ArticlePloS one2013
A DNA element regulates drug tolerance and withdrawal in Drosophila.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Receptors and Channels Associated with Alcohol Use: Contributions fromNeuroscience insights · 2021Review
- Mechanisms Underlying the Risk to Develop Drug Addiction, Insights From Studies inFrontiers in physiology · 2018Review
- Genetics and genomics of alcohol responses in Drosophila.Neuropharmacology · 2017Review
- Behavioral Deficits Following Withdrawal from Chronic Ethanol Are Influenced by SLO Channel Function inGenetics · 2017Article
- Alcohol-Induced Neuroadaptation Is Orchestrated by the Histone Acetyltransferase CBP.Frontiers in molecular neuroscience · 2017Article
- Review
- A DNA element in the slo gene modulates ethanol tolerance.Alcohol (Fayetteville, N.Y.) · 2016Article
- Modulation of BK Channels by Ethanol.International review of neurobiology · 2016Review
- A histone modification identifies a DNA element controlling slo BK channel gene expression in muscle.Journal of neurogenetics · 2015Article
- How the Ganetzky lab drove me to alcohol.Journal of neurogeneticsArticle
- Article
- BK channels and alcohol tolerance: Insights from studies onMedicine internationalArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Drug tolerance and withdrawal are insidious responses to drugs of abuse; the first increases drug consumption while the second punishes abstention. Drosophila generate functional tolerance to benzyl alcohol sedation by increasing neural expression of the slo BK-type Ca(2+) activated K(+) channel gene. After drug clearance this change produces a withdrawal phenotype-increased seizure susceptibility. The drug-induced histone modification profile identified the 6b element (60 nt) as a drug responsive element. Genomic deletion of 6b produces the allele, slo (Δ6b), that reacts more strongly to the drug with increased induction, a massive increase in the duration of tolerance, and an increase in the withdrawal phenotype yet does not alter other slo-dependent behaviors. The 6b element is a homeostatic regulator of BK channel gene expression and is the first cis-acting DNA element shown to specifically affect the duration of a drug action.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.