ArticleTranslational psychiatry2019
Identification of HIVEP2 as a dopaminergic transcription factor related to substance use disorders in rats and humans.
Article in Translational psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Extensive genetic interactions (epistasis) linked to alcohol use disorder in a high-risk population.Communications biology · 2026Article
- Transcription factors implicated in substance use disorder, from immediate early genes to altered gene expression.Brain research · 2026Review
- Adult-Onset Parkinsonism as Late Manifestation of HIVEP2-Associated Developmental Disorder.Movement disorders clinical practice · 2024Article
- Parental gonadossomatic mosaicism inFrontiers in genetics · 2023Article
- Transcriptome sequencing reveals circRNA expression profile in Parkinson's disease-like mice after aerobic exercise.Turkish journal of biology = Turk biyoloji dergisi · 2022Article
- Article
- Epistatic evidence for gender-dependant slow neurotransmission signalling in substance use disorders: PPP1R12B versus PPP1R1B.EBioMedicine · 2020Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Playing an important role in the etiology of substance use disorder (SUD), dopamine (DA) neurons are subject to various regulations but transcriptional regulations are largely understudied. For the first time, we report here that the Human Immunodeficiency Virus Type I Enhancer Binding Protein 2 (HIVEP2) is a dopaminergic transcriptional regulator. HIVEP2 is expressed in both the cytoplasm and nuclei of DA neurons. Therein, HIVEP2 can target the intronic sequence GTGGCTTTCT of SLC6A3 and thereby activate the gene. In naive rats from the bi-directional selectively bred substance-preferring P vs -nonpreferring NP rat model of substance abuse vulnerability, increased gene activity in males was associated with the vulnerability, whereas decreased gene activity in the females was associated with the same vulnerability. In clinical subjects, extensive and significant HIVEP2-SLC6A3 interactions were observed for SUD. Collectively, HIVEP2-mediated transcriptional mechanisms are implicated in dopaminergic pathophysiology of SUD.
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Registered trials
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