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Vance
Lemmon , Ph.D.
Walter
G. Ross Chair in Developmental Neuroscience
Miami Project to Cure Paralysis
Professor
of Neurological Surgery
Lois
Pope LIFE Center, Room 4-16
1095 NW 14th Terrace
Miami, Florida 33136
Telephone: 305-243-6793
FAX: 305-243-3921
e-mail:
vlemmon@miami.edu
Vance
Lemmon Lab Web Site
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Curriculum Vitae:
| B.A. |
1973 |
Biology,
Revelle College, UCSD |
| Ph.D. |
1978 |
Anatomy,
Emory University |
| Postdoctorate
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1978-1981 |
Neurobiology
(with Alan Pearlman and David Gottlieb), Washington University,
St. Louis, MO |
| Assistant
Professor |
1981-1983 |
Anatomy,
MUSC, Charleston, SC |
| Assistant
Professor |
1983-1988 |
Neurobiology,
University of Pittsburgh |
| Associate
Professor |
1988-1995 |
Neurosciences,
CWRU, Cleveland, OH |
| Professor
|
1995-2003 |
Neurosciences,
CWRU, Cleveland, OH |
| Professor |
2003-present |
Neurological
Surgery, University of Miami |
Research
Interests:
L1 is a
neural cell adhesion molecule of the Ig superfamily. It was
identified independently in the 1970's and 1980's by several
labs,
mostly by people making monoclonal antibodies to neural tissue.
It's most striking feature is its strong expression on axons
in the CNS and PNS. Early cell culture experiments from different
labs indicated that L1 was involved in axon growth. In 1987
Carl Lagenaur and I showed that purified L1 was a potent promoter
of axon growth. These observations have led many investigators
to study L1 in development and in nerve regeneration. Indeed
it has been implicated in a variety of systems and processes,
including neural cell migration, learning and neural plasticity.
The discovery that mutations in the L1 gene caused X-linked
hydrocephalus, confirmed the importance of L1 for brain development.
As a result, along with NCAM, L1 is one of the best studied
neural CAMs.
For the past 10 years my lab has focused on understanding how
the L1 cytoplasmic domain is involved in L1 function. We are
convinced that L1 is not simply a passive sticky material that
glues axons together or to other cells. Rather it has important
signaling properties critical for axon growth and guidance.
The L1 cytoplasmic domain binds to several cytoplasmic proteins
that are critical in this process and these include cytoskeletal
components and proteins involved in protein trafficking as well
as kinases and phosphatases. Cell biological, biochemical and
molecular studies are in progress to further our understanding
of these phenomena.
At the Miami
Project to Cure Paralysis we are also using advanced molecular
biological approaches combined with in vivo experimentation
to study how axons grow long distances through the adult central
nervous system in the hopes of identifying molecules that can
help promote regeneration in damaged spinal cords.
Selected
Publications:
A.W.
Schaefer, Y. Kamei, H. Kamiguchi, E.V. Wong, I. Rapoport, T.
Kirchhausen, C.M. Beach, G. Landreth, S.K. Lemmon, V. Lemmon.
(2002) L1 endocytosis is controlled by a phosphorylation-dephosphorylation
cycle stimulated by outside-in signaling by L1. J.
Cell Biology, 157:1223-1232.
De Angelis, E., Brümmendorf, T., Cheng, L., Lemmon, V.,
and Kenwrick, S. (2001) Alternative use of a mini exon of the
L1 gene affects L1 binding to neural ligands. J.
Biol. Chem., 276:32738-32742.
Long, K.E., Asou, H., Snider, M.D., Lemmon, V. (2001) The role
of endocytosis in regulating L1-mediated adhesion. J.Biol.Chem.,
276:1285-1290.
Kamiguchi, H., Long, K.E., Pendergast, M., Schaefer, A.W., Rapoport,
I., Kirchhausen, T., Lemmon, V. (1998) The neural cell adhesion
molecule L1 interacts with the AP-2 adaptor and is endocytosed
via the clathrin-mediated pathway. J.Neurosci.,
18:5311-5321.
Last
updated August 28, 2003
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