Molecular, Cellular & Developmental Biology; Member of
the Center for Neuroscience
Department of Molecular, Cellular & Developmental
Biology, Campus Box 347
Porter Biosciences Room B047
University of Colorado at Boulder
Boulder, CO 80309-0347
Dr. Han is an Associate Professor of Molecular, Cellular,
and Developmental Biology at the University of Colorado at
Boulder, an assistant investigator of the Howard Hughes Medical
Institute, a member of the Cancer Center at the University
of Colorado Health Sciences Center, Denver and Adjunct Professor
at Fudan University, Shanghai. He obtained his Ph.D. degree
in molecular biology at the University of California, Los
Angeles, with Michael Grunstein. He began his research on
Caenorhabditis elegans as a postdoctoral fellow with Paul
Sternberg at the California Institute of Technology. Dr. Han
was a Life Science Research Foundation fellow, a Lucille P.
Markey Scholar, a Searle Scholar and a Basil O'Connor Scholar.
Dr. Hans laboratory uses the nematode Carenorhabditis
elegans and mouse to study several basic biological problems
including mechanisms of Ras-mediated signal transduction and
its interaction with other regulatory pathways, control of
cell division, fusion, shape and movement during morphogenesis
and nuclear migration and anchorage. The laboratory has also
initiated a project to study the functions of lipid synthesis/metabolism
in development, behavior and human diseases. Research in his
laboratory is supported by funds from the Howard Hughes Medical
Institute and National Institute of Health.
Hanna-Rose, W. and Han, M. (2002). The Caenorhabditis elegans
EGL-26 protein mediates vulval cell morphogenesis. Devel.
Bio. 24, 247-258. (Cover)
Fay, D., Keneen, S. and Han, M. (2002) fzr-1 and lin-35/Rb
Function Redundantly to Control Cell Proliferation in C. elegans
as Revealed by a Nonbiased Synthetic Screen. Genes & Dev.
In press. (Cover)
Kniazeva, M., Sieber, M. McCauley. S. Zhang, K. Watts, J.,
Han, M. (2002). Suppression of C. elegans ELO-2 function results
in disruption of palmitic acid elongation and causes multiple
physiological defects including abnormal ultradian rhythms.