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Faculty Detail     Name JAMES F COLLAWN   Campus Address MCLM 395A Zip 0005 Phone 205-934-1002 E-mail jcollawn@uab.edu Other websites

Education Graduate  Medical University of South Carolina    1986  Ph.D.

Faculty Appointment(s) Appointment Type Department Division Rank Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor Secondary  Microbiology  Microbiology Associate Professor Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor Center  Center for AIDS Research  Center for AIDS Research Professor Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor Center  Cystic Fibrosis Research Center  Cystic Fibrosis Research Center Professor Center  Medicine  Nephrology Res & Trng Ctr Professor

Graduate Biomedical Sciences Affiliations Cell, Molecular, & Developmental Biology  Cellular and Molecular Biology Program  Medical Scientist Training Program  Microbiology  Pathobiology and Molecular Medicine

Biographical Sketch  James F. Collawn, Professor of Cell Biology, received his B.S. degree from the University of South Carolina and his Ph.D. degree in Biochemistry from the Medical University of South Carolina (1986). He completed his postdoctoral training in cellular immunology at The Scripps Research Institute and in cell biology at The Salk Institute in La Jolla, California. After working for two years as a Staff Scientist at The Salk Institute, Dr. Collawn joined the Department of Cell Biology in 1993. Dr. Collawn became an Established Investigator of the American Heart Association and Director of the Cell Biology Graduate Program in 2000.

Society Memberships Organization Name Position Held Org Link American Physiological Society

Research/Clinical Interest Title Role of ion channels in cystic fibrosis Description Our laboratory studies receptor-mediated endocytosis (RME) and protein trafficking. Our studies examine the polarized trafficking of two integral membrane proteins in epithelial cells, the transferrin receptor (TR) and the cystic fibrosis transmembrane conductance regulator (CFTR). TR is expressed in nearly all mammalian cells and its itinerary is well characterized by us and others. CFTR is a cAMP activated chloride channel and its transit through the secretory and endocytic pathways is just beginning to be understood. Cystic fibrosis (CF), the most common genetic disorder in the Caucasian population, results from defective processing or function of the CFTR protein. Therapeutic approaches have focused on increasing the amount or improving the function of defective CFTR at the apical membrane. However, until the exact physiological functions and trafficking pathways of wild-type CFTR have been characterized, such treatments remain only empirical. Using biochemical and physiological approaches, we are studying the cellular mechanisms that regulate wild-type CFTR biogenesis, endocytosis, recycling and function. We are also comparing the above features of the wild type protein to naturally-occurring CFTR mutants in order to understand the metabolic and functional defects in these proteins that result in a certain disease phenotype.

Selected Publications  Publication PUBMEDID Collawn, J. F., and Matalon, S. (2012) The role of CFTR in transepithelial liquid transport in pig alveolar epithelia. Am J Phyiol Lung Cell Mol Physiol. 303:L489-91.  22797251  Collawn, J. F., and Matalon, S. (2012) The role of CFTR in transepithelial liquid transport in pig alveolar epithelia. Am J Physiol Lung Cell Mol Physiol. 303:L489-91.  22797251  Collawn, J. F., Lazrak, A., Bebok, Z., and Matalon, S. (2012) The CFTR and ENaC Debate – How Important is ENaC in CF Lung Disease? Am J Physiol Lung Cell Mol Physiol. 302:L1141-6.   22492740  Bartoszewski, R., Brewer, J., Rab, A., Crossman, D. K., Bartoszewska, S., Kapoor, N., Fuller, C., Collawn, J. F., and Bebok, Z. (2011) The unfolded protein response (UPR)-activated transcription factor XBP1 induces micro-RNA-346 expression that targets the human antigen peptide transporter 1 (TAP1) mRNA and governs immune regulatory genes. J. Biol. Chem. 286:41862-70.   22002058  Fu, L., Rab, A., Tang, L. P., Rowe, S. M., Bebok, Z., and Collawn, J. F. (2012) Dab2 is a key regulator of endocytosis and post-endocytic trafficking of the cystic fibrosis transmembrane conductance regulator. Biochem J. 441:633-643.   21995445  Lazrak, A., Jurkuvenaite, A., Chen, L., Keeling, K. M., Collawn, J. F., Bedwell, D. M., and Matalon, S. (2011) Enhancement of alveolar epithelial sodium channel activity with decreased cystic fibrosis transmembrane conductance regulator expression in mouse lung. Am. J. Physiol Lung Cell Mol Physiol. 301:L557-567.   21743028  Bai, M., Gad, H., Turacchio, G., Cocucci, E., Yang, J-S., Li, J., Beznoussenko, G. V., Nie, Z., Luo, R., Fu, L., Collawn, J. F., Kirchhausen, T., Luini, A., and Hsu, V. W. (2011) ARFGAP1 promotes AP-2-dependent endocytosis. Nature Cell Biol. 13:559-67.  21499258  Bartoszewski, R., Rab, A., Fu, L., Bartoszewska, S., Collawn, J. F., and Bebok, Z. (2011) The unfolded protein response and its effect on CFTR expression. Methods in Enzymology 491:3-24.   21329791  Collawn, J. F., Fu, L., and Bebok, Z. (2010) Targets for cystic fibrosis therapy: proteomic analysis and correction of mutant cystic fibrosis transmembrane conductance regulator. Expert Rev. Proteomics 7:495-506.   20653506  Bartoszewski, R. A., Jablonsky, M., Bartoszewska, S., Stevenson, L., Dai, Q., Kappes, J., Collawn, J. F., and Bebok, Z. (2010) A synonymous single nucleotide polymorphism in DeltaF508 CFTR enhances the expression of the mutant protein. J. Biol. Chem. 285:28741-48.   20628052  First Prev   1 2 of  2  Next Last

Keywords Cystic Fibrosis; Endocytosis; Protein Trafficking

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