Jonathan Allen Cohn, MD


Professor of Medicine
Professor in Pediatrics
Associate Professor of Cell Biology
Department / Division:
Medicine / Medicine - Gastroenterology
Address:
466 Sands Bldg
Durham, NC 27710
Office Telephone:
(919) 684-6879
Training:
  • MD, Weill Cornell Medical College (New York), 1978
Residency:
  • Medicine, University of Alabama Medical Center, Birmingham, 1978-1980
  • Medicine, UCSF Medical Center (California), 1980-1981
Fellowship:
  • Gastroenterology, Yale Medical Center (Connecticut), 1981-1984
Research Interests:
In many epithelial tissues, the protein mainly responsible for controlling transepithelial fluid movement is the the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR was originally identified as the protein product of the gene causing cystic fibrosis (CF). CFTR functions as a chloride channel regulated by protein kinase A (PKA). This laboratory is studying the role and regulation of CFTR. One project focuses on how PKA acts on CFTR. In this project, recombinant peptide models are being used to model the cytoplasmic domains of CFTR responsible for activating the protein's chloride's chloride channel function. Site-directed mutagenesis is being used to produce modified peptides to study how different individual serine phosphoryation contribute to CFTR regulation. A second project concerns DF508, the most common mutation among patients with CF. This mutation affects CFTR function by preventing normal folding and intracellular trafficking of the newly synthesized mutant protein. This project is examining the mislocalization of DF508-CFTR in tissues and cell lines with the long term goal of developing strategies to prevent the mutant protein from mislocalizing. A third project concerns the role of CFTR in chronic pancreatitic diseases. Emerging data about the role of CFTR during normal pancreatic secretion suggests that dysfunction of this protein may lead to pancreatic diseases such as chronic pancreatitis and pancreatic cancer. Patients with these chronic pancreatic diseases are being tested for CFTR mutations and for evidence of defective CFTR function.
Representative Publications:
  • Noone, PG; Zhou, Z; Silverman, LM; Jowell, PS; Knowles, MR; Cohn, JA. Cystic fibrosis gene mutations and pancreatitis risk: relation to epithelial ion transport and trypsin inhibitor gene mutations. Gastroenterology. 2001;121:1310-1319.  Abstract
  • Cohn, JA; Friedman, KJ; Noone, PG; Knowles, MR; Silverman, LM; Jowell, PS. Relation between mutations of the cystic fibrosis gene and idiopathic pancreatitis. New England Journal of Medicine. 1998;339:653-658.  Abstract
  • Stutts, MJ; Canessa, CM; Olsen, JC; Hamrick, M; Cohn, JA; Rossier, BC; Boucher, RC. CFTR as a cAMP-dependent regulator of sodium channels. Science. 1995;269:847-850.  Abstract
  • Cohn, JA; Strong, TV; Picciotto, MR; Nairn, AC; Collins, FS; Fitz, JG. Localization of the cystic fibrosis transmembrane conductance regulator in human bile duct epithelial cells. Gastroenterology. 1993;105:1857-1864.  Abstract
  • Fitz, JG; Basavappa, S; McGill, J; Melhus, O; Cohn, JA. Regulation of membrane chloride currents in rat bile duct epithelial cells. Journal of Clinical Investigation. 1993;91:319-328.  Abstract
  • Cohn, JA; Nairn, AC; Marino, CR; Melhus, O; Kole, J. Characterization of the cystic fibrosis transmembrane conductance regulator in a colonocyte cell line. Proceedings of the National Academy of Sciences of USA. 1992;89:2340-2344.  Abstract
  • Marino, CR; Matovcik, LM; Gorelick, FS; Cohn, JA. Localization of the cystic fibrosis transmembrane conductance regulator in pancreas. Journal of Clinical Investigation. 1991;88:712-716.  Abstract
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