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Dr. Peter K. Lauf received his M.D. degree in 1960 at the University
of Freiburg, Germany after his thesis work under neurophysiologist
Paul Hoffmann and his successor Albrecht Fleckenstein. From 1960-1962,
he was Fellow at the Institute of Pathology at the University of Freiburg.
From 1962-1964, he was Research Fellow at the Max Planck Institute
of Immunochemistry (Otto Westphal) in Freiburg/Germany. From 1964-1967,
he was Research Associate at the Child Research Center of Michigan
in Detroit; 1966-67, Assistant Professor of Biochemistry at Wayne State
University. In 1968, he joined Dan Tosteson's Department of Physiology
and Pharmacology at Duke as Assistant Professor, where he became Associate
Professor in 1971 and Professor in 1978. In 1985, he accepted the Chair
of Physiology and Biophysics at Wright State University, which he held
until June 30, 2003. On July 1, 2003, he assumed his new position as
University Professor within the School of Medicine at Wright State
University. Dr. Lauf has over 300 publications, book chapters and abstracts,
his NIH-funded research is on erythrocyte cation transport system,
especially the Na/K pumps and the electroneutral K-Cl cotransporter.
During his career, he has trained numerous Ph.D.'s and postdoctoral
fellows. He has held visiting professorships in Germany, Japan, Sweden
and Australia, and joint appointments in the Department of Immunology
at Duke and in Physiology and Biophysics at the University of Cincinnati
College of Medicine. Dr. Lauf has received several awards such as an
NIH career award in 1971, the Golding Research Professorship at Wright
State in 1988, the 1998 Research Award from the Affiliate Society Council
of Engineering in Dayton, OH, and the University Professor Title at
Wright State University in 2003. In 1986, Dr. Lauf founded the Ohio
Physiological Society; he currently serves as member of the APS CAMP
Steering Committee, and of the Senior Physiologist Committee. Most
recently, he organized the III International Symposium on Cell Volume
and Signaling held at Wright State University in Dayton, Ohio.
Control of Erythrocyte Volume Through Membrane Transport Processes
Erythrocytes of all species maintain their cellular volume by active
transport of sodium (Na) and potassium (K) through specifically designed
pumps counteracting the constant dissipation of inward Na and outward
K gradients across their plasma membranes. Using various cellular models,
this laboratory has been studying for many years the properties of
Na/K pump fluxes, as well as the mechanisms by which K together with
chloride (Cl) leaves the cell through a cation-anion coupled transport
mechanism, the K-Cl cotransporter. More recently this laboratory's
research is attempting to shed further light on the kinetic and thermodynamic
properties of K-Cl cotransport because they reveal how the transporter
works, how ions bind and are translocated, and which is the nature
of the driving forces. It has been discovered that crucial thiol groups,
intracellular magnesium, as well as anions and protons are crucial
for the regulation of the K-Cl cotransporter's activity through regulatory
mechanisms such as enzymes and cofactors still to be revealed. Studies
are now in progress on the molecular identity of the K-Cl cotransporter
and its regulatory machinery through the use of pharmacological probes
such as inhibitors like loop diuretics, disulfonic stilbenes and quinolines,
and by molecular-biological techniques aimed at cloning and reconstituting
the protein macromolecules. Knowledge gained in these studies will
benefit the understanding of disorders of cell volume regulation in
general, and of processes leading to cellular dehydration through K-Cl
and water loss as it occurs in erythrocytes with genetically abnormal
hemoglobins such as hemoglobin S and C.
Selected Publications
K-C1 cotransport in vascular smooth muscle and erythrocytes: Possible
implication in vasodilation. N.C. Adragna, R.E. White, S.N. Orlof
and P.K. Lauf. Am. J. Physiol, Cell Pysiol. 278:C381-390,
2000.
Lithium inhibits swelling-activared K-C1 cotransport and reveals
a complete phosphatidylinositol cycle in low K sheep erythrocytes.
C. Ferrell, P.K. Lauf, B. Wilson,
and N.C. Adragna. Submitted to J. Memb Biology, 2000.
K-Cl Cotransport: Properties and Molecular Mechanism. P.K. Lauf, N.C.
Adragna. J. Cell Phys. and Biochem. 10:341-354, 2000.
Lithium and Protein Kinsase C. Moculators Regulate Swelling-Activated
K-Cl Cotransport and Reveal a Complete Phosphatidylinositol Cycle
in Low K Sheep Erythrocytes. C. Perrell, P.K. Lauf, B. Wilson,
and N.C. Adragna. J Memb. Biology, 177: 81-93, 2000.
