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Faculty Detail Faculty Entry   
Name MARK OLIVER BEVENSEE  
Campus Address MCLM 812 Zip 0005
Phone 205-975-9084
E-mail bevensee@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:bevensee@uab.edu">bevensee@uab.edu</a>
URL http://138.26.61.118/depts/MEB/SOMResearchFaculty/currentfacultydata.asp?ID=mbevensee
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Civitan International Research Center  Civitan International Research Center Associate Professor
Center  General Clinical Research Center  Comprehensive Neuroscience Center Associate Professor
Center  Ctr for Glial Bio in Med  Ctr for Glial Bio in Med Associate Professor
Center  Medicine  Med - Nephrology Associate Professor
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Associate Professor
Secondary  Neurobiology  Neurobiology Assistant Professor

Biographical Sketch 
Dr. Mark Bevensee, Associate Professor, received his Ph.D. in 1996 from the laboratory of Dr. Walter F. Boron in the Department of Cellular and Molecular Physiology at Yale University. His postdoctoral work was also done at Yale under the direction of Dr. Boron. In the Fall of 2000, Dr. Bevensee joined the faculty at UAB.

Society Memberships
Organization Name Position Held Org Link
American Physiological Society  Member   
American Society for Biochemistry and Molecular Biology  Member   
American Society for Cell Biology  Member   
Society for Neuroscience  Member   
 

Research/Clinical Interest
Title
Cellular and Molecular Physiology of Acid-base Transporters and pH Regulation
Description
My laboratory is interested in the cellular and molecular physiology of intracellular pH (pHi) regulation and acid-base transport in tissues such as the brain, heart, and kidney. We are also interested in how acid-base transporters, as well as ion channels such as the epithelial Na+ channel (ENaC) contribute to Na+ hyperabsorption in mouse models of autosomal recessive polycystic kidney disease (ARPKD). Transporters that move acids (e.g., H+) or bases (e.g., bicarbonate or HCO3– ) across the plasma membrane of cells contribute to many cellular processes, including the regulation of pHi, secretion or reabsorption of ions, and modulation of neuronal activity. Some of these transporters include Na-H exchangers, electrogenic and electroneutral Na/HCO3 cotransporters, and Na-dependent and -independent Cl-HCO3 exchangers. In our cellular studies, we use fluorescence approaches with ion-sensitive dyes and electrophysiological techniques (e.g., patch-clamping) to identify and characterize the function and regulation of ion channels and transporters involved in ion movement and acid-base transport across plasma membranes. In our neuroscience research, we are also interested in the effects of pHi changes and transporter activity on neuronal firing. The laboratory is also elucidating the molecular nature of Na/bicarbonate cotransporters (NBCs) and related proteins present in brain, heart, and kidney. The laboratory is characterizing structure-function relationships, ion translocation, and regulation of the cloned proteins expressed in either frog oocytes impaled with microelectrodes, or transfected mammalian cells loaded with ion-sensitive dyes. Electrophysiological recordings from excised membrane patches from oocytes enable us to identify and characterize intracellular regulators of NBC activity. The results from our cellular and molecular studies will enhance our understanding of the physiology of pHi regulation and the biophysics of bicarbonate transport, as well as elucidate the contribution of acid-base transporters and ion channels to polycystic kidney disease.

Postdoc Positions Available
Date Posted Position Title
No records
 

Selected Publications 
Publication PUBMEDID
Current Topics in Membranes. Vol. 70. Co-transport Systems. MO Bevensee, ed. Amsterdam: Academic Press, 2012.   
Thornell IA, Wu J, Liu X & Bevensee MO (2012). PIP2 hydrolysis stimulates electrogenic Na/bicarbonate cotransporter NBCe1-B and -C variants expressed in Xenopus laevis oocytes. J. Physiol. 590: 5993-6011.  22966160 
Bevensee MO & Boron WF (in press). Control of Intracellular pH. In: Seldin and Giebisch's The Kidney: Physiology and Pathophysiology, Fifth Edition. RJ Alpern, M Caplan, OW Moe, eds. New York: Elsevier, Inc.   
Olteanu D, Liu X, Liu W, Roper VC, Sharma N, Yoder BK, Satlin LM, Schwiebert EM & Bevensee MO (2012). Increased Na+/H+ exchanger activity on the apical surface of a cilium-deficient cortical collecting duct principal cell model of polycystic kidney disease. Am. J. Physiol.: Cell. Physiol. 302: C1436-C1451.  22301060 
Majumdar D & Bevensee MO (2010). Na-coupled bicarbonate transporters of the Slc4 family in the nervous system: function, localization, and relevance to neurologic function. Neuroscience 171: 951-972.  20884330 
Lee S, Lee HJ, Park HJ, Yang HS, Thornell IM, Bevensee MO & Choi I (2010). Na/bicarbonate cotransporter NBCn1 in the kidney medullary thick ascending limb cell line is upregulated under acidic conditions and enhances ammonium transport. Exp. Physiol. 95:926-937.  20591978 
Wang W, Wu J, Bernard K, Li G, Wang G, Bevensee MO & Kirk KL (2010). ATP-independent CFTR channel gating and allosteric modulation by phosphorylation. Proc. Natl. Acad. Sci., U.S.A. 107:3888-3893.  20133716 
Wu J, McNicholas CM & Bevensee MO (2009). Phosphatidylinositol 4,5-bisphosphate (PIP2) stimulates the electrogenic Na/bicarbonate cotransporter NBCe1-A expressed in Xenopus oocytes. Proc. Natl. Acad. Sci., U.S.A. 106: 14150-14155.  19667194 
Majumdar D, Maunsbach AB, Shacka JJ, Williams JB, Berger UV, Schultz KP, Harkins LE, Boron WF, Roth KA & Bevensee MO (2008). Localization of electrogenic Na/bicarbonate cotransporter NBCe1 variants in rat brain. Neuroscience 155:818-832  18582537 
Bevensee MO & Boron WF (2008). Effects of hypoxia on intracellular-pH regulation in astrocytes cultured from rat hippocampus. Brain Res 1193C:143-152  18190894 
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Keywords
acid-base, bicarbonate, transporter, brain, fluorescence dyes, glia , heart, intracellular pH, microelectrodes, neuron, Xenopus oocyte, neuronal firing, kidney, polycystic kidney disease, epithelial sodium channel

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