A novel high-throughput in-cell Western assay for the quantitative measurement of signaling dynamics in DNA damage signaling networks : cell decision processes in response to DNA double strand breaks

Following exposure to DNA damage, cells initiate a stress response involving multiple protein kinase signaling cascades. The DNA damage response results in one of several possible cell-fate decisions, or cellular responses: induction of cell-cycle arrest, initiation of DNA repair, activation of transcriptional programs, and either apoptosis, necrosis or cell senescence. The mechanisms by which cells make these decisions, and how cell fate depends upon variables such as DNA damage type and dose, and other environmental factors, is unknown. The process by which cells select among alternate fates following such stimuli, or "cues" is likely to involve a dynamic, multi-variate integration of signals from each of the kinase signaling components. A major goal of signal transduction research is to understand how information flows through signal transduction pathways downstream of a given cue, such as DNA damage, and how signals are integrated, in order to mediate cellular responses. Mathematical modeling approaches are necessary to advance our understanding of these processes.

Department dc:contributor.department

Massachusetts Institute of Technology. Biological Engineering Division.

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2006

Author dc:creator

• Tentner, Andrea R. (Andrea Ruth)

Advisor dc:contributor.advisor

• Michael B. Yaffe.

• Biological Engineering Division.

Statement dc:rights

• MIT theses are protected by copyright. They may be viewed, downloaded, or printed from this source but further reproduction or distribution in any format is prohibited without written permission.

Licence dc:rights.uri

• http://dspace.mit.edu/handle/1721.1/7582

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/1721.1/34561

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/34561