Abstract

Aim 1: Develop and Implement High-Throughput Kinase Assays for Monitoring the Signaling Response to DNA Damage.
Aim 2 : Monitor Kinase Localization, Cell Cycle Progression, and Apoptosis in Response to DNA Damage.
Aim 3 : Construct a Quantitative Predictive Systems Biology Model for Protein Kinase Network Responses During DNA Damage Signaling.
Aim 4. Utilize Knock-Out Mutant Analysis, shRNA Technologies, and Genetic Engineering in Cells and Mice to Test Hypotheses Generated from the Model and to Further Probe DNA Damage Signaling Networks.
Aim 5 - Discovery of New Kinase Substrates that Play Key Roles in the DNA Damage Response.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Specialized Center--Cooperative Agreements (U54)
Project #
5U54CA112967-05
Application #
7694417
Study Section
Special Emphasis Panel (ZCA1)
Project Start
Project End
Budget Start
2008-09-01
Budget End
2009-08-31
Support Year
5
Fiscal Year
2008
Total Cost
$419,885
Indirect Cost

  Institution

Name
Massachusetts Institute of Technology
Department
Type
DUNS #
001425594
City
Cambridge
State
MA
Country
United States
Zip Code
02139

  Publications

Kulkarni, Madhura; Tan, Tuan Zea; Syed Sulaiman, Nurfarhanah Bte et al. (2018) RUNX1 and RUNX3 protect against YAP-mediated EMT, stem-ness and shorter survival outcomes in breast cancer. Oncotarget 9:14175-14192
Oudin, Madeleine J; Barbier, Lucie; Schäfer, Claudia et al. (2017) MENA Confers Resistance to Paclitaxel in Triple-Negative Breast Cancer. Mol Cancer Ther 16:143-155
Bruno, Peter M; Liu, Yunpeng; Park, Ga Young et al. (2017) A subset of platinum-containing chemotherapeutic agents kills cells by inducing ribosome biogenesis stress. Nat Med 23:461-471
Werbin, Jeffrey L; Avendaño, Maier S; Becker, Verena et al. (2017) Multiplexed Exchange-PAINT imaging reveals ligand-dependent EGFR and Met interactions in the plasma membrane. Sci Rep 7:12150
Miller, Miles A; Sullivan, Ryan J; Lauffenburger, Douglas A (2017) Molecular Pathways: Receptor Ectodomain Shedding in Treatment, Resistance, and Monitoring of Cancer. Clin Cancer Res 23:623-629
Nagel, Zachary D; Kitange, Gaspar J; Gupta, Shiv K et al. (2017) DNA Repair Capacity in Multiple Pathways Predicts Chemoresistance in Glioblastoma Multiforme. Cancer Res 77:198-206
de Picciotto, Seymour; Dickson, Paige M; Traxlmayr, Michael W et al. (2016) Design Principles for SuCESsFul Biosensors: Specific Fluorophore/Analyte Binding and Minimization of Fluorophore/Scaffold Interactions. J Mol Biol 428:4228-4241
Lescarbeau, Rebecca S; Lei, Liang; Bakken, Katrina K et al. (2016) Quantitative Phosphoproteomics Reveals Wee1 Kinase as a Therapeutic Target in a Model of Proneural Glioblastoma. Mol Cancer Ther 15:1332-43
Miller, Miles A; Oudin, Madeleine J; Sullivan, Ryan J et al. (2016) Reduced Proteolytic Shedding of Receptor Tyrosine Kinases Is a Post-Translational Mechanism of Kinase Inhibitor Resistance. Cancer Discov 6:382-99
Lescarbeau, Rebecca S; Lei, Liang; Bakken, Katrina K et al. (2016) Quantitative phosphoproteomics reveals Wee1 kinase as a therapeutic target in a model of proneural glioblastoma. Mol Cancer Ther :

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