Postdoctoral Fellow Position open in the Kuliopulos Lab at Tufts Medical Center in Boston, MA
We have a position immediately available for a Post-doctoral Fellow to work in the Kuliopulos Laboratory in the field of Metabolism and GPCR Pharmacology at Tufts Medical Center located in Boston.
Emerging evidence suggests that certain G protein-coupled receptors (GPCR) such as Protease-activated receptor-2 (PAR2) may play a pivotal role in inflammation, however, inappropriate PAR2 activity may underlie the pathogenesis of several diseases including metabolic disorders involving the liver and other organs. Our unique approach to controlling GPCR activity in these diseases is to use cell-penetrating pepducin technology. Pepducins can block virtually any receptor signaling pathway in animals affording the fellow a unique opportunity to study the role of poorly-understood signaling networks in inflammatory/metabolic disorders of the liver and other affected tissues. The post-doctoral fellow will investigate the molecular mechanism and (patho)physiologic relevance of PAR2 signaling in metabolic disorders and study their role(s) in the orchestration of signaling and disease progression.
The position requires excellent quantitative and analytical skills and experience with tissue culture techniques. Applicants with a strong background in pharmacology/biochemistry are preferred. Experience using in vivo animal models is desirable but not necessary.
Education and experience:
Qualifications for this position are a Ph.D.
To apply, please contact:
Athan Kuliopulos, MD, PhD
Professor of Medicine and Biochemistry
Director, Hemostasis and Thrombosis Laboratory
Tufts Medical Center, Box 7510
800 Washington Street
Boston, MA 02111
please visit http://jobs.tuftsmedicalcenter.org/ and search for “fellow MORI.”
Turning receptors on and off with intracellular pepducins: new insights into G-protein-coupled receptor drug development. O'Callaghan K, Kuliopulos A, Covic L. J Biol Chem. 2012 Apr 13;287(16):12787-96
Interdicting protease-activated receptor-2-driven inflammation with cell-penetrating pepducins. Sevigny LM, Zhang P, Bohm A, Lazarides K, Perides G, Covic L, Kuliopulos A. Proc Natl Acad Sci U S A. 2011 May 17;108(20):8491-6