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The MAPK pathways regulate
cell proliferation, metastasis, and programmed
cell death (apoptosis). My goal is to
understand how drugs that modulate the ras
oncogene downstream pathways can selectively
modify these pathways to decrease tumor cell
proliferation or cause tumor cells to initiate
apoptotic cell death.
 
Current Publications
Janulis, M.,
Silberman, S., Ambegaokar, A., Gutkind, J.S.,
and Schultz, R.M., Role of the Mitogen‑Activated
Protein Kinases and c‑Jun/AP‑1 trans‑Activating
Activity in the Regulation of Protease mRNAs and
the Malignant Phenotype in NIH 3T3 Fibroblasts,
J. Biol. Chem 274, 801-813, 1999.
Qi, X., Borowicz1,
S., Pramanik, R. Schultz, R.M., Han, J., and
Chen, G., Estrogen receptor inhibits
c-Jun-dependent stress-induced cell death by
binding and modifying c-Jun activity in human
breast cancer cells, J. Biol. Chem.
279, 6769-6777, 2004.
Qi, X., Tang,
J., Pramanik, R., Schultz,
R.M., Shirasawa, S., Sasazuki,
T., Han, J., and Chen, G., p38 MAPK
activation selectively induces cell death in K-ras
mutated human colon cancer cells through
regulation of vitamin D receptor, J. Biol.
Chem, 279, 22138-22144, 2004.
Schultz, R.M.,
“Cell Cycle, Apoptosis and Cancer" in
Textbook of Biochemistry with Clinical
Correlations, 6th Ed., (T. Devlin, ed.), New
York, John Wiley and Sons, in press, 2005.
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