anti-Monoamine Oxidase B (MAOB) Antibodies

Zebrafish Monoamine Oxidase B (MAOB) interaction partners

1. Conspecific alarm substance acutely elicits fear-induced aggression and decreases brain Z-MAO activity in WT and leo zebrafish populations. However, the reduced aggressive behavior could be associated to a decreased locomotion following the chronic exposure, which did not change Z-MAO activity.

2. Zebrafish MAO (zMAO) exhibits functional properties similar to human hMAO A as well as exhibits its own unique behavior.

3. expression, purification & characterization of zebrafish monoamine oxidase (zMAO) using Pichia pastoris expression system is described; zMAO possesses little differential sensitivity to acetylenic inhibitors than exhibited by either human MAO A & MAO B

4. this study confirm the presence of functionally active MAO in zebrafish brain and other tissues and characterize the neural systems that express MAO and areas of intense activity in the brain.

Human Monoamine Oxidase B (MAOB) interaction partners

1. The MAOB (rs1799836) polymorphism predicts putaminal dopamine turnover in early Parkinson's disease with the MAOB(TT) allele linked to high enzyme activity leading to higher intrinsic dopamine turnover, which has been demonstrated to constitute a risk factor for motor complications

2. elevated expression of MAOA and MAOB were found in epithelial and/or stromal components of human prostate hyperplasia samples compared with normal prostate tissues.

3. Study on the involvement of MAO-B in the constitutive expression of genes coding MAO, Bcl-2 and neurotrophic factors in human U118MG cell line. MAO-B might function as a repressor and MAO-A as a mediator in the constitutional expression of pro-survival genes, and that MAO-B and MAO-A might regulate different signal pathways for rasagiline and selegiline to induce neuroprotective genes.

4. levels of monoamine oxidase-B were, independently of gender, elevated in Alzheimer's disease patients (+52%; p=0.009) but unaltered in mild cognitive impairment compared to control subjects.

5. Resveratrol 4'-glucoside was the only compound which inhibited MAO-A, but itself, resveratrol 3-glucoside, and pterostilbene 4'-glucoside failed to inhibit MAO-B. Additional studies are needed to establish the effects of these compounds on MAO-A and/or MAO-B in humans

6. Our observations provide new information on the genotype-phenotype relations of MAOA/B and EFHC2 genes involved in the contiguous deletions of Norrie disease.Based on the case of our observation, contiguous deletion with only one of the MAO genes (MAOB) may not cause psychomotor disability, and deletion of EFHC2may not contribute to epilepsy.

7. the mean methylation values of the CpG sites studied in the MAOA gene were related to smoking behavior in women. Similarly, several methylation patterns in the MAOB gene were associated with a smoking history, with each CpG site showing a remarkable sex dependence. Smoking behavior seems to be related to the genetic and epigenetic profile of MAO genes, with considerable individual and sex-related differences

8. This study shows that MAO-B levels are increased not only in astrocytes but also in pyramidal neurons in Alzheimer disease brain and also suggests that MAO-B regulates Abeta production in neurons via gamma-secretase

9. The findings may suggest that MAO-B is an important sensor in iron-stressed neuronal cells.

10. Childhood trauma interacts with haplotypes in COMT, MAOA and MAOB, increasing risk for OCD.

11. brain protein levels of MAOB are normal or elevated in the three parkinsonian conditions-with MAOB increase generally associated with elevations in levels of astrocyte markers. Brain MAOA concentrations were, somewhat surprisingly, not decreased in Parkinson's disease, Progressive Supranuclear palsy or multiple system atrophy with the exception of the atrophic putamen in MSA, despite loss of dopamine neurons.

12. MAOA and MAOB variants may contribute to the etiology of Attention deficit hyperactivity disorder (ADHD) in the Indo-Caucasoid population and could be responsible for higher occurrence of ADHD in the boys.

13. MAOB gene variants are contributing to the etiology of ADHD in the Indo-Caucasoid population

14. This study suggests that MAOB increases ASD risk in males, possibly through its sex-specific regulatory effect on 5-HT metabolism and behavior.

15. These findings suggest an association of platelet MAO-B activity, but a lack of association of MAOB rs1799836 and MAOA-uVNTR, with selected psychotic symptoms in ethnically homogenous veterans with PTSD.

