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Faculty Detail    
Name JAMES A SCHAFER
 
Campus Address MCLM 834 Zip 0005
Phone 205-934-7106
E-mail jschafer@uab.edu
Other websites http://www.physiology.uab.edu/Schafer.htm
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor Emeritus
Center  Cystic Fibrosis Research Center  Cystic Fibrosis Research Center Professor Emeritus
Center  Medicine  Nephrology Res & Trng Ctr Professor Emeritus

Biographical Sketch 
James A. Schafer (b. 1941) received B.S. (Biophysics, 1963) Ph.D. (Physiology, 1968) degrees from the University of Michigan. He joined UAB in 1970, following postdoctoral fellowships at Gustav-Embden Center, Frankfurt, Germany, and Duke University. Dr. Schafer received the second Robert F. Pitts Memorial Award from the International Union of Physiology in 1983, The Homer W. Smith Award of the American Heart Association and the American Society of Nephrology in 1993, Max-Planck Prize of the Max-Planck Society and the von Humboldt Foundation of Germany in 1994, and the Carl W. Gottschalk Distinguished Lectureship and Robert W. Berliner Awards of the American Physiological Society in, respectively, 2001 and 2003, all for excellence in renal physiology research. In 1995 he was elected to honorary membership in the American Society for Clinical Investigation. He has served as the editor of the American Journal of Physiology (1983-1989); as the secretary-treasurer of the American Society of Nephrology and Member of Council (1989-1992); and as the chair of the Research Committee of the National Kidney and Urologic Diseases Advisory Board, US Dept. of Health & Human Services. Dr. Schafer is a past president of the American Physiological Society (1996-1997) and served as a Member of Council (1992-1998). He also served on the Board, Executive Committee, and Public Affairs Executive Committee of FASEB (1995-1999).

Society Memberships
Organization Name Position Held Org Link
American Heart Association  Member  http://americanheart.org 
American Physiological Society  President
Member of Council 
http://www.the-aps.org/index.htm 
American Society of Clinical Investigation  Honorary Member  http://www.asci-jci.org/ 
American Society of Nephrology  Secretary-Treasurer
Member of Council 
http://www.asn-online.org/ 
Biophysical Society  Member  http://www.biophysics.org/ 
FASEB  Member of Board
Public Affairs Executive Committee 
http://faseb.org/ 
International Society of Nephrology  Member  http://www.isn-online.org 
International Union of Physiological Sciences  US delegate
Member 
http://iups.mcw.edu 

Research/Clinical Interest
Title
Regulation of Salt and Water Reabsorption by the Distal Nephron
Description
Research in our laboratory concerns the regulation of Na+ and water reabsorption, and K+ secretion, by the aldosterone-responsive segments of the nephron. Of particular interest is the interaction of the two hormones that are the primary regulators of salt and water reabsorption in this segment: vasopressin (AVP or ADH), which is secreted by the posterior pituitary, and aldosterone, a mineralocorticoid produced by the adrenal glands. We are also studying the effects of other autacoids in modulating the primary hormonal effects. Such autocoids include: epinephrine, norepinephrine, dopamine, natriuretic peptides, prostaglandins, and bradykinin. It appears that all of these substances ultimately regulate Na+ and water reabsorption, and K+ secretion, by determining the activity of corresponding channels in the luminal membrane of the collecting duct. Using physiological, biochemical, cellular, and molecular biological approaches, we are examining the effects of dietary salt intake and genotype on the expression of autacoid receptor isoforms and their intracellular second messengers as an approach to understanding possible etiologies of salt-dependent hypertension. We are also studying the regulation of the trafficking of the epithelial Na+ channel that is regulated by these hormones and autocoids. These studies use a surface labeling approach to determine the density of these channels in the apicalmembrane of cultured epithelial cells. These cells are produced by transfection with epitopically-tagged Na+ channel subunits using retroviral methodology, and are studied by electrophysiological techniques and radioactively-labeled antibodies to the epitopes.

Selected Publications 
Publication PUBMEDID
Schafer JA, Andreoli TE, and Weinstein A. Milestones in Nephrology: Fluid absorption and active and passive flows in the rabbit superficial pars rects. J. Am. Soc. Nephrol. 11:784-800, 2000. [Original publication of Schafer et al. Am. J. Physiol.-Renal Physiol. 233:F154-F167, 1977 republished as part of the series "Milestones in Nephrology" with commentaries.]  888957 
Schafer JA. Interaction of modeling and experimental approaches to understanding renal salt and water balance. Ann. Biomed. Eng. 28:1002-1009, 2000  11144661 
Schafer JA. Abnormal regulation of ENaC: syndromes of salt retention and salt wasting by the collecting duct. Am. J. Physiol. 283:F221-F235, 2002.   
Morris RG and Schafer JA. cAMP increases density of ENaC subunits in MDCK cells in direct proportion to amiloride-sensitive Na+ transport. J. Gen. Physiol. 120:71-85, 2002.   
Yoder BK, Tousson A, Millican L, Wu JH, Bugg CE, Jr., Schafer JA, and Balkovetz DF. Polaris, a protein disrupted in orpk mutant mice is required for the assembly of renal cilium. Am. J. Physiol. 282:F541-F552, 2002.   
Schafer JA, Li L, Sun D, Morris RG and Wilborn, TW.  Regulation of amiloride-sensitive Na+ channels in the renal collecting duct.  Current Topics in Membranes, 47:109-131, 1999.   
Sun D, Wilborn TW and Schafer JA. Dopamine D4 receptor isoform mRNA and protein is expressed in the rat cortical collecting duct. Am. J. Physiol. 275: F742-F751, 1998.   
Li, L and Schafer JA. Dopamine inhibits vasopressin-dependent cAMP production in the rat cortical collecting duct. Am. J. Physiol. 275: F62-F67, 1998   
Morris RG, Tousson A, Benos DJ and Schafer JA.  Microtubule disruption prevents an AVP-stimulated chloride secretion but not sodium reabsorption in A6 cells.   Am. J. Physiol. 274: F300-F314, 1998.   
Schafer JA.  Salt and water homeostasis:  Is it just a matter of good bookkeeping?  [Homer W. Smith Award Lecture at the American Society of Nephrology Meeting 1993.]  J. Am. Soc. Nephrol.   4: 1933-1950, 1994.   

Keywords
kidney physiology, epithelial transport, sodium, potassium, chloride