Institute for Biochemistry, Johannisallee 30, 04103 Leipzig, Faculty for Medicine

Prof. Dr. Torsten Schöneberg

In our recent research focus are newly identified neurotransmitter receptors of the G-protein-coupled receptor family (GPCRs).

GPCRs are involved in almost every physiologic process. More than 60% of all drugs influence function GPCR. Therefore, one can expect new physiologic insights and the identification of new therapeutic drug targets by analysing orphan GPCRs. Further, mutations in GPCRs can cause inherited human diseases such as obesity. Our lab diagnoses and analyses GPCR dysfunction in affected patients.

Specifically, we focus on orphan GPCR which are expressed in neuronal and immunologic relevant tissues. Here, biochemical, genetic and pharmacologic methods are used for basic research. The functional relevance of orphan GPCR is studies in transgenic animal models. Further, analysis of the evolutionary history of GPCR can provide valuable information about the functional relevance. Comparison of species can provide valuable information about the advantage or disadvantage of GPCR gain or inactivation in primates and humans. We expect from these studies new insights into mechanisms and specific reasons for gain and loss of GPCR-signalling abilities during evolution toward the human brain.

This project already benefits from ongoing collaborations with the groups of S. Pääbo (primate and population genetics) and A. Beck-Sickinger (GPCR) as well as from the strong local expertise in neurophysiology (J. Eilers, A. Reichenbach, P. Illes).

Fig.: Mutations in neuronal GPCR can cause deseases. Inactivating mutations in the hypothalamic melanocortin type 4 receptor cause an inherited form of obesity because of abnormal feeding behaviour. Left: normal mouse, right: mouse with a defect melanocortin type 4 receptor.