Untersuchungen zur Hangover Funktion während der Entwicklung von Alkoholtoleranz und der zellulären Stressantwort

酒精耐受发展过程中的解酒功能和细胞应激反应的研究

• 批准号: 102110757
• 负责人: Professorin Dr. Henrike Scholz
• 金额: --
• 依托单位: AG Molecular Mechanisms of Addcitive Behaviors
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2009
• 资助国家: 德国
• 起止时间: 2008-12-31 至 2014-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/102110757?language=en
• 关键词: Untersuchungen; zur; Hangover; Funktion; hrend

The goal is to understand how a cellular stress pathway might cause changes in neuronal adaptation and how these changes in turn contribute to ethanol induced behavior. Previously we have identified the hangover mutant in Drosophila. This mutant develops reduced ethanol tolerance. By phenotypic and molecular genetic analyzing the hangover mutants we have shown that the behavioral response to ethanol is on the molecular level similar in part similar to a cellular stress response to heat and oxidative stress and involves the hangover gene (Scholz et al., 2005). Key questions to address now are whether the defects are developmental or directly caused by a cellular stress response to ethanol, to define the biochemical activities of the Hangover protein that are required for tolerance, to identify possible interaction partners and to identify target genes that are regulated by Hangover. With these analyses we want to gain insight into the mechanism by which Hangover acts on the cellular level to promote the development of tolerance.

目的是了解细胞应力途径如何导致神经元适应的变化以及这些变化如何促进乙醇诱导的行为。以前，我们已经确定了果蝇中的宿醉突变体。该突变体会降低乙醇的耐受性。通过表型和分子遗传分析宿醉突变体我们已经表明，对乙醇的行为反应在分子水平上，部分类似于与热应激和氧化应激的细胞应激反应相似，并且涉及宿醉基因（Scholz等，2005）。现在要解决的关键问题是缺陷是由于对乙醇的细胞应力反应而直接引起的，以定义耐受性所需的宿醉蛋白的生化活性，以识别可能的相互作用伴侣并识别受宿醉调节的靶基因。通过这些分析，我们希望深入了解宿醉在细胞水平上促进耐受性发展的机制。