Receptor tyrosine kinases (RTKs) form part of the mitogen response pathway involved in the signaling events that control both cell proliferation and differentiation. Mutations in RTKs or their intracellular signal transducer proteins are among the chief causes of oncogenic cell growth. Analysis of the potent actions of these mutant oncoproteins is essential to understanding the mechanics of oncogenesis. The experiments described in this proposal are focused on determining the role of ion channels as targets and physiological mediators of this signaling. We have shown in fibroblasts, that the expression of the oncogenic protein Ras, induces a small conductance, Ca2+ activated K+ channel (SK). Induction of SK channel expression via the activation of growth factor receptor tyrosine kinases known to activate normal Ras, correlates with regulation of cell proliferation. Such a role for K+ channels in mitogenesis could be shown to be an effective target for therapeutic drugs intended to inhibit or stimulate cell proliferation. Thus, the overall goal of this proposal is aimed to specifically analyze mitogenic signaling events in relation to the ion channel activities which they evoke.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31GM018523-02
Application #
2459289
Study Section
Minority Programs Review Committee (MPRC)
Project Start
1997-08-01
Project End
Budget Start
1997-08-01
Budget End
1998-07-31
Support Year
2
Fiscal Year
1997
Total Cost
Indirect Cost
Name
Purdue University
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
072051394
City
West Lafayette
State
IN
Country
United States
Zip Code
47907