We are seeking a highly motivated, recent PhD or MD/PhD graduate to join the translational respiratory disease research team led by Drs. Blackburn and Karmouty-Quintana. Our research is focused on identifying novel molecular mechanisms involved in the pathogenesis of chronic lung disease, with an emphasis on studying the role of adenosine in acute and chronic lung injury. The research will involve the use of experimental models of disease, including transgenic mice, in vitro research, as well as studies utilizing isolated human lung tissue from patients with diverse diseases including COPD and IPF.
This is an exceptional opportunity for a highly talented and ambitious young investigator with a strong background in respiratory biology and/or nucleoside biochemistry. The successful applicant will be expected to make major discoveries related to molecular mechanisms involved in the pathogenesis of acute and chronic lung disease. Operating funds from the lab will fund the position; however, the successful candidate will be strongly encouraged to apply for a postdoctoral fellowship. Interested individuals with a recent PhD or MD/PhD, strong publication record and excellent academic credentials are encouraged to apply. Prior expertise in molecular biology, respiratory physiology/pharmacology and/or nucleoside biochemistry is desirable. The successful candidate will be expected to develop his/her own independent project within the interests of the team.
Please submit a cover letter, curriculum vitae, and the names and full contact information for three professional references. The cover letter should include a description of your previous research experience and long-term career goals. Electronic applications should be sent to email@example.com.
A central hypothesis of our laboratory is that the signaling nucleoside adenosine is an amplifier of lung inflammation and damage. Adenosine is generated in response to cell stress or damage and is therefore a byproduct of the inflammation and damage set-up by any number of initiators of lung inflammation. It is our belief that as adenosine levels increase in the lung, they access pathways that serve to promote airway inflammation and remodeling. Adenosine signals by engaging specific adenosine receptors on target cells such as mast cells, lymphocytes, eosinophils, macrophages, airway epithelial cells and smooth muscle cells. Most of the projects in my laboratory focus on understanding the mechanisms by which adenosine receptor signaling influences the activities of these cells in the context of lung inflammation and remodeling.
We make extensive use of genetically modified mice to examine the role of adenosine signaling in chronic lung disease. This includes knockout mice deficient in enzymes of adenosine metabolism, and knockout mice deficient in the various adenosine receptors. In addition, we utilize transgenic mice that overexpress components of adenosine signaling specifically in the lung. With these genetic tools we can assess the contribution of specific aspects of adenosine signaling in chronic lung diseases in the context of the whole animal.