Biomarker Variants of Dopamine Receptor Genes Influence the Binding Interaction Between Dopamine Receptor and Risperidone

多巴胺受体基因的生物标志物变异影响多巴胺受体与利培酮的结合相互作用

阅读:3

Abstract

INTRODUCTION: Risperidone is atypical antipsychotic medication commonly used to control behavioral symptoms in children with autism and widely considered a first-line treatment for acute and maintenance treatment of schizophrenia and bipolar mania. However, the response to risperidone is varied between patients due to genetic factors such as dopamine receptor genes. METHODS: Using state-of-the-art tools, the current study designed to predict the most deleterious SNPs of the five (DRD1, DRD2, DRD3, DRD4 and DRD5) dopamine receptors genes, and their impact on the function and structure of dopamine receptor protein and the binding with risperidone. In-silico tools such as SIFT, PolyPhen2, PANTHER, PROVEAN, SNPs & GO, CRAVAT-VEST score, Mutation Assessor, FannsDB-CONDEL score, predict SNP and SNAP2 were subjected to predicting the deleterious nature of 1581 non-synonymous SNPs (nsSNP) of dopamine receptors genes. RESULTS: The analysis predicted the most deleterious nsSNPs in each dopamine receptor: rs759268810 in DRD1, rs866976053 in DRD2, rs1274871399 in DRD3, rs745604469 in DRD4, and rs778635010 in DRD5. Significant reduction in the binding free energy in the mutant (F198C: S score = -7.29 kcal/mol) in the D2 subtype of the dopamine receptor compared to the wild (F198: S score = -8.73 kcal/mol) at the interaction analysis with risperidone. Cumulative analysis of the interaction between risperidone and dopamine receptor protein revealed the rs866976053 as the most deleterious nsSNP among the 1581 nsSNPs of the dopamine receptor genes. CONCLUSION: The observation of the state-of-the-art tools-based analysis and observations of MD simulations prioritized the F198C of DRD2 as a candidate variant for wet lab studies to find its impact on drug efficacy for managing autism, schizophrenia and bipolar mania.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。