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Validated All-in-One™ qPCR Primer for MAOB(NM_000898.4) Search again
Product ID:
HQP011008
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
-
Gene Description:
monoamine oxidase B
Target Gene Accession:
NM_000898.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The protein encoded by this gene belongs to the flavin monoamine oxidase family. It is a enzyme located in the mitochondrial outer membrane. It catalyzes the oxidative deamination of biogenic and xenobiotic amines and plays an important role in the metabolism of neuroactive and vasoactive amines in the central nervous sysytem and peripheral tissues. This protein preferentially degrades benzylamine and phenylethylamine.
Gene References into function
- X ray structure to 3 A resolution
- Substrates but not inhibitors alter the redox potentials of monoamine oxidases.
- Analysis of conserved active site residues in monoamine oxidase A and B and their three-dimensional molecular modeling
- Activation of human monoamine oxidase B gene expression by a protein kinase C MAPK signal transduction pathway involves c-Jun and Egr-1.
- Association of monoamine oxidase A gene polymorphism with Alzheimer's disease and Lewy body variant.
- a strong gender difference exists with respect to the modifying effect of MAO-B genotype on the smoking association with parkinson disease
- MAO-B polymorphisms are associated with smoking behaviour
- study shows that the monoamine oxidase A structure is "more flexible" than that of monoamine oxidase B and that clorgyline and pargyline inactivation increase structural stability of both enzymes
- There was no interaction of smoking and the G allele and risk of Parkinson disease.
- molecular models and binding sites of inhibitors
- MAO B gene expression is selectively induced by a decreased Sp3/Sp1 ratio and reduced DNA methylation
- The 1.7-A structure of the reversible isatin-MAO-B complex has been determined; it forms a basis for the interpretation of the enzyme's structure when bound to either reversible or irreversible inhibitors.
- MAO-B elevation was found to abolish the spare alpha-ketoglutarate dehydrogenase threshold capacity, which can normally be significantly inhibited before it affects maximal mitochondrial oxygen consumption rates.
- Smoking is associated with low platelet MAO activity not only because of the direct inhibitory effect of tobacco constituents on the enzyme, but also because subjects with low platelet MAO activity are more likely to become smokers.
- The structural details of the interactions of the covalent 8alpha-S-cysteinyl-FAD with the protein moiety in monoamine oxidase B (MAO B) based on the MAO B crystal structure are described in this review.
- In the promoter region, a new polymorphism consisting of a C to T single base change was detected in position -1,114 from ATG, with an allelic frequency of 3.5%, but it was not associated with PD risK.
- (TGF)-beta-inducible early gene (TIEG)2 increased MAO B gene expression at promoter, mRNA, protein, and catalytic activity levels in both SH-SY5Y and HepG2 cells.
- Results show that I(2)-imidazoline receptor density and monoamine oxidase-B activity are only weakly correlated in platelets.
- No mutations found in platelets of patients with Huntington disease.
- There was no evidence of epistatic interaction between MAOA, MOAB, and COMT genes on Overt aggression scale scores.
- This review addresses several factors contributing to a possible role for MAO-B in normal brain aging and neurological disease.
- maoa and maob genes play important role in dopamine degradation.
- Low MAOB, and consequently expectedly high phenylethylamine levels in neonates is consistent with phenylketonuria in newborns (review)
- results are consistent with those of the hypothesis of MAO-B acting as a modifying gene in phenylketonuria
- Examination of the regional distribution of MAO-B revealed lower [(3)H]lazabemide binding to MAO-B in the lateral and basal nuclei of the amygdala and higher binding in the medial nucleus
- This longitudinal analysis provides preliminary evidence that changes in platelet MAO activity and cholesterol, which may reflect changes in central serotonergic activity are associated with attention deficit in adolescents.
- important component of the active site structure of hMAO A is the loop conformation of residues 210-216, which differs from that of hMAO B and rat MAO A
- ERs compete with ERRs for binding to the MAO-B promoter at selective AGGTCA motifs, thereby changing the chromatin status and cofactor recruitment to a repressed state.
- This study found a relationship between the A/G polymorphism in intron 13 of the MAO-B gene and intensity of postoperative pain in males. Higher average intensity of postoperative pain was detected in males with the G allele.
- Our results add to the evidence of involvement of MAOB in PD and suggest that the effect may be stronger in women.
- MAOB allele A was an independent factor predisposing to early onset of Parkinson's disease.
- After controlling for smoking, veterans with psychotic PTSD had significantly higher platelet MAO-B activity than veterans with or without PTSD, or healthy subjects.
- Results show that the two markers of lower serotonergic capacity, 5-HTTLPR S allele and low platelet MAO activity, have a similar and partly synergistic influence on self-reported as well as performance measures of impulsivity.
- MAOB A644G single nucleotide polymorphism is involved in the outcome of treatment with mirtazapine or paroxetine in females with major depression
- Analyzed the genotype distributions and allele frequencies for the MAO-A and MAO-B polymorphism of the MAO gene among the patients with fibromyalgia syndrome.
- this study provides the strongest evidence for the involvement of MAOB gene in the etiology of ADHD to date, at least in Han Chinese population
- These data suggest that the structural properties of the active site cavities in rat MAOs are significantly different from the two human enzymes, which correlates with the differences in the inhibitor specificities between human and rat MAOs.
- Variants in FGF20 and MAOB show evidence of statistical interactions and potential patterns of biological interaction contributing to Parkinson disease risk.
- an association in girls between low platelet MAO-B activity and symptoms of Oppositional Defiant Disorder.
- mechanistic studies of mofegiline inhibition of recombinant human monoamine oxidase B