Adhesion is an important regulator of phagocyte function. The investigator's long-term goal is to understand how activation of phagocytes regulates integrin- mediated adhesion. Recent publications or work in press from the investigator's laboratory have demonstrated that l-plastin (LPL), an F actin-bundling protein, undergoes enhanced phosphorylation on Ser5 in response to cell activation. LPL phosphorylation is correlated with enhanced cellular aggregation and/or adhesion mediated by integrins. Peptides derived from the amino terminus of LPL mimic this effect and mutation of Ser5 abolishes this effect. The investigator hypothesizes that the state of LPL phosphorylation regulates integrin-mediated adhesion. The proposed studies include the determination of the mechanisms of LPL activation of integrin function, the determination of LPL interactions required for integrin activation, and the characterization of LPL knockout mice and cells.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI035811-07
Application #
6170085
Study Section
Special Emphasis Panel (ZRG2-IMS (02))
Program Officer
Kraemer, Kristy A
Project Start
1994-05-01
Project End
2004-04-30
Budget Start
2000-05-01
Budget End
2001-04-30
Support Year
7
Fiscal Year
2000
Total Cost
$224,232
Indirect Cost
Name
University of California San Francisco
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
073133571
City
San Francisco
State
CA
Country
United States
Zip Code
94143