W, Pearce D (May 1997). "Androgen and glucocorticoid receptor heterodimer formation. A possible mechanism for mutual inhibition of transcriptional activity". The Journal of Biological Chemistry 272 (22): 14087–92. doi:10.1074/jbc.272.22.14087. PMID 9162033.
- ^ Ono H, Shirakawa O, Nishiguchi N, Nishimura A, Nushida H, Ueno Y, et al. (Apr 2002). "No evidence of an association between a functional monoamine oxidase a gene polymorphism and completed suicides". American Journal of Medical Genetics 114 (3): 340–2. doi:10.1002/ajmg.10237. PMID 11920860.
- ^ Wang TJ, Huang SY, Lin WW, Lo HY, Wu PL, Wang YS, et al. (Jan 2007). "Possible interaction between MAOA and DRD2 genes associated with antisocial alcoholism among Han Chinese men in Taiwan". Progress in Neuro-Psychopharmacology & Biological Psychiatry 31 (1): 108–14. doi:10.1016/j.pnpbp.2006.08.010. PMID 17007976.
- ^ Lee SY, Hahn CY, Lee JF, Huang SY, Chen SL, Kuo PH, et al. (Jul 2010). "MAOA interacts with the ALDH2 gene in anxiety-depression alcohol dependence". Alcoholism, Clinical and Experimental Research 34 (7): 1212–8. doi:10.1111/j.1530-0277.2010.01198.x. PMID 20477771.
- ^ Caspi A, McClay J, Moffitt TE, Mill J, Martin J, Craig IW, et al. (Aug 2002). "Role of genotype in the cycle of violence in maltreated children". Science 297 (5582): 851–4. doi:10.1126/science.1072290. PMID 12161658. Lay summary – eurekalert.org (2002-08-01).
- ^ Frazzetto G, Di Lorenzo G, Carola V, Proietti L, Sokolowska E, Siracusano A, et al. (2007). "Early trauma and increased risk for physical aggression during adulthood: the moderating role of MAOA genotype". PloS One 2 (5): e486. doi:10.1371/journal.pone.0000486. PMC 1872046. PMID 17534436.
- ^ Fergusson DM, Boden JM, Horwood LJ, Miller A, Kennedy MA (Feb 2012). "Moderating role of the MAOA genotype in antisocial behaviour". The British Journal of Psychiatry 200 (2): 116–23. doi:10.1192/bjp.bp.111.093328. PMID 22297589.
- ^ Sjöberg RL, Ducci F, Barr CS, Newman TK, Dell'osso L, Virkkunen M, et al. (Jan 2008). "A non-additive interaction of a functional MAO-A VNTR and testosterone predicts antisocial behavior". Neuropsychopharmacology 33 (2): 425–30. doi:10.1038/sj.npp.1301417. PMC 2665792. PMID 17429405.
- ^ Ficks CA, Waldman ID (Sep 2014). "Candidate genes for aggression and antisocial behavior: a meta-analysis of association studies of the 5HTTLPR and MAOA-uVNTR". Behavioral Genetics 44 (5): 427–44. doi:10.1007/s10519-014-9661-y. PMID 24902785.
- ^ Gallardo-Pujol D, Andrés-Pueyo A, Maydeu-Olivares A (Feb 2013). "MAOA genotype, social exclusion and aggression: an experimental test of a gene-environment interaction". Genes, Brain, and Behavior 12 (1): n/a–n/a. doi:10.1111/j.1601-183X.2012.00868.x. PMID 23067570.
- ^ McDermott R, Tingley D, Cowden J, Frazzetto G, Johnson DD (Feb 2009). "Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation". Proceedings of the National Academy of Sciences of the United States of America 106 (7): 2118–23. doi:10.1073/pnas.0808376106. PMC 2650118. PMID 19168625.
- ^ Hook GR (2009). ""Warrior genes" and the disease of being Māori". MAI Review (2): 1–11.
- ^ Cases O, Seif I, Grimsby J, Gaspar P, Chen K, Pournin S, et al. (Jun 1995). "Aggressive behavior and altered amounts of brain serotonin and norepinephrine in mice lacking MAOA". Science 268 (5218): 1763–6. doi:10.1126/science.7792602. PMC 2844866. PMID 7792602.
- ^ a b c d Scott AL, Bortolato M, Chen K, Shih JC (May 2008). "Novel monoamine oxidase A knock out mice with human-like spontaneous mutation". Neuroreport 19 (7): 739–43. doi:10.1097/WNR.0b013e3282fd6e88. PMC 3435113. PMID 18418249.
- ^ a b Vishnivetskaya GB, Skrinskaya JA, Seif I, Popova NK (2007). "Effect of MAO A deficiency on different kinds of aggression and social investigation in mice". Aggressive Behavior 33 (1): 1–6. doi:10.1002/ab.20161. PMID 17441000.
- ^ a b Brunner HG, Nelen M, Breakefield XO, Ropers HH, van Oost BA (Oct 1993). "Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A". Science 262 (5133): 578–80. doi:10.1126/science.8211186. PMID 8211186.
