The tumor suppressor Rb is functionally inactivated in most human, cancers and the consequent deregulation of E2F family members and their transcriptional targets is believed to be a crucial step in tumorigenesis. Based on their opposing transcriptional properties, the E2Fs can be divided into two classes: the activating E2Fs and the repressive E2Fs. There has been much debate about the relative roles of the activating versus repressive E2Fs in controlling the proliferation of both normal and tumor cells. Moreover, the role of these proteins in ES cell regulation has not yet been addressed. The goal of this proposal is to create a novel shRNA vector system that will enable inducible knockdown of multiple E2Fs in either cultured cells or mouse models. These studies will allow us to directly address the requirement of the activating E2Fs in ES cells, primary fibroblasts and in tumor development. Moreover, it will also provide a valuable vector resource to the community that can be used for efficient, simultaneous knockdown of genes of choice. ? ? ?

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32CA119625-01
Application #
7054877
Study Section
Special Emphasis Panel (ZRG1-F09 (20))
Program Officer
Jakowlew, Sonia B
Project Start
2006-07-01
Project End
2009-06-30
Budget Start
2006-07-01
Budget End
2007-06-30
Support Year
1
Fiscal Year
2006
Total Cost
$48,796
Indirect Cost
Name
Massachusetts Institute of Technology
Department
Internal Medicine/Medicine
Type
Schools of Arts and Sciences
DUNS #
001425594
City
Cambridge
State
MA
Country
United States
Zip Code
02139