ArticleAlcoholism, clinical and experimental research2014
The expression of KLF11 (TIEG2), a monoamine oxidase B transcriptional activator in the prefrontal cortex of human alcohol dependence.
Article in Alcoholism, clinical and experimental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Results from a randomized controlled trial of zonisamide in the treatment of alcohol use disorder.Journal of psychiatric research · 2024Trial
- Effects of sex, treatment resistance, and antidepressant treatment on monoamine oxidase B total distribution volume.medRxiv : the preprint server for health sciences · 2026Article
- MAO-B status in alcohol use disorder: a [Molecular psychiatry · 2026Article
- Krüppel-Like Factors Modulate Susceptibility To Neuropsychiatric Disorders.Molecular neurobiology · 2025Review
- Type A monoamine oxidase; its unique role in mood, behavior and neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- CGRP causes anxiety via HP1γ-KLF11-MAOB pathway and dopamine in the dorsal hippocampus.Communications biology · 2024Article
- Development and Clinical Application of Positron Emission Tomography Imaging Agents for Monoamine Oxidase B.Frontiers in neuroscience · 2021Review
- Chronic Voluntary Ethanol Drinking in Cynomolgus Macaques Elicits Gene Expression Changes in Prefrontal Cortical Area 46.Alcoholism, clinical and experimental research · 2020Article
- The Antidepressant-like Effect of Flavonoids fromMolecules (Basel, Switzerland) · 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
- Binge ethanol exposure increases the Krüppel-like factor 11-monoamine oxidase (MAO) pathway in rats: Examining the use of MAO inhibitors to prevent ethanol-induced brain injury.Neuropharmacology · 2016Article
- 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
- Chronic Social Stress and Ethanol Increase Expression of KLF11, a Cell Death Mediator, in Rat Brain.Neurotoxicity research · 2015Article
- Evidence revealing deregulation of the KLF11-MAO A pathway in association with chronic stress and depressive disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundThe biochemical pathways underlying alcohol abuse and dependence are not well understood, although brain cell loss and neurotoxicity have been reported in subjects with alcohol dependence. Monoamine oxidase B (MAO B; an enzyme that catabolizes neurotransmitters such as dopamine) is consistently increased in this psychiatric illness. MAO B has been implicated in the pathogenesis of alcohol dependence and alcohol-induced brain neurotoxicity. Recently, the cell growth inhibitor protein, Kruppel-like factor 11 (KLF11), has been reported to be an MAO transcriptional activator. KLF11 is also known as TIEG2 (transforming growth factor-beta-inducible early gene 2) and mediates apoptotic cell death. This study investigates the protein expression of KLF11 and its relationship with MAO B using human postmortem prefrontal cortex from subjects with alcohol dependence.
methodsTwelve subjects with alcohol dependence and the respective psychiatrically normal control subjects were investigated. Expression of KLF11 and MAO B proteins in the prefrontal cortex was measured by Western blot analysis. Correlation studies involving KLF11 and MAO B protein expression were performed. Localization of KLF11 in the human prefrontal cortex was also determined by immunohistochemistry.
resultsLevels of KLF11 protein were significantly increased by 44% (p < 0.03) in the postmortem prefrontal cortex of subjects with alcohol dependence as compared to age- and gender-matched, psychiatrically normal control subjects. Furthermore, KLF11 levels were significantly and positively correlated with both the increased MAO B protein levels and blood alcohol content in alcohol-dependent subjects. In addition, KLF11 protein expression was visualized in both neuronal and glial cells.
conclusionsThis novel study shows the important role of KLF11, an MAO transcriptional activator, in human alcohol dependence. It further supports that the KLF11-MAO B cell death cascade may contribute to chronic alcohol-induced brain damage. This argues a case for KLF11-MAO B inhibition as a novel therapeutic strategy that may impact this highly prevalent illness.
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