Ras protein, a guanosine triphosphatase (GTPase), is a molecular switch in signal transduction pathways that control cell growth and differentiation. In human cells, point mutations in crucial regions of ras can cause uncontrolled cell growth, or tumors. At least 30% of human cancers show that presence of mutationally activated ras. Structural studies of ras-GTP with its effectors and putative effectors will contribute greatly to the understanding of the molecular mechanism of the interaction and ras inhibitors design. Our studies on ras and RalGDS will enable us to further understand the structural basis for molecular communication in this system.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Biotechnology Resource Grants (P41)
Project #
5P41RR001209-23
Application #
6586733
Study Section
Project Start
2002-03-01
Project End
2003-02-28
Budget Start
Budget End
Support Year
23
Fiscal Year
2002
Total Cost
$143,176
Indirect Cost
Name
Stanford University
Department
Type
DUNS #
800771545
City
Stanford
State
CA
Country
United States
Zip Code
94305
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