CR2, CD19, MEMBRANE Ig AND B CELL SIGNAL TRANSDUCTION

Cooper, Neil R.

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: National Institute of Allergy and Infectious Diseases (NIAID)
• Type: Research Project (R01)
• Project #: 3R01AI033244-02S1
• Application #: 3148332
• Study Section: Experimental Immunology Study Section (EI)
• Project Start: 1992-01-01
• Project End: 1996-12-31
• Budget Start: 1993-01-01
• Budget End: 1993-12-31
• Support Year: 2
• Fiscal Year: 1993

Institution

• Name: Scripps Research Institute
• City: La Jolla
• State: CA
• Country: United States
• Zip Code: 92037

Publications

Roberts, M L; Cooper, N R (1998) Activation of a ras-MAPK-dependent pathway by Epstein-Barr virus latent membrane protein 1 is essential for cellular transformation. Virology 240:93-9

Sugano, N; Chen, W; Roberts, M L et al. (1997) Epstein-Barr virus binding to CD21 activates the initial viral promoter via NF-kappaB induction. J Exp Med 186:731-7

Roberts, M L; Luxembourg, A T; Cooper, N R (1996) Epstein-Barr virus binding to CD21, the virus receptor, activates resting B cells via an intracellular pathway that is linked to B cell infection. J Gen Virol 77 ( Pt 12):3077-85

Luxembourg, A T; Cooper, N R (1994) T cell-dependent, B cell-activating properties of antibody-coated small latex beads. A new model for B cell activation. J Immunol 153:604-14

Luxembourg, A T; Cooper, N R (1994) Modulation of signaling via the B cell antigen receptor by CD21, the receptor for C3dg and EBV. J Immunol 153:4448-57