K-Cl Cotransport: Immunohistochemical and Ion Flux Studies in Human
Embryonic Kidney (HEK293) Cells Transfected with Full-Length and
C-Terminal-Domain-Truncated KCCl cDNAs. P.K. Lauf, J. Zhang,
E. Delpire, R.E.W. Fyffe, and N.C. Adragna. Cellular Physiology
and Biochemistry.11:143-160, 2001.
Protein kinase G regulates the potassium-chloride cotransporter-3
(KCC3) expression in primary cultures of rat vascular smooth muscle
cells. M. Di Fulvio, T.M. Lincoln, P.K. Lauf, and N.C. Adragna. J.
Biol. Chem., 276:21046-21052, 2001.
Erthrocyte K-Cl Cotransport: Immunocytochemical and Functional
Evidence for More than One KCC Isoform in HK and LK Sheep Red Blood
Cells. P.K. Lauf, J. Zhang, E. Delpire, R.E.W. Fyffe, D.B.
Mount, N.C. Adragna. Comparative Biochemistry and Physiology, 130:
499-509, 2001.
K-Cl cotransport in vascular smooth muscle and erythrocytes: Possible implication
in vasodilation. N.C. Adragna, R.E. White, S.N. Orlof and P.K. Lauf. Am.
J. Physiol., Cell Physiol., 278:C381-390, 2000.
Lithium and Protein Kinase C Modulators Regulate Swelling-Activated K-Cl Cotransport
and Reveal a Complete Phosphatidylinositol Cycle in Low K Sheep Erythrocytes.
C. Ferrell, P.K. Lauf, B. Wilson, and N.C. Adragna. J. Memb. Biol,
177:81-93, 2000.
Erythrocyte K-Cl cotransport: immunohistochemical and ion flux studies in human
embryonic kidney (HEK293) cells transfected with full-length and C-terminal-domain-truncated
KCC1 cDNAs. P.K. Lauf, J. Zhang, E. Delpire, R.E.W. Fyffe, and N.C. Adragna. Cell
Physiol Biochem, 11:143-160, 2001.
Protein kinase G regulates the potassium-chloride cotransporter-3 (KCC3) e
xpression
in primary cultures of rat vascular smooth muscle cells. M. Di Fulvio, T.M. Lincoln, P.K.
Lauf, and N.C. Adragna. J. Biol. Chem., 276:21046-210552, 2001.
Nitric oxide signaling pathway regulates the postassium-chloride cotransporter-1
mRNA expression in vascular smooth muscle cells. M. Di Fulvio, P.K. Lauf,
and N.C. Adragna. J. Biol.Chem. 276:44534-44540, 2001.
Effect of GSH depletion on K-Cl cotransort and regulatory volume decrease in
high K/high GSH dog red blood cells. Fujise, H., Higa, K., Kanemaru, T., Fukuda,
M., Adragna, N.C., and P.K. Lauf. Am. J. Physiol. 281:C2003-C2009,
2001.
K-Cl Cotransport Regulation and Protein Kinase G in Cultured Vascular Smooth
Muscle Cells. N.C. Adragna, J. Zhang, M. DiFulvio, T.M. Lincoln, and P.K.
Lauf. J. Memb. Biol.187:157-165, 2002.
Platelet-Derived Growth Factor Regulates K-Cl Cotransport in Vascular Smooth
Muscle Cells. J. Zhang, P.K. Lauf, and N.C. Adragna. Am. J. Physiol.
Cell. 284:C674-C680, 2003.
NONOates regulate potassium-chloride cotransporter-1 and -3 mRNA expression in
vascular smooth muscle cells. M. DiFulvio, P.K. Lauf, S.Shah, and N.C.
Adragna. Am. J. Physiol., Heart Circulation Physiol, Jan. 9, 2003.
Research Projects
PROTEOMICS OF M-L ANTIGENS MODULATING CATION TRANSPORT
PRINCIPAL INVESTIGATOR
AGENCY: NIH 1 R21 DK064140
(7/1/03-6/30/05).
The major goal of this project is to use new proteomics technology to elucidate
the biochemical nature of the M-L antigens that are associated with monvalent
cation transport in sheep erythrocytes. This project deals with immunological
aspects of surface antigens and membrane transporters.
THIRD SYMPOSIUM ON
CELL VOLUME AND SIGNALING
PRINCIPAL INVESTIGATOR
AGENCY: NIH 1R13 DK064886-01
(7/1/03-6/30/04).
The major goal of this project is to manage the 3rd international symposium on
Cell Volume and Signaling.
ROLE OF ION TRANSPORTERS AND APOPTOSIS IN THE PATHOGENESIS OF HUMAN CATARACT
PRINCIPAL INVESTIGATOR
AGENCY: WRIGHT STATE UNIVERSITY SCHOOL OF MEDICINE
(5/1/03-4/30/04).
This project examines the involvement of membrane transporters in the origin
of lens cataract in humans. |