- ^ Vishnivetskaya GB, Skrinskaya JA, Seif I, Popova NK (1 January 2007). "Effect of MAO A deficiency on different kinds of aggression and social investigation in mice". Aggressive Behavior 33 (1): 1–6. doi:10.1002/ab.20161. PMID 17441000.
- ^ Hebebrand J, Klug B (Sep 1995). "Specification of the phenotype required for men with monoamine oxidase type A deficiency". Human Genetics 96 (3): 372–6. doi:10.1007/BF00210430. PMID 7649563.
- ^ Jiang Y, Langley B, Lubin FD, Renthal W, Wood MA, Yasui DH, et al. (Nov 2008). "Epigenetics in the nervous system". The Journal of Neuroscience 28 (46): 11753–9. doi:10.1523/JNEUROSCI.3797-08.2008. PMID 19005036.
- ^ Philibert RA, Gunter TD, Beach SR, Brody GH, Madan A (Jul 2008). "MAOA methylation is associated with nicotine and alcohol dependence in women". American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics 147B (5): 565–70. doi:10.1002/ajmg.b.30778. PMC 3685146. PMID 18454435.
- ^ Philibert RA, Wernett P, Plume J, Packer H, Brody GH, Beach SR (Jul 2011). "Gene environment interactions with a novel variable Monoamine Oxidase A transcriptional enhancer are associated with antisocial personality disorder". Biological Psychology 87 (3): 366–71. doi:10.1016/j.biopsycho.2011.04.007. PMC 3134149. PMID 21554924.
- ^ Wong CC, Caspi A, Williams B, Craig IW, Houts R, Ambler A, et al. (Aug 2010). "A longitudinal study of epigenetic variation in twins". Epigenetics 5 (6): 516–26. doi:10.4161/epi.5.6.12226. PMC 3322496. PMID 20505345.
- ^ Barber N (2010-07-13). "Pity the poor murderer, his genes made him do it". The Human Beast: Why we do what we do. Psychology Today. Retrieved 2010-10-17.
- ^ Hagerty BB (2010-07-01). "Can Your Genes Make You Murder?". News > Science > Inside The Criminal Brain. National Public Radio. Retrieved 2010-10-17.
- ^ Pietrangeli P, Mondovì B (Jan 2004). "Amine oxidases and tumors". Neurotoxicology 25 (1-2): 317–24. doi:10.1016/S0161-813X(03)00109-8. PMID 14697906.
- ^ Huang L, Frampton G, Rao A, Zhang KS, Chen W, Lai JM, et al. (Oct 2012). "Monoamine oxidase A expression is suppressed in human cholangiocarcinoma via coordinated epigenetic and IL-6-driven events". Laboratory Investigation; A Journal of Technical Methods and Pathology 92 (10): 1451–60. doi:10.1038/labinvest.2012.110. PMID 22906985.
- ^ Wu JB, Shih JC (Oct 2011). "Valproic acid induces monoamine oxidase A via Akt/forkhead box O1 activation". Molecular Pharmacology 80 (4): 714–723. doi:10.1124/mol.111.072744. PMC 3187529. PMID 21775495.
Further reading
- "'Warrior Gene' Predicts Aggressive Behavior After Provocation". Science News. Science Daily. 2009-01-23.
- McDermott R, Tingley D, Cowden J, Frazzetto G, Johnson DD (Feb 2009). "Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation". Proceedings of the National Academy of Sciences of the United States of America 106 (7): 2118–23. doi:10.1073/pnas.0808376106. PMC 2650118. PMID 19168625.
- Edmondson DE, Binda C, Mattevi A (Jan 2004). "The FAD binding sites of human monoamine oxidases A and B". Neurotoxicology 25 (1-2): 63–72. doi:10.1016/S0161-813X(03)00114-1. PMID 14697881.
- Craig IW (Mar 2007). "The importance of stress and genetic variation in human aggression". BioEssays 29 (3): 227–36. doi:10.1002/bies.20538. PMID 17295220.
