Cell death plays a critical role in normal development and homeostasis as well as in disease. An essential aspect of cell death is the efficient and rapid removal of cell corpses by phagocytosis before toxic intracellular contents are released. My long-term goal is to elaborate molecular mechanisms of phagocytosis using the C. elegans model system. I will apply molecular and genetic approaches uniquely applicable in this system to: 1) Determine the roles of CD36 phagocytosis scavenger receptor homologues in elimination of necrotic and apoptotic cells 2) Focus on 1 receptor to determine its expression pattern and cellular focus of action 3) Use a novel genetic approach toward identification of new genes required for phagocytosis. Elimination of cell corpses is a component of autoimmune diseases, the clearing of necrotic damage following a stroke, and a complication of chemotherapy. The development of a model system to elaborate molecular mechanisms of cell corpse removal could lead to an understanding that significantly alters our approach in the treatment of these conditions.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
3F32NS010948-02S1
Application #
6446531
Study Section
Special Emphasis Panel (ZRG1 (01))
Program Officer
Behar, Toby
Project Start
2001-03-01
Project End
Budget Start
2001-03-01
Budget End
2002-02-28
Support Year
2
Fiscal Year
2001
Total Cost
$59,146
Indirect Cost
Name
Rutgers University
Department
Biochemistry
Type
Schools of Arts and Sciences
DUNS #
038633251
City
New Brunswick
State
NJ
Country
United States
Zip Code
08901