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email: mschneid@umaryland.edu
EDUCATION 1959-63 B.S., Biochemistry, Yale University
1963-65 No degree, Medicine, Tufts Medical School
1965-66 No degree, Physiology & Biophysics, University College,
London
1966-69 Ph.D. Physiology, Duke University POST GRADUATE EDUCATION 1969-72 Research Associate with Dr. W.K. Chandler
Yale University, Department of Physiology
New Haven CT
PROFESSIONAL EXPERIENCE
Faculty Appointments
1969-72 Research Associate in Physiology, Yale Medical
School
1972-78 Assistant Professor of Physiology
University of Rochester
1978-82 Associate Professor of Physiology, University of
Rochester
1979-80 Visiting Scientist
Neurobiol. Lab, Ecole Normale Superieure, Paris, France
1982-85 Assoc. Prof. of Physiology (unlimited tenure)
University of Rochester`
1984-85 Visiting Assoc. Prof. of Biological Chemistry
Univ. of Maryland at Baltimore
1985-88 Research Prof. of Biological Chemistry
Univ. of Maryland at Baltimore
1986- Full Member of Graduate Faculty
Univ. of Maryland at Baltimore
1988- Professor of Biological Chemistry (unlimited tenure)
Univ. of Maryland at Baltimore
1990- Professor of Biophysics Univ. of Maryland at Baltimore
1994- Director, Interdisciplinary Program in Muscle Biology Univ.
of Maryland at Baltimore and Univ. of Maryland Baltimore
County | 
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Associated Site : Interdisciplinary Training in Muscle Biology
Research Description
We are investigating the basic cellular, sub-cellular and molecular mechanisms underlying the generation and reversal of cytosolic Ca2+ signals and how the cytosolic Ca2+ signals in turn regulate a variety of cell functions over a time scale ranging from milliseconds to days. Our major emphasis is on intracellular Ca2+ movements in skeletal muscle fibers, where we are investigating mechanisms by which changes in the electrical voltage across the plasma membrane regulates calcium release channels in the intracellular sarcoplasmic reticulum during muscle activation and how the calcium binding sites and calcium transport systems in the muscle fiber function in the removal of the released Ca2+ during relaxation when release has halted. Monitoring of local subcellular changes in [Ca2+] both within the cytosol and within intracellular stores is being carried out using high spatio-temporal resolution digital and confocal fluorescence imaging using multiple simultaneous indicators in order to investigate the roles of local [Ca2+] in the function of skeletal muscle fibers as well as in neurons and various normal or transfected tissue cultured cell lines. The roles of Ca2+ ions and activity patterns in long term regulation of cell properties and gene expression is being studied using new procedures currently being developed in our laboratory for long term tissue culture, electrical stimulation and optical monitoring of [Ca2+] in cultured adult skeletal muscle fibers.
Selected Publications:
Liu, Y., Randall, W.R., and Schneider, M.F. (2005) Activity-depenedent and –independent nuclear fluxes of HDAC4 mediated by different kinases in adult skeletal muscle. J. Cell Biology. 168: 887-897 Rodney GG, Wilson GM and Schneider MF.(2005) A calmodulin binding domain of RyR increases activation of spontaneous Ca2+ sparks in frog skeletal muscle. J Biol Chem. 280:11713-11722 Cseresnyes, Z. and Schneider, M. F. (2004) Peripheral hot spots for local Ca2+ release after single action potentials in sympathetic ganglion neurons. Biophys. J. 86:163-181. Ward, C.W., Feng, W., Tu, J., Pessah, I.N., Worley, P.K., and Schneider, M.F. (2004) Homer protein increases activation of Ca2+ sparks in permeabilized skeletal muscle. J. Biol. Chem. 279:5791-5787 Schneider MF and Rodney GG.(2004) Peptide and protein modulation of local Ca2+ release events in permeabilized skeletal muscle fibers. Biol Res 37: 613-616. |
