This project seeks to understand the biological function of signaling molecules Pleiotrophin (PTN) and Midkine (MK). PTN and MK have proposed signaling functions in angiogenesis, oncogenesis, and chemotaxis. They are putative ligands for Anaplastic Lymphoma Kinase (ALK), a human proto- oncogene. The Drosophila homologue of ALK, DAIk, mediates visceral mesoderm development, and is activated by the secreted molecule Jelly belly (Jeb). The study seeks to elucidate the developmental roles of PTN and MK by examining the loss-of-function effects of Miple 1 and Miple 2, Drosophila homologues to PTN and MK, during embryogenesis. It will address three topics: the role of PTN and MK in DAIk-mediated visceral mesoderm development, the gain-of-function effects of PTN and MK, and the participation of PTN and MK in other developmentally required signaling pathways.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
1F31NS048764-01
Application #
6792520
Study Section
Special Emphasis Panel (ZRG1-F05 (20))
Program Officer
Finkelstein, Robert
Project Start
2004-06-15
Project End
2007-06-14
Budget Start
2004-06-15
Budget End
2005-06-14
Support Year
1
Fiscal Year
2004
Total Cost
$39,696
Indirect Cost
Name
Oregon Health and Science University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
096997515
City
Portland
State
OR
Country
United States
Zip Code
97239