Abstracts Keynote & Plenary

Chemistry and Biochemistry Department, UCLA, Los Angeles, CA 90095-1569
As nanoscale experiments continually shrink in size, the scale over which light moves becomes closer
and closer to molecular scale. At present, metal particles with a diameter of a few nanometers can be
fabricated and placed in arrays. We show that at these scales, molecules can have significant dipole
moment to stir the near-field light propagated between the molecules. This is an example of what we
label as nanopolaritonics, the combined action of metal plasmons and molecular excitations. The
versatility and controllability inherent in molecules, when combined with the large dipole moments
of
metal plasmons, can therefore be combined to stir and modulate light on the nano and sub-nano scale.
PL-010
In silico Modeling
of Wnt Signaling Pathway: Effects of GSK3� Phosphorylation, -catenin
Phosphorylation, and -catenin Degradation in Kinetics
Ying-Chieh Sun
Department of Chemistry,
National Taiwan Normal University, 88, TingChow Road Section 4, Taipei
116, Taiwan
Email address: sun@ntnu.edu.tw
Background
Recent experiments have explored effects of activities of kinases other than the well-studied kinase,
GSK3, in the signaling of wnt pathway, particularly in the level of -catenin. In addition, it was
found that the kinase PKA can attenuate degradation of -catenin. However, the role of these
kinases in the level of -catenin, degradation of -catenin, and the resulting downstream transcription
activity remains to be clarified. Furthermore, the effect of GSK3 phosphorylation in -catenin
level was not examined computationally. In the present study, effects of phosphorylation of GSK3,
�phosphorylations and degradation of -catenin in the kinetics of wnt signaling pathway were
examined computationally.
Methods
The well-known
computational Lee-Heinrich kinetic model of wnt pathway was modified to include
these effects. The rate laws of reactions in the modified model were solved numerically to examine
these effects in -catenin level.
Results
The computations
gave that the -catenin level is almost linearly proportional to the
phosphorylation activity of GSK3. The dependence of -catenin level on activity of
phosphorylation and degradation of free -catenin and downstream TCF activity can be analyzed
with an approximate, simple function of kinetic parameters of added reaction steps associated with
examined effects in order to rationalize observed experimental results.
Conclusions
The phosphorylations
of -catenin by kinases other than GSK3 should take place at free
unphorphorylated -catenin instead of the GSK3 -phosphorylated -catenin*. In order
to
account for observed enhanced TCF activity, the step of -catenin dephosphorylation is essential, and
the kinetic parameters of -catenin phosphorylation and degradation need to meet a condition,
describing in the text below. These findings should be useful for future experiments.
PL-011
Computational
Drug Design for Cancer Using Tubulin as a Target
Jack A. Tuszynski
Cross Cancer Institute,
Edmonton, Alberta, Canada