Coreceptor Modification of Tcr Tyrosine Kinase Signals

Miceli, M Carrie

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: National Cancer Institute (NCI)
• Type: First Independent Research Support & Transition (FIRST) Awards (R29)
• Project #: 5R29CA065979-02
• Application #: 2109177
• Study Section: Experimental Immunology Study Section (EI)
• Project Start: 1994-12-08
• Project End: 1999-11-30
• Budget Start: 1995-12-01
• Budget End: 1996-11-30
• Support Year: 2
• Fiscal Year: 1996

Institution

• Name: University of California Los Angeles
• Department: Microbiology/Immun/Virology
• Type: Schools of Medicine
• DUNS #: 119132785
• City: Los Angeles
• State: CA
• Country: United States
• Zip Code: 90095

Publications

Chung, C D; Patel, V P; Moran, M et al. (2000) Galectin-1 induces partial TCR zeta-chain phosphorylation and antagonizes processive TCR signal transduction. J Immunol 165:3722-9

Vespa, G N; Lewis, L A; Kozak, K R et al. (1999) Galectin-1 specifically modulates TCR signals to enhance TCR apoptosis but inhibit IL-2 production and proliferation. J Immunol 162:799-806

Moran, M; Miceli, M C (1998) Engagement of GPI-linked CD48 contributes to TCR signals and cytoskeletal reorganization: a role for lipid rafts in T cell activation. Immunity 9:787-96

Lewis, L A; Chung, C D; Chen, J et al. (1997) The Lck SH2 phosphotyrosine binding site is critical for efficient TCR-induced processive tyrosine phosphorylation of the zeta-chain and IL-2 production. J Immunol 159:2292-300

Chung, C D; Lewis, L A; Miceli, M C (1997) T cell antigen receptor-induced IL-2 production and apoptosis have different requirements for Lck activities. J Immunol 159:1758-66