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John Kyriakis, Ph.D. |
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Professor of Medicine
Biochemistry
jkyriakis@tuftsmedicalcenter.org
Our laboratory studies signal transduction
pathways recruited by proinflammatory cytokines and growth
factors, and how these pathways affect inflammation, cardiac
pathology and cell proliferation. Our current studies focus
on three projects. First, we are examining the biological and
biochemical function and the regulation of the Ste20 homologue
germinal center kinase (GCK). GCK is required for the activation,
by pathogenic endotoxins, of the Jun-N-terminal kinases. Our
results indicate that GCK is activated by transient suppression
of the proteasomal degradation of the GCK polypeptide. Work
with gck-/- mice seeks to elucidate the role of GCK in sepsis.
In a second study, we are examining the MAPK-kinase-kinase
(MAP3K) mixed lineage kinase-3 (MLK3) and its role in the regulation
of Raf family MAP3Ks, and the inhibition of MLK3 by the neurofibromatosis-2
tumor suppressor. Finally, we have identified two transcripts,
p8 and gene 33 that are induced, respectively, in heart failure
and acute myocardial infarction. Our cellular studies suggest
that the p8 and Gene 33 proteins are important to the pathophysiology
of heart disease. Ongoing studies will determine the molecular
mechanisms by which p8 and Gene 33 function, as well as identify
in vivo roles for these proteins.
Visit the Kyriakis
research web site |
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