DEPARTMENT OF PHYSIOLOGY AND BIOPHYSICS

Bio

CV

Research

Publications

 

 

 

 

   KEVIN L. KIRK, Ph.D.
Professor

  Email:  klkirk@uab.edu
  Telephone: 205.934.3122
  Fax: 205.975.9028
  Bldg/Room: MCLM 982B
Dr. Kevin L. Kirk, Professor, completed undergraduate studies in Psychobiology at Luther College in Decorah, Iowa (B.A., 1976) and did graduate work in Physiology and Biophysics at the University of Iowa (Ph.D., 1981). He came to UAB in 1981 as a postdoctoral fellow and joined the Department of Physiology and Biophysics in 1984.   Dr. Kirk has received several awards for his research including the Karlin Henze Memorial Award for Cystic Fibrosis Research; a Searle Scholar Award and an Established Investigatorship from the American Heart Association.
 

Research

Our research centers on the epithelial chloride channel (CFTR) that is encoded by the gene that is defective in cystic fibrosis. This chloride channel is implicated in two major human diseases: cystic fibrosis (low CFTR activity in lung) and secretory diarrhea (excessive CFTR activity in gut). We have identified novel CFTR binding proteins (e.g., SNAREs) that govern the functional activity of this chloride channel in epithelial tissues. In addition, we have identified several small molecules and dietary compounds that potently activate CF mutant channels.  Our goal is to define the mechanism and biologic relevance of each of these interactions with the hope that these projects will: (i) provide important insights into the basic functional and regulatory properties of the CFTR channel and (ii) lead to the development of new strategies for treating diseases such as cystic fibrosis.

 
 

Selected Publications

  • Wang W, K Bernard, G Li and KL Kirk.  Curcumin opens CFTR channels by a novel mechanism that requires neither ATP binding nor dimerization of the nucleotide binding domains.  J Biol Chem 282:4533-4544, 2007.

  • Wang W, C. Oliva, G Li, A. Holmgren, CH Lillig, and KL Kirk.  Reversible silencing of CFTR chloride channels by glutathionylation. J. General Physiol.  125:127-141, 2005.

  • Wang W, G Li, JP Clancy, and KL Kirk.  Activating CFTR channels with pore blocker analogs.  J. Biol. Chem.  280:23622-23630, 2005.

  • Cormet-Boyaka E, M Jablonsky, AP Naren, PL Jackson, DD Muccio, and KL Kirk.  Rescuing cystic fibrosis transmembrane conductance regulator (CFTR)-processing mutants by transcomplementation. Proc. Natl. Acad. Sci. USA 101:8221-8226, 2004.

  • Ganeshan R, A. Di, DJ Nelson, MW Quick and KL Kirk.  The interaction between syntaxin 1A and CFTR Cl- channels is mechanistically distinct from syntaxin 1A-SNARE interactions.  J. Biol. Chem. 278(5):2876-2885, 2003.

  • Cormet-Boyaka E, A Di, SY Chang, AP Naren, A Tousson, DJ Nelson and KL Kirk. CFTR chloride channels are regulated by a SNAP-23/syntaxin1A complex. Proc. Natl. Acad. Sci.  99(19):12477-12482, 2002.

  • Fu J, HJ Li, AP Naren and KL Kirk.  A cluster of negative charges at the amino terminal tail of CFTR regulates ATP dependent channel gating. J. Physiol. 536(2):459-470, 2001.

  • Fu J and KL Kirk. Cysteine scanning mutagenesis reveals dual regulatory roles of the amino terminal tail of CFTR in controlling ATP-dependent channel gating. J. Biol. Chem. 276(38):35668, 2001.