UV irradiation of cells elicits complicated cellular responses, called the stress response. Based on Preliminary Data, experiments are proposed to test the hypothesis that UV irradiation causes activation of membrane receptors such as the Fas receptor and TNF receptor I, which results in reduction of apoptosis that is analogous to Fas ligand and TNF2-induced apoptosis. Studies will test the hypothesis that UV irradiation induces apoptosis by activating Fas receptor and subsequent interaction with FADD as a pathway to UV-induced apoptosis. The subsequent role in activation of FLICE will be tested followed by investigation of the role of ICE-like proteases in UV-induced apoptosis. These studies will provide a detailed picture of the pathway for UV-induced apoptosis.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA078041-03
Application #
6137673
Study Section
Radiation Study Section (RAD)
Program Officer
Pelroy, Richard
Project Start
1998-01-01
Project End
2001-06-30
Budget Start
2000-01-01
Budget End
2001-06-30
Support Year
3
Fiscal Year
2000
Total Cost
$159,655
Indirect Cost
Name
University of Michigan Ann Arbor
Department
Radiation-Diagnostic/Oncology
Type
Schools of Medicine
DUNS #
073133571
City
Ann Arbor
State
MI
Country
United States
Zip Code
48109
Wu, Shiyong; Loke, Heather N; Rehemtulla, Alnawaz (2002) Ultraviolet radiation-induced apoptosis is mediated by Daxx. Neoplasia 4:486-92
Taneja, N; Tjalkens, R; Philbert, M A et al. (2001) Irradiation of mitochondria initiates apoptosis in a cell free system. Oncogene 20:167-77
Rehemtulla, A; Hamilton, A C; Taneja, N et al. (1999) A caspase-resistant form of Bcl-X(L), but not wild type Bcl-X(L), promotes clonogenic survival after ionizing radiation. Neoplasia 1:63-70