16. No significant association was found between severe agitation and MAOA uVNTR or MAOB rs1799836 polymorphism, revealing that these individual polymorphisms in MAO genes are not related to severe agitation in subjects with schizophrenia and conduct disorder. Higher platelet MAO-B activity was found in subjects with severe agitation vs. non-agitated subjects. Platelet MAO-B activity was not associated with MAOB rs1799836

17. we performed a meta-analysis in the Chinese population to provide comprehensive data on the association between the MAOB polymorphism and Parkinson's disease. Overall, no significant association was found between the MAOB A644G polymorphism and Parkinson's disease risk in the Chinese population.

18. inhibition of MAO-B using selegiline reversed the cigarette smoke-induced oxidative stress and inflammation in bronchial epithelial cells.

19. Monoamine oxidase B levels are highly expressed in gliomas.

20. The results of this meta-analysis suggest that people in the Asian population with the MAOB intron 13 A allele have an increased risk of Parkinson disease, especially when combined with the COMT LL genotype.

Pig (Porcine) Monoamine Oxidase B (MAOB) interaction partners

1. cloning and characterization of monoamine oxidase A and B genes in pig

Mouse (Murine) Monoamine Oxidase B (MAOB) interaction partners

1. mice lacking both MAO isoforms, MAOA and MAOB, exhibit smaller prostate mass and develop epithelial atrophy in the ventral and dorsolateral prostates.

2. findings thus support that AEP-mediated cleavage of alpha-Syn at N103 is required for the association and activation of MAO-B, mediating Parkinson's disease pathogenesis.

3. Hydralazine (Hdz) abrogated the degradation of tele-methylhistamine (tMH) catalyzed by monoamine oxidase B (MAO-B) in vitro.

4. Huntington disease neural cells exhibit increased Monoamine oxidase-A and Monoamine oxidases-B expression and activity

5. Activity of monoamine oxidase B in the striatum is reduced during the presymptomatic stage, but returns to the control level during the symptomatic stage of Parkinsonism in mice.

6. These findings demonstrate that regulation of monoamine levels by Mao activity in beta cells is pivotal for physiological insulin secretion and that loss of MaoB expression may contribute to the beta cell dysfunction in type 2 diabetes.

7. Monoamine oxidase B deficiency (along with monoamine oxidase A) resulted in an array of abnormalities similar to autism-spectrum disorder.

8. chronic elevations of monoamines, because of the absence of MAO A and MAO B, cause functional alterations that are accompanied with changes in the cellular mechanisms underlying learning and memory.

9. MAO-B is involved in the acute neurotoxicity of MPTP in embryonic and newborn mice

10. Data suggest that both IR1 (imidazoline receptor 1) and IR2/Maob play roles in acquisition of behavioral responses in alcoholism; activation of IR1 and IR2/Maob may serve as molecular targets in prevention (and possibly treatment) of alcoholism.

11. The results of our study further confirms that the dox-inducible astrocytic MAO-B transgenic mouse displays similar age-related behavioral and neuropathological features to other models of Parkinson's disease

12. MAO-B seems to exert a critical role in the development of postoperative and neuropathic pain

13. The temporal sequence of events following MAO-B elevation initially involves increased oxidative stress followed by mitochondrial complex I inhibition and finally neurodegeneration.

14. Data indicate that the activity of MAOB could modulate the regular and amphetamine-perturbed expression of GAD(67) and pCREB, and suggest interactions among the MAOB activity, GABA content of OlfB, and olfaction.

15. The findings of this study revealed novel roles for MAO-b and serotonin in the regulation of intermediate progenitor cells proliferation in the developing brain.

16. a monoamine-oxidase epigenetic regulation is involved in effects of smoking

17. these results suggest that MAO B deficiency may lead to behavioral disinhibition and decreased anxiety-like responses partially through regional increases of Phenylethylamine levels.

18. Observed chase/escape and anxiety-like behavior in the MAO A/B KO mice, different from MAO A or B single KO mice, suggest that varying monoamine levels result in both a unique biochemical and behavioral phenotype.

19. Moreover, MAOB is region-dependently involved in responses of the brain to Amph and baclofen, supporting interactions between GABA and monoamines.

20. Elevated astrocytic MAO-B mimicking age related increase resulted in specific, selective and progressive loss of dopaminergic neurons in the substantia nigra, accompanied by decreases in mt complex I activity and increased mt oxidative stress.