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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  PhD 


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor
Secondary  Microbiology  Microbiology Professor
Center  Center for Biophysical Sciences/Engineering  Center for Biophysical Sciences/Engineering Professor
Center  Comp Arthritis, MSK, Bone & Autoimmunity Ctr  Comp Arthritis, MSK, Bone & Autoimmunity Ctr Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  Cystic Fibrosis Research Center  Cystic Fibrosis Research Center Professor
Center  GL Ctr for Craniofacial, Oral, & Dental Disorders  GL Ctr for Craniofacial, Oral, & Dental Disorders Professor
Center  General Clinical Research Center  Nephrology Research & Training Center 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 was an Established Investigator of the American Heart Association and Director of the Cell Biology Graduate Program from 2000 to 2017. He was an Associate Editor for the American Journal of Physiology-Lung Cellular and Molecular Physiology from 2011 to 2018 and is Vice-chairman of the Department of Cell, Developmental and Integrative Biology.

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
Serocki, M., Bartoszewska, S., Janaszak-Jasiecka, A., Ochocka, R. J., Collawn, J. F., and Bartoszewski, R. (2018) miRNAs regulate the HIF switch during hypoxia: a novel therapeutic approach. Angiogenesis 21(2):183-202.  29383635 
Bartoszewska, S., Kamysz, W., Jakiela, B., Sanak, M., Króliczewski, J., Bebok, Z., Bartoszewski, R., Collawn, J. F. (2017) miR-200b downregulates CFTR during hypoxia in human lung epithelial cells. Cell Mol Biol Letters 34:132-139. doi: 10.1016/j.coph.2017.09.013  29167681 
Solomon, G. M., Fu, Lianwu, Rowe, S., and Collawn, J. F. (2017) The therapeutic potential of CFTR modulators for COPD and other airway diseases. Current Opinion in Pharmacology doi: 10.1016/j.coph.2017.09.013.  29132121 
Bartoszewski, R., Matalon, S., and Collawn, J. F. (2017) Ion channels of the lung and their role in disease pathogenesis. Am. J. Physiol. Lung Aug 3:ajplung.00244.2017. doi: 10.1152/ajplung.00244.2017.  29025712 
Bartoszewski, R., Kroliczewski, J., Piotrowski, A., Janaszak-Jasieck, A., Bartoszewska, S., Vecchio-Pagan, Fu, L., Matalon, S., Cutting, G. R., Rowe, S. M., and Collawn, J. F. (2016). Codon bias and the folding dynamics of the cystic fibrosis transmembrane conductance regulator. Cell Mol Biol Letters 21(1):23, DOI 10.1186/s11658-016-0025-x.  28536625 
Sabusap, C. M., Wang, W., McNicholas, C. M., Chung, W. J., Fu, L., Wen, H., Mazur, M., Kirk, K. L., Collawn, J. F., Hong, J. S., and Sorscher, E. J. (2016) Analysis of cystic fibrosis-associated P67L illustrates barriers to personalized therapeutics for orphan diseases. JCI Insight 1(14):e86581, doi:10.1172/jci.insight.86581.  27660821 
Janaszak-Jasieck, A., Bartoszewska, S., Kochan, K., Kalinowski, L., Kamysz, W., Ochocka, R. J., Bartoszewski, R., and Collawn, J. F. (2016) miR-429 regulates the transition between Hypoxia-Inducible Factor (HIF)-1α and HIF-3α expression in human endothelial cells. Scientific Reports (Nature) doi: 10.1038/srep22775.  29954587 
Matalon, S., Bartoszewski, R., and Collawn, J. F. (2015) Role of epithelial sodium channels in lung fluid homeostasis. Am J Physiol Lung Cell Mol Physiol 309:L1229-38.  26432872 
Fu, L., Rab, A., Tang, L-P., Bebok, Z., Rowe, S., Bartoszewski, R., and Collawn, J. F. (2015) ΔF508 CFTR Surface Stability Is Regulated by DAB2 and CHIP-mediated Ubiquitination in Post-endocytic Compartments. PLoS One 10:e0123131.  25879443 
Lazrak, A., Fu, L., Bali, V., Bartoszewski, R., Rab, A., Havasi, V., Keiles, S., Kappes, J., Kumar, R., Lefkowitz, E. J., Sorscher, E. J., Matalon, S., Collawn, J. F., and Bebok, Z. (2013) The silent codon change, I507-ATC->ATT, contributes to the severity of the ΔF508 CFTR channel dysfunction. FASEB J. 27:4630-4645.  23907436 
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 
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 ∆F508 CFTR enhances the expression of the mutant protein. J. Biol. Chem. 285:28741-48.  20628052 
   

Keywords
Cystic Fibrosis; Endocytosis; Protein Trafficking, chymase, heart failure