Abstract
The H4R is the latest addition of the histamine receptor family. This GPCR was found to be involved in a multitude of allergic and inflammatory diseases. Antagonizing H4Rs results in profound anti-inflammatory effects in various animal disease models, and a first phase 2a clinical trial in patients suffering from atopic dermatitis has already been conducted.
In order to accelerate and expand current drug discovery at H4R, in-depth understanding of its molecular mechanisms and signaling pathways are key. Complexity of H4R signaling pathways was high- lighted by the discovery of so-called biased ligands, which can initiate differential efficacies in various GPCR responses. This chapter will provide an overview of commonly applied methods used to elucidate the molecular pharmacological aspects of the H4R from receptor-ligand-binding interactions to down- stream gene transcription.
In order to accelerate and expand current drug discovery at H4R, in-depth understanding of its molecular mechanisms and signaling pathways are key. Complexity of H4R signaling pathways was high- lighted by the discovery of so-called biased ligands, which can initiate differential efficacies in various GPCR responses. This chapter will provide an overview of commonly applied methods used to elucidate the molecular pharmacological aspects of the H4R from receptor-ligand-binding interactions to down- stream gene transcription.
| Original language | English |
|---|---|
| Title of host publication | Histamine receptors as drug targets |
| Editors | Ekaterini Tiligada, Madeleine Ennis |
| Publisher | Humana Press |
| Chapter | 6 |
| Pages | 157-181 |
| Number of pages | 26 |
| ISBN (Electronic) | 9781493968435 |
| ISBN (Print) | 9781493968411, 9781493983155 |
| DOIs | |
| Publication status | Published - 2017 |
Publication series
| Name | Methods in Pharmacology and Toxicology |
|---|---|
| Publisher | Humana Press |
| ISSN (Print) | 1557-2153 |
| ISSN (Electronic) | 1940-6053 |
Funding
The authors participated in the European COST Action BM0806. ECHO grant (711.013.014) of the Netherlands Organization of Scientific Research supported this work.
| Funders | Funder number |
|---|---|
| European Cooperation in Science and Technology | BM0806, 711.013.014 |
| Nederlandse Organisatie voor Wetenschappelijk Onderzoek |
