The Grimsey lab focuses on the impact of G protein-coupled receptor (GPCR) mediated non-canonical p38 Mitogen Activated Protein (MAP) kinase signaling in vascular inflammation, angiogenesis and chronic lung disease. Our laboratory fosters a collaborative working environment, taking a multidisciplinary approach to address our research goals. In addition to using primary human vascular cells, some of the key techniques currently used in the laboratory are live cell fluorescence imaging, in vitro and in vivo angiogenesis models, and the development of novel Fluorescence Resonance Energy Transfer (FRET) biosensors, inhibitor peptides and therapeutic biologics.
The p38 mitogen-activated protein kinase (MAPK) pathway is a key mediator of vascular inflammatory responses in lung disease and is an important drug target for the treatment of chronic obstructive pulmonary disease (COPD) and cancer. Despite the wealth of information available, it is still unclear exactly how p38 MAPK signaling pathways are regulated by many GPCRs, with current p38 targeted therapies having failed to meet clinical needs.
GPCRs and MAPK-dependent signaling pathways regulate many physiological and pathophysiological processes and are the principle targets of more than 50% of current therapeutics.
Our studies have revealed a novel mechanism for GPCR dependent activation of non-canonical p38 signaling. Defining how non-canonical p38 signaling is regulated will enable us to identify new strategies and alternative targets for drug development.
Our research focus is driven by two key questions: 1) How do cells regulate the spatiotemporal kinetics of signaling cascades? and 2) How can we harness these processes to treat chronic inflammatory diseases?
Molecular Biology, Cell Biology, Vascular Biology, Biochemistry, Bioinformatics, Live Cell Microscopy, Drug Discovery, Pharmacology, Cell Signaling.
