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Faculty Detail Faculty Entry   
Name JAMES F COLLAWN  
Campus Address MCLM 395A Zip 0005
Phone 205-934-1002
E-mail jcollawn@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:jcollawn@uab.edu">jcollawn@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
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  Med - Nephrology Professor
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor
Secondary  Microbiology  Microbiology Associate Professor

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.

Postdoc Positions Available
Date Posted Position Title
12/28/2007  Postdoctoral Fellow 
Postdoctoral fellow to conduct research on trafficking of the CFTR protein in human airway epithelial cells. Experience in cell biology and biochemistry would be helpful.   
 

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 
Jurkuvenaite, A., Chen, L., Bartoszewski, R., Goldstein, R., Bebok, Z., Matalon, S., and Collawn, J. F. (2010) Functional stability of rescued DeltaF508 Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) in Airway Epithelial Cells. Am J Respir Cell Mol. Biol. 42:363-72.   19502384 
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 
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 
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 
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 
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 
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Keywords
Cystic Fibrosis; Endocytosis; Protein Trafficking

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