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PDB gallery
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2bxr: HUMAN MONOAMINE OXIDASE A IN COMPLEX WITH CLORGYLINE, CRYSTAL FORM A
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2bxs: HUMAN MONOAMINE OXIDASE A IN COMPLEX WITH CLORGYLINE, CRYSTAL FORM B
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CH-NH2 oxidoreductases (EC 1.4) - primarily amino acid oxidoreductases
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| 1.4.1: NAD/NADP acceptor |
- Glutamate dehydrogenase
- Glutamate synthase (NADPH)
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| 1.4.3: oxygen acceptor |
- D-amino acid oxidase
- Amine oxidase
- Lysyl oxidase
- Monoamine oxidase
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| 1.4.4: disulfide acceptor |
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| 1.4.99: other acceptors |
- D-amino acid dehydrogenase
- Amine dehydrogenase
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- Biochemistry overview
- Enzymes overview
- By EC number: 1.1
- 2
- 3
- 4
- 5
- 6
- 7
- 8
- 10
- 11
- 13
- 14
- 15-18
- 2.1
- 3.1
- 4.1
- 5.1
- 6.1-3
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Mitochondrial proteins
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| Outer membrane |
| fatty acid degradation |
- Carnitine palmitoyltransferase I
- Long-chain-fatty-acid—CoA ligase
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| tryptophan metabolism |
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monoamine neurotransmitter
metabolism |
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| Intermembrane space |
- Adenylate kinase
- Creatine kinase
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| Inner membrane |
| oxidative phosphorylation |
- Coenzyme Q – cytochrome c reductase
- Cytochrome c
- NADH dehydrogenase
- Succinate dehydrogenase
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| pyrimidine metabolism |
- Dihydroorotate dehydrogenase
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| mitochondrial shuttle |
- Malate-aspartate shuttle
- Glycerol phosphate shuttle
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| other |
- Glutamate aspartate transporter
- Glycerol-3-phosphate dehydrogenase
- ATP synthase
- Carnitine palmitoyltransferase II
- Uncoupling protein
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| Matrix |
| citric acid cycle |
- Citrate synthase
- Aconitase
- Isocitrate dehydrogenase
- Oxoglutarate dehydrogenase complex
- Succinyl coenzyme A synthetase
- Fumarase
- Malate dehydrogenase
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| anaplerotic reactions |
- Aspartate transaminase
- Glutamate dehydrogenase
- Pyruvate dehydrogenase complex
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| urea cycle |
- Carbamoyl phosphate synthetase I
- Ornithine transcarbamylase
- N-Acetylglutamate synthase
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| alcohol metabolism |
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| Other/to be sorted |
| steroidogenesis |
- Cholesterol side-chain cleavage enzyme
- Steroid 11-beta-hydroxylase
- Aldosterone synthase
- Frataxin
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- Mitochondrial membrane transport protein
- Mitochondrial permeability transition pore
- Mitochondrial carrier
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| Mitochondrial DNA |
| Complex I |
- MT-ND1
- MT-ND2
- MT-ND3
- MT-ND4
- MT-ND4L
- MT-ND5
- MT-ND6
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| Complex III |
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| Complex IV |
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| ATP synthase |
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| tRNA |
- MT-TA
- MT-TC
- MT-TD
- MT-TE
- MT-TF
- MT-TG
- MT-TH
- MT-TI
- MT-TK
- MT-TL1
- MT-TL2
- MT-TM
- MT-TN
- MT-TP
- MT-TQ
- MT-TR
- MT-TS1
- MT-TS2
- MT-TT
- MT-TV
- MT-TW
- MT-TY
|
|
|
|
see also mitochondrial diseases
|
Index of cells
|
|
| Description |
- Structure
- Organelles
- peroxisome
- cytoskeleton
- centrosome
- epithelia
- cilia
- mitochondria
- Membranes
- Membrane transport
- ion channels
- vesicular transport
- solute carrier
- ABC transporters
- ATPase
- oxidoreduction-driven
|
|
| Disease |
- Structural
- peroxisome
- cytoskeleton
- cilia
- mitochondria
- nucleus
- scleroprotein
- Membrane
- channelopathy
- solute carrier
- ATPase
- ABC transporters
- other
- extracellular ligands
- cell surface receptors
- intracellular signalling
- Vesicular transport
- Pore-forming toxins
|
|
|
|
Enzymes involved in neutrotransmission
|
|
| monoamine |
| histidine → histamine |
| anabolism: |
|
|
| catabolism: |
- Histamine N-methyltransferase
- Amine oxidase
|
|
|
| tyrosine→dopamine→epinephrine |
| anabolism: |
- Tyrosine hydroxylase
- Aromatic L-amino acid decarboxylase
- Dopamine beta hydroxylase
- Phenylethanolamine N-methyltransferase
|
|
| catabolism: |
- Catechol-O-methyl transferase
- Monoamine oxidase
|
|
|
| glutamate→GABA |
| anabolism: |
|
|
| catabolism: |
- 4-aminobutyrate transaminase
|
|
|
| tryptophan→serotonin→melatonin |
- Tryptophan hydroxylase
- Aromatic L-amino acid decarboxylase
- Acetylserotonin O-methyltransferase
|
|
|
| arginine→NO |
- Nitric oxide synthase (NOS1, NOS2, NOS3)
|
|
| choline→Acetylcholine |
| anabolism: |
- Choline acetyltransferase
|
|
| catabolism: |
- Cholinesterase (Acetylcholinesterase, Butyrylcholinesterase)
|
|
|
|
Index of the central nervous system
|
|
| Description |
- Anatomy
- meninges
- cortex
- association fibers
- commissural fibers
- lateral ventricles
- basal ganglia
- diencephalon
- mesencephalon
- pons
- cerebellum
- medulla
- spinal cord
- Physiology
- Development
|
|
| Disease |
- Addiction
- Cerebral palsy
- Meningitis
- Demyelinating diseases
- Seizures and epilepsy
- Headache
- Stroke
- Sleep
- Congenital
- Injury
- Neoplasms and cancer
- Other
- Symptoms and signs
- head and neck
- eponymous
- lesions
- Tests
|
|
| Treatment |
- Procedures
- Drugs
- general anesthetics
- analgesics
- dependence
- epilepsy
- cholinergics
- migraine
- Parkinson's
- vertigo
- other
|
|
|
