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post-doc opportunity - amyloid/apoptosis/gene expression

Steven Estus, Ph.D. sestus at aging.coa.uky.edu
Tue Jul 23 09:07:11 EST 1996


Postdoctoral position available to examine the molecular mechanisms
underlying neuronal apoptosis/necrosis. 

Our laboratory is focused on identifying genes induced in several model
systems, evaluating the "apoptotic" role of  genes already identified, and
elucidating the mechanisms leading to the gene inductions, with particular
emphasis on oxidative stress and kinase pathways.  Systems under analysis
include (i) a model of physiologically-appropriate programmed cell death
during development, i.e., NGF-deprived sympathetic neurons, (ii) a model
of physiologically-inappropriate neuronal death with potential disease
relevance, i.e., beta-amyloid treated primary cortical cultures, (iii)
models comparing oxidative-stressed induced apoptosis and necrosis, and, 
(iv) Alzheimers disease and control autopsy brain tissue.  This is an NIH
R01 funded position at a P50 Alzheimer Center, which has relevant
strengths in oxidative stress and neuronal death. Excellent opportunity to
work in a stimulating research area in a positive lab environment, and
live in an enjoyable college town.  Fax or email brief statement of
research interests, curriculum vitae, and names and addresses of three
references to Steven Estus, Ph.D., Center on Aging,  Univ. Kentucky,
Lexington, KY 40536, fax: (606) 323-2866, email: 
sestus at aging.coa.uky.edu.

Relevant Publications include:  

R. S. Freeman, S. Estus, K. Horigome, and E. M. Johnson, Jr.. Cell death
genes in 
        invertebrates and (maybe) vertebrates.  Curr. Opin. Neurobiology. 
3: 25-
        31 (1993).

R. S. Freeman, S. Estus, K. Horigome, and E. M. Johnson, Jr..  Analysis of cell 
        cycle-related genes in post-mitotic neurons:  selective induction
of cyclin D1 
        during programmed cell death.  Neuron  12 343-355 (1994).

S. Estus, W. J. Zaks, R. S. Freeman, M. Gruda, R. Bravo, and E. M.
Johnson, Jr..  
        Altered gene expression in neurons during programmed cell death; 
identification 
        of c-jun as necessary for neuronal apoptosis.  J. Cell Biol. 127:
1717-1727 
        (1994).

J. Ham, C. Babij, J. Whitfield, C.M. Pfarr, D. Lallemand, M. Yaniv, L.L.
Rubin.  A 
        c-Jun dominant negative mutant protects sympathetic neurons
against programmed 
        cell death.  Neuron 14: 927-939 (1995).

A. J. Anderson, C. J. Pike, C.W. Cotman.   Differential induction of
immediate early
        gene proteins in cultured neurons by ß-amyloid (Aß):  Association
of c-jun with
        Aß-induced apoptosis  J. Neurochem.  65: 1487-1498 (1995).

S. Estus, C. van Rooyen, M. Mattson, E.F. Brigham, and R.E. Rydel. 
Comparison of 
        altered gene expression during neuronal death induced by NGF
withdrawal, 
        amyloid ß-protein treatment, or glucose deprivation.  Soc.
Neuroscience Abs. 21:
        1721 (1995).



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