Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM042388-05
Application #
2181333
Study Section
Allergy and Immunology Study Section (ALY)
Project Start
1990-07-01
Project End
1999-06-30
Budget Start
1996-07-01
Budget End
1997-06-30
Support Year
5
Fiscal Year
1996
Total Cost
Indirect Cost

  Institution

Name
Scripps Research Institute
Department
Type
DUNS #
City
La Jolla
State
CA
Country
United States
Zip Code
92037

  Publications

Field, K A; Apgar, J R; Hong-Geller, E et al. (2000) Mutant RBL mast cells defective in Fc epsilon RI signaling and lipid raft biosynthesis are reconstituted by activated Rho-family GTPases. Mol Biol Cell 11:3661-73
Frigeri, L; Apgar, J R (1999) The role of actin microfilaments in the down-regulation of the degranulation response in RBL-2H3 mast cells. J Immunol 162:2243-50
Apgar, J R (1997) Increased degranulation and phospholipase A2, C, and D activity in RBL cells stimulated through FcepsilonR1 is due to spreading and not simply adhesion. J Cell Sci 110 ( Pt 6):771-80
Apgar, J R (1995) Activation of protein kinase C in rat basophilic leukemia cells stimulates increased production of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate: correlation with actin polymerization. Mol Biol Cell 6:97-108
Apgar, J R (1994) Polymerization of actin in RBL-2H3 cells can be triggered through either the IgE receptor or the adenosine receptor but different signaling pathways are used. Mol Biol Cell 5:313-22
Ucker, D S; Obermiller, P S; Eckhart, W et al. (1992) Genome digestion is a dispensable consequence of physiological cell death mediated by cytotoxic T lymphocytes. Mol Cell Biol 12:3060-9
O'Rourke, A M; Mescher, M F; Apgar, J R (1992) IgE receptor-mediated arachidonic acid release by rat basophilic leukemia (RBL-2H3) cells: possible role in activating degranulation. Mol Immunol 29:1299-308
Apgar, J R (1991) Association of the crosslinked IgE receptor with the membrane skeleton is independent of the known signaling mechanisms in rat basophilic leukemia cells. Cell Regul 2:181-91