ArticleMolecular pharmacology2011
Transcription factor E2F-associated phosphoprotein (EAPP), RAM2/CDCA7L/JPO2 (R1), and simian virus 40 promoter factor 1 (Sp1) cooperatively regulate glucocorticoid activation of monoamine oxidase B.
Article in Molecular pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Effects of sex, treatment resistance, and antidepressant treatment on monoamine oxidase B total distribution volume.medRxiv : the preprint server for health sciences · 2026Article
- ICF syndrome: An epigenetic paradigm for primary immunodeficiencies.Journal of human immunity · 2026Review
- Activation of Genes by Nuclear Receptor/Specificity Protein (Sp) Interactions in Cancer.Cancers · 2025Review
- Reduced Platelet MAO-B Activity Is Associated with Psychotic, Positive, and Depressive Symptoms in PTSD.Biomolecules · 2022Article
- Molecular cloning, characterization, and functional analysis of the uncharacterized C11orf96 gene.BMC veterinary research · 2022Article
- Natural Products for the Treatment of Post-stroke Depression.Frontiers in pharmacology · 2022Review
- Article
- Development and Clinical Application of Positron Emission Tomography Imaging Agents for Monoamine Oxidase B.Frontiers in neuroscience · 2021Review
- Monoamine Oxidase B Total Distribution Volume in the Prefrontal Cortex of Major Depressive Disorder: An [11C]SL25.1188 Positron Emission Tomography Study.JAMA psychiatry · 2019Article
- Type A and B monoamine oxidases distinctly modulate signal transduction pathway and gene expression to regulate brain function and survival of neurons.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Repetitive transcranial magnetic stimulation inhibits Sirt1/MAO-A signaling in the prefrontal cortex in a rat model of depression and cortex-derived astrocytes.Molecular and cellular biochemistry · 2018Article
- Modulation of monoamine oxidase (MAO) expression in neuropsychiatric disorders: genetic and environmental factors involved in type A MAO expression.Journal of neural transmission (Vienna, Austria : 1996) · 2016Review
- Inhibition of Excessive Monoamine Oxidase A/B Activity Protects Against Stress-induced Neuronal Death in Huntington Disease.Molecular neurobiology · 2015Article
- Multiple cellular proteins interact with LEDGF/p75 through a conserved unstructured consensus motif.Nature communications · 2015Article
- Mutations in CDCA7 and HELLS cause immunodeficiency-centromeric instability-facial anomalies syndrome.Nature communications · 2015Article
- Chronic Social Stress and Ethanol Increase Expression of KLF11, a Cell Death Mediator, in Rat Brain.Neurotoxicity research · 2015Article
- Near-infrared fluorescence imaging of cancer mediated by tumor hypoxia and HIF1α/OATPs signaling axis.Biomaterials · 2014Article
- Monoamine oxidase A mediates prostate tumorigenesis and cancer metastasis.The Journal of clinical investigation · 2014Article
- Dynamics of the ternary complex formed by c-Myc interactor JPO2, transcriptional co-activator LEDGF/p75, and chromatin.The Journal of biological chemistry · 2014Article
- Mineralocorticoid receptor interaction with SP1 generates a new response element for pathophysiologically relevant gene expression.Nucleic acids research · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Glucocorticoid steroid hormones play important roles in many neurophysiological processes such as responses to stress, behavioral adaption, and mood. One mechanism by which glucocorticoids exert functions in the brain is via the modulation of neurotransmission systems. Glucocorticoids are capable of inducing the activities of monoamine oxidases (MAOs), which degrade monoamine neurotransmitters including serotonin, norepinephrine, phenylethylamine, and dopamine. However, the molecular mechanisms for such induction are not yet fully understood. Here, we report that dexamethasone, a synthetic glucocorticoid hormone, stimulates MAO B (an isoform of MAOs) promoter and catalytic activities via both the fourth glucocorticoid response element (GRE) and simian virus 40 promoter factor 1 (Sp1) binding sites in MAO B promoter. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation analysis demonstrated that glucocorticoid receptor binds to the fourth GRE in vitro and in vivo. Using Sp1-binding motifs as bait in a yeast one-hybrid system, we identified two novel transcriptional repressors of MAO B, E2F-associated phosphoprotein (EAPP) and R1 (RAM2/CDCA7L/JPO2), that down-regulate MAO B via MAO B core promoter, which contains Sp1 sites. EMSA suggested that EAPP and R1 competed with Sp1 for binding to the Sp1 site in vitro. Moreover, EAPP and R1 reduced Sp1-activated glucocorticoid activation of MAO B promoter. In response to dexamethasone, lower occupancy by EAPP and R1 and higher occupancy by Sp1 were shown at the natural MAO B core promoter. Together, this study uncovers for the first time the molecular mechanisms for glucocorticoid activation of MAO B gene and provides new insights into the hormonal regulation of MAO.
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