Jonathan Allen Cohn, MD

Professor of Medicine
Associate Professor of Cell Biology
Professor in Pediatrics
Campus mail DUMC Box 3256, Durham, NC 27710
Phone (919) 684-6879
Email address jonathan.cohn@duke.edu

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.

Education and Training

  • Fellow in Gastroenterology, Medicine, Yale University, 1981 - 1984
  • Medical Resident, Medicine, University of California San Francisco, School of Medicine, 1980 - 1981
  • Medical Resident, Medicine, University of Alabama Birmingham, 1978 - 1980
  • M.D., Cornell University, 1978

Publications

Whitcomb, D. C., J. A. Cohn, and C. D. Ulrich. “Inherited diseases of the pancreas: Preface.” Medical Clinics of North America 84, no. 3 (January 1, 2000). https://doi.org/10.1016/s0025-7125(05)70236-4.

Full Text

Friedman, K. J., J. Kole, J. A. Cohn, M. R. Knowles, L. M. Silverman, and R. Kole. “Correction of aberrant splicing of the cystic fibrosis transmembrane conductance regulator (CFTR) gene by antisense oligonucleotides.” J Biol Chem 274, no. 51 (December 17, 1999): 36193–99. https://doi.org/10.1074/jbc.274.51.36193.

PMID
10593905
Full Text

Friedman, K. J., W. E. Highsmith, Z. Zhou, P. G. Noone, A. Spock, J. A. Cohn, L. M. Silverman, and M. R. Knowles. “D1152H: A common CFTR mutation associated with highly variable disease expression.” In American Journal of Human Genetics, 65:A295–A295. UNIV CHICAGO PRESS, 1999.

Scholars@Duke

Cohn, J. A., Z. Zhou, J. D. Bornstein, K. J. Friedman, P. S. Jowell, S. M. Branch, J. Baillie, L. M. Silverman, M. R. Knowles, and P. G. Noone. “CFTR mutations and idiopathic chronic pancreatitis.” Pediatric Pulmonology 28, no. SUPPL. 19 (September 1, 1999): 130–31.

Scholars@Duke

Cohn, J. A. “Is idiopathic chronic pancreatitis a form of cystic fibrosis?” Pediatric Pulmonology 28, no. SUPPL. 19 (September 1, 1999): 91.

Scholars@Duke

Cohn, J. A., and P. S. Jowell. “Are mutations in the cystic fibrosis gene important in chronic pancreatitis?” Surg Clin North Am 79, no. 4 (August 1999): 723–viii. https://doi.org/10.1016/s0039-6109(05)70038-4.

PMID
10470322
Full Text

Cohn, J. A., L. Chien, L. D. Howell, and J. Kole. “Heirarchical phosphorylation of CFTR serine-737.” In Gastroenterology, 116:A870–A870. W B SAUNDERS CO-ELSEVIER INC, 1999.

Scholars@Duke

Cohn, J. A., L. M. Silverman, and M. R. Knowles. “Mutations of the cystic fibrosis gene and pancreatitis - Reply.” New England Journal of Medicine 340, no. 3 (January 21, 1999): 239–239.

Scholars@Duke

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