Projects
Eight funded projects
Non-canonical CXCR7 signaling mechanisms in in platelets
We aim to disclose the unknown molecular interacting partners in the non-canonical signaling cascade, by which physiological and pharmacological CXCR7 agonists increase cGMP production, and consequently stabilize cAMP levels in platelets and endothelial cells. In later stages of the project, we will analyze the role of CXCR7 in affecting cGMP and cAMP levels and thrombo-inflammation in vivo and validate the therapeutic efficacy of pharmacological CXCR7 agonists in venous thrombosis, which is primarily governed by vascular and thrombo-inflammatory complications. Thus, the planned investigations will uncover the role and therapeutic potential of non-canonical CXCR7 signaling in vascular pathophysiology.
Dissecting non-canonical from canonical Gαi-dependent pathways in ischemia- reperfusion injury
Cardiovascular diseases and stroke belong to the leading causes of death worldwide. After ischemia, the subsequent reperfusion process promotes a local inflammation mediated by infiltrating neutrophils and ROS, exacerbating tissue damage and leading to reperfusion injury. G protein signal transduction modulates cell recruitment into inflammatory tissue, however Gi-driven canonical vs. non-canonical contribution is still elusive..
Mode of action of the Gαi/ Gpsm2 and the RGS4 / neurabin complex in cochlear hair cells
During the development of the inner ear, Gai3 and its non-canonical regulator Gpsm2 play an essential role for orienting sensory hair cells. In addition, in the mature organ of Corti, Gai3 signalling is involved in protective mechanisms during noise trauma.
Modulation of heterotrimeric G protein activity by nucleoside diphosphate kinase
Nucleoside diphosphate kinases (NDPKs) form complexes with heterotrimeric G proteins and provide GTP for the activation of these signal transducers. Thus, their function as activator of G protein signaling (AGS) is investigated in this project.