Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A

Science ◽  
1993 ◽  
Vol 262 (5133) ◽  
pp. 578-580 ◽  
Author(s):  
H. Brunner ◽  
M Nelen ◽  
X. Breakefield ◽  
H. Ropers ◽  
B. van Oost
Keyword(s):  
Monoamine Oxidase ◽  
Point Mutation ◽  
Structural Gene ◽  
Monoamine Oxidase A ◽  
Abnormal Behavior

scholarly journals A Spontaneous Point Mutation Produces Monoamine Oxidase A/B Knock-out Mice with Greatly Elevated Monoamines and Anxiety-like Behavior

2004 ◽  
Vol 279 (38) ◽  
pp. 39645-39652 ◽  
Author(s):  
Kevin Chen ◽  
Daniel P. Holschneider ◽  
Weihua Wu ◽  
Igor Rebrin ◽  
Jean C. Shih
Keyword(s):  
Monoamine Oxidase ◽  
Point Mutation ◽  
Monoamine Oxidase A ◽  
Knock Out ◽  
Knock Out Mice

scholarly journals Insights into enzyme point mutation effect by molecular simulation: phenylethylamine oxidation catalyzed by monoamine oxidase A

2016 ◽  
Vol 18 (19) ◽  
pp. 13346-13356 ◽  
Author(s):  
Gabriel Oanca ◽  
Miha Purg ◽  
Janez Mavri ◽  
Jean C. Shih ◽  
Jernej Stare
Keyword(s):  
Monoamine Oxidase ◽  
Point Mutation ◽  
Molecular Simulation ◽  
Active Site ◽  
Monoamine Oxidase A ◽  
Substrate Molecule

The active site of monoamine oxidase A with a phenylethylamine substrate molecule and residue 335 subjected to mutation.

scholarly journals High-dose testosterone treatment reduces monoamine oxidase A levels in the human brain: a preliminary report

2021 ◽  
pp. 105381
Author(s):  
Georg S. Kranz ◽  
Marie Spies ◽  
Chrysoula Vraka ◽  
Ulrike Kaufmann ◽  
Eva-Maria Klebermass ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Human Brain ◽  
Preliminary Report ◽  
Monoamine Oxidase A ◽  
High Dose ◽  
Testosterone Treatment

Monoamine Oxidase A (MAOA) methylation in acrophobia: an epigenetic correlate of therapy response?

2019 ◽  
Vol 29 ◽  
pp. S203-S204
Author(s):  
M. Schiele ◽  
C. Ziegler ◽  
L. Kollert ◽  
A. Katzorke ◽  
D. Gromer ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Therapy Response ◽  
Monoamine Oxidase A

scholarly journals Association between monoamine oxidase A promoter polymorphism and the risk of sudden infant death syndrome: a meta-analysis

2021 ◽  
Author(s):  
Qiaoxia Zhou ◽  
Daoyin Gong ◽  
Yu Zhang ◽  
Feijun Huang
Keyword(s):  
Monoamine Oxidase ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Protective Factor ◽  
Meta Analysis ◽  
Variable Number Tandem Repeat ◽  
Sudden Infant Death ◽  
Monoamine Oxidase A ◽  
Sudden Infant ◽  
Increased Risk

Abstract Introduction The etiology of sudden infant death syndrome (SIDS) remains an unsolved problem. The aim of this meta-analysis is to investigate the potential association between monoamine oxidase A (MAOA) promoter variable number tandem repeat (VNTR) polymorphism and SIDS risk. Methods A systematic review and meta-analysis were conducted on studies from accessible electronic databases. Each VNTR variant was examined in each gender independently by comparing with the pooled results of other alleles. Results A total of six independent case–control studies including 1022 SIDS cases and 1839 controls were enrolled in this meta-analysis. In both of the whole populations and Caucasian populations, male infants with the low-MAOA-expression alleles (2R+3R) were found to exhibit a statistically significant increased risk of SIDS, whereas those with a 4R allele exhibited a reduced risk of SIDS. Besides, an increased risk of SIDS was detected in male Caucasian infants with 2R or 3R alleles. However, none of the allele or genotype variants was associated with SIDS in female victims. Conclusion In male Caucasian infants, the low expression of MAOA promoter VNTR alleles (2R and 3R) is associated with an increased risk of SIDS, and the existence of the 4R allele could be regarded as a protective factor.

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