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The Human Serotonin Type 3 Receptor Gene ( HTR3A‐E ) Allelic Variant Database
Author(s) -
Celli Jacopo,
Rappold Gudrun,
Niesler Beate
Publication year - 2017
Publication title -
human mutation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 162
eISSN - 1098-1004
pISSN - 1059-7794
DOI - 10.1002/humu.23136
Subject(s) - pharmacogenetics , biology , allele , phenotype , nausea , gene , genetics , bioinformatics , serotonin transporter , receptor , genotype , database , pharmacology , medicine , computer science
Serotonin type 3 (5‐HT 3 ) receptors are ligand‐gated ion channels formed by five subunits (5‐HT3A‐E), which are encoded by the HTR3A , HTR3B , HTR3C , HTR3D , and HTR3E genes. Functional receptors are pentameric complexes of diverse composition. Different receptor subtypes confer a predisposition to nausea and vomiting during chemotherapy, pregnancy, and following surgery. In addition, different subtypes contribute to neurogastroenterologic disorders such irritable bowel syndrome (IBS) and eating disorders as well as comorbid psychiatric conditions. 5‐HT 3 receptor antagonists are established treatments for emesis and IBS and are beneficial in the treatment of psychiatric diseases. Several case–control and pharmacogenetic studies have demonstrated an association between HTR3 variants and psychiatric and neurogastroenterologic phenotypes. Recently, their potential as predictors of nausea and vomiting and treatment of psychiatric disorders became evident. This information is now available in the serotonin receptor 3 HTR3 gene allelic variant database ( www.htr3.uni-hd.de ), which contains five sub‐databases, one for each of the five different serotonin receptor genes HTR3A ‐ E . Information on HTR3 variants, their functional relevance, associated phenotypes, and pharmacogenetic data such as drug response and side effects are available. This central information pool should help clinicians as well as scientists to evaluate their findings and to use the relevant information for subsequent genotype–phenotype correlation studies and pharmacogenetic approaches.