Kathryn W. Peters, PhD

  • Research Assistant Professor

The overall goal of the proposed research is to understand the mechanisms that regulate the apical membrane density of the cystic fibrosis transmembrane conductance regulator (CFTR). The most common mutation, DF508, leads to endoplasmic reticulum associated-degradation (ERAD), production of an incompletely glycosylated CFTR, Band B, and inadequate numbers of mature CFTR, Band C, in the apical membrane. The initial challenge was the identification and characterization of CFTR2 mutants that produce Band C CFTR when co-expressed with PIAS4 (an E3 SUMO ligase) in the presence or absence of the corrector C18. Three categories emerged: intransigent (no Band C produced), throughput responsive (an increase in Band C less than Band B) and folding responsive (the increase in Band C greater than Band B). These results have expanded into three areas of investigation to aid in our understanding of the expression/degradation of CFTR in relation to its SUMOylation.  These goals include: identification of the SUMO paralog, including levels of expression, that contributes to surface CFTR; the roles of NHERF interactions with CFTR and their effect on SUMOylation; and the role of K1468 in SUMO modification. In addition to this career interest in cystic fibrosis research through the understanding of CFTR, is the intense gratification of teaching and guiding students to ask and answer questions in the laboratory. 

Professional and Scientific Society Memberships

  • Society of General Physiologists, 2000-2007
  • Association for Women in Science, 1992-1995
  • American Association for the Advancement of Science, 1990-1994



Education & Training

  • Dental Hygiene, University of Pittsburgh School of Dental Medicine, 1968
  • BS, Education, California University of Pennsylvania, 1973
  • BS, Biology, California University of Pennsylvania, 1986
  • MS, Biology, California University of Pennsylvania, 1988
  • PhD, California University of Pennsylvania, 1996
  • Cell Biology and Physiology, University of Pittsburgh, 1996-1999
  • Molecular Biology Summer Workshop, Smith College, 2003

Selected Publications

Liang, X., A.C. Da Paula, Z. Bozóky, H. Zhang, C.A. Bertrand, K.W. Peters, J.D. Forman-Kay, and R.A. Frizzell ( 2012 ). Phosphorylation-dependent 14-3-3 protein interactions regulate CFTR biogenesis. Mol. Biol. Cell. 23: 996-1009.

Liang, X., M.B. Butterworth, K.W. Peters, R.A. Frizzell (2010). AS160 modulates aldosterone stimulated epithelial sodium channel (ENaC) trafficking. Mol. Biol. Cell 21: 2024-2033.

Lewarchik, C.M., K.W. Peters, J. Qi, and R.A. Frizzell (2008). Regulation of CFTR trafficking by its R domain. J. Biol. Chem. 283: 28401-28412.

Liang, X., M.B. Butterworth, K.W. Peters, W.H. Walker, and R.A. Frizzell (2008). An obligatory heterodimer of 14-3-3β and 14-3-3ε is required for aldosterone regulation of the epithelial sodium channel. J. Biol. Chem. 283: 27418-27425.

Hill, W.G., M.B. Butterworth, H. Wang, R.S. Edinger, J. Lebowitz, K.W. Peters, R.A. Frizzell, and J. P. Johnson (2007). The epithelial sodium channel (ENaC) traffics to apical membrane in lipid rafts in mouse cortical collecting duct cells. J. Biol. Chem. 282: 37402-37411.

Moser, A.J., A. Gangopadhyay, N.A. Bradbury, K.W. Peters, R.A. Frizzell, and R.J. Bridges (2007). Electrogenic bicarbonate secretion by prairie dog gallbladder. Am. J. Physiol. 292: G1683-94.

Myerburg, M.M., M.B. Butterworth, E.E. McKenna, K.W. Peters, R.A. Frizzell, T.R. Kleyman, and J.M. Pilewski (2006). Airway surface liquid volume regulates ENaC by altering the serine protease-protease inhibitor balance: a mechanism for sodium hyperabsorption in cystic fibrosis J. Biol. Chem. 281: 27942-27949.

Kreindler, J.L., K.W. Peters, R.A. Frizzell, R.J. Bridges (2006). Identification and membrane localization of electrogenic sodium bicarbonate cotransporters in Calu- 3 cells. Biochim. Biophys. Acta. 1762: 704-710. Acta. 1762: 704-710.

Liang, X., K.W. Peters, M.B. Butterworth, and R.A. Frizzell (2006). 14-3-3 isoforms are induced by aldosterone and participate in its regulation of epithelial sodium channels. J Biol. Chem. 281: 16323-16332

Wang, H., L.M. Traub, K.M. Weixel, M.J. Hawryluk, N. Shah, R.S. Edinger, C.J. Perry, L. Kester, M. B. Butterworth, K.W. Peters, T.R. Kleyman, R.A. Frizzell, J.P. Johnson (2006). Clathrin-mediated endocytosis of the epithelial sodium channel. Role of epsin. J. Biol. Chem. 281: 4129-14135.

Full Publication List via NIH PubMed »