- Home
- About Us
- Divisions
- Adolescent and Young Adult Medicine
- Allergy and Immunology
- Blood and Marrow Transplantation and Cellular Therapies
- Cardiology
- Child Advocacy
- Emergency Medicine
- Endocrinology
- Gastroenterology, Hepatology and Nutrition
- General Academic Pediatrics
- Genetic and Genomic Medicine
- Health Informatics
- Hematology-Oncology
- Infectious Diseases
- Nephrology
- Neurology and Child Development
- Newborn Medicine
- Paul C. Gaffney Division of Pediatric Hospital Medicine
- Pulmonology
- Rheumatology
- Centers & Institutes
- Center for Pediatric Research in Obesity and Metabolism
- Center for Rare Disease Therapy
- Children's Neuroscience Institute
- Cystic Fibrosis Research Center
- Institute for Infection, Inflammation, and Immunity in Children
- Pediatric Asthma Center
- Pediatric Institute for Heart Regeneration and Therapeutics
- Richard King Mellon Foundation Institute for Pediatric Research
- Pittsburgh Vaccine Trials Unit
- The Pittsburgh Study
- Research
- Diversity
- Education
- Faculty Affairs
- News
- People
- Podcasts
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.