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Faculty Detail    
Name CATHERINE M FULLER
 
Campus Address VH 610 Zip 0019
Phone  (205) 934-6227
E-mail  fuller@physiology.uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Center  Cystic Fibrosis Research Center  Cystic Fibrosis Research Center Professor
Center  Nephrology Research & Training Center  Nephrology Research & Training Center Professor
Center  Center for Biophysical Sciences/Engineering  Center for Biophysical Sciences/Engineering Professor
Center  Ctr for Glial Bio in Med  Ctr for Glial Bio in Med Professor
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor
Secondary  Dept of Medical Education  Dept of Medical Education Associate Professor
Secondary  Cell Biology (Org Ret)  Cell Biology (Org Ret) Associate Professor

Graduate Biomedical Sciences Affiliations
Cancer Biology 
Integrative Biomedical Sciences 
Medical Scientist Training Program 
Neuroscience 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Cathy Fuller, Ph.D. (Associate Professor), received her B.Sc. (Hons.) degree from the University of London (1982), and her Ph.D. from the University of Liverpool (1985), in the laboratory of Prof. O.H. Petersen. She was a post-doctoral fellow in the laboratory of Dr. I. Schulz at the Max Planck Institut fur Biophysik (Frankfurt, Germany), from 1985-1988. She joined the Dept. of Physiology and Biophysics as a post-doctoral fellow in the laboratory of Dr. Dale J. Benos in 1988. She joined the faculty of the department in 1995.

Society Memberships
Organization Name Position Held Org Link
American Physiological Society  Steering Committee, Cell and Molecular Physiology Section  www.the-aps/org 



Research/Clinical Interest
Title
ENaC/ASIC Ion Channels;
Description
My lab is interested in the molecular mechanisms underlying the function of epithelial and astrocyte Na+ channels. These cell membrane proteins have important roles to play in the regulation of whole-body salt and water homeostasis, as well as in cell migration and proliferation in disease states such as cancer and renal disease. Current projects in the lab include analysis of ASIC/ENaC family members and their interaction with MAPK/ERK signaling pathways with relevance to migration and proliferation in gliomas, trafficking of these channel subunits in gliomas and their role in lipid rafts, and the role of a novel ENaC/ASIC chnnel in polycystic kidney disease. We use techniques such as fluorescence imaging, RT-PCR, site-directed mutagenesis and electrophysiology.

Selected Publications 
Publication PUBMEDID
Kapoor, N., Lee, W., Clark, E, Bartoszewski, R., McNicholas, C.M., Latham, C., Bebok, Z., Parpura, V., Fuller, C.M., Palmer, C., Benos, D.J. Acidosis increases ASIC1 plasma membrane expression in glioblastoma multiforme. Am. J. Physiol. Cell Physiol. 300: C1246-C1259, 2011. Selected for “Highlights from the Literature” Editorial Section in Physiology
 
21346156 
Clark, E.B., Jovov, B., Rooj, A.K., Fuller, C.M., and Benos, D.J. Proteolytic cleavage of the human acid-sensing ion channel 1 by the serine protease matriptase. J. Biol. Chem. 285:27130-27143, 2010.  20601429 
Qadri, Y.J., Y. Song, C.M. Fuller, and D.J. Benos. Amiloride docking to acid-sensing ion channel 1. J. Biol. Chem. 285:9627-9635, 2010.  20048170 
Kapoor, N., R. Bartoszewski, Y.J. Qadri, Z. Bebok, J.K. Bubien, C.M. Fuller, and D.J. Benos. Knockdown of ASIC1 and ENaC subunits inhibits glioblastoma whole cell current and cell migration. J. Biol. Chem. 284:24526-24541, 2009.  19561078 
Qadri, Y.J., B.K. Berdiev, Y. Song, H.L. Lippton, C.M. Fuller, and D.J. Benos. Psalmotoxin-1 docking to human acid-sensing ion channel 1. J. Biol. Chem. 284: 17625-17633, 2009.  19395383 
Bashari, E., Y.J. Qadri, Z.H. Zhou, N. Kapoor, S.J. Anderson, R.H. Meltzer, C.M. Fuller and D.J. Benos. Two PKC consensus sites on human acid-sensing ion channel 1b differentially regulate its function. Am. J. Physiol. 296: C372-C384, 2008.  19091960 
Vila-Carriles, W., Z.-H. Zhou, C.M. Fuller, and D.J. Benos. Participation of the chaperone Hsc70 in the trafficking and functional expression of ASIC2 in glioma cells. J. Biol. Chem (2007) 282:34381-34391  17878160 
Ross, S.B. C.M. Fuller, J.K. Bubien, and D.J. Benos. Amiloride and psalmotoxin-sensitive Na+ channels contribute to regulatory volume increases in high grade glioma cells. Am. J. Physiol. Cell Physiol. (2007) 293:C1181-C1185.   17615161  
Meltzer, R.H., N. Kapoor, Y.J. Qadri, S.J. Anderson, C.M. Fuller and D.J. Benos. Heteromeric assembly of ASIC and ENaC subunits in glioma. (2007) J. Biol. Chem. 282:25548-25559.  17613525 
Vila-Carriles, W., G. Gy. Kovacs. Y. Qadri, B. Jovov, Z.-H. Zhou, A.K. Pahwa, G. Colby, O. Esimai, G.Y. Gillespie, T.B. Mapstone, J.M. Markert, C.M. Fuller, J.K. Bubien, and D.J. Benos, Surface expression of ASIC2 inhibits the amiloride sensitive current and migration of glioma cells (2006) J. Biol. Chem. 281, 19220-32  16704974  
Kovacs, G. Gy., A. Zsembery, S.J. Anderson, P. Komlosi, G.Y. Gillespie, P.D. Bell, D.J. Benos, and C.M. Fuller. (2005) Changes in intracellular calcium and pH in response to thapsigargin in human glioblastoma cells and normal astrocytes. Am. J. Physiol. Cell 289:C361-C371  15800052  
Bubien, J.K., H.-L. Ji, G. Y. Gillespie, C.M. Fuller, J.M. Markert, T.B. Mapstone, and D.J. Benos. (2004) Cation selectivity and inhibition of malignant glioma Na+ channels by Psalmotoxin 1. Am J Physiol: Cell 287:C1282-C1291  15253892  
Berdiev, B.K., B. Jovov, H.L. Ji, R. Ganeshan, W. Tucker, A.P. Naren, C.M. Fuller, E.R. Chapman, K.L. Kirk, and D.J. Benos. (2004) ENaC subunit-subunit interactions and inhibition by syntaxin 1A. Am. J. Physiol. Renal 286: F1100-F1106  14996668  
Berdiev, B.K., J. Xia, L.-A. McLean, J.M. Markert, G. Y. Gillespie, T. B. Mapstone, A. P. Naren, B. Jovov, J.K. Bubien, H.-L. Ji, C. M. Fuller, K. L. Kirk, and D.J. Benos. (2003) Acid-sensing ion channels in malignant gliomas. J. Biol. Chem. 278:15023-15034.  12584187 

Keywords
Sodium channels, glioma, migration, proliferation, cancer, signaling, polycystic kidney disease