Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
5R29AI032136-05
Application #
2067047
Study Section
Experimental Immunology Study Section (EI)
Project Start
1992-07-01
Project End
1997-04-30
Budget Start
1996-05-01
Budget End
1997-04-30
Support Year
5
Fiscal Year
1996
Total Cost
Indirect Cost

  Institution

Name
National Jewish Health
Department
Type
DUNS #
City
Denver
State
CO
Country
United States
Zip Code
80206

  Publications

Routes, J M; Colton, L A; Ryan, S et al. (2000) CREB (cAMP response element binding protein) and C/EBPalpha (CCAAT/enhancer binding protein) are required for the superstimulation of phosphoenolpyruvate carboxykinase gene transcription by adenoviral E1a and cAMP. Biochem J 352 Pt 2:335-42
Routes, J M; Li, H; Bayley, S T et al. (1996) Inhibition of IFN-stimulated gene expression and IFN induction of cytolytic resistance to natural killer cell lysis correlate with E1A-p300 binding. J Immunol 156:1055-61
Klemm, D J; Colton, L A; Ryan, S et al. (1996) Adenovirus E1A proteins regulate phosphoenolpyruvate carboxykinase gene transcription through multiple mechanisms. J Biol Chem 271:8082-8
Routes, J M; Cook, J L (1995) E1A gene expression induces susceptibility to killing by NK cells following immortalization but not adenovirus infection of human cells. Virology 210:421-8
Routes, J M; Ryan, S (1995) Oncogenicity of human papillomavirus- or adenovirus-transformed cells correlates with resistance to lysis by natural killer cells. J Virol 69:7639-47
Routes, J M (1993) Adenovirus E1A inhibits IFN-induced resistance to cytolysis by natural killer cells. J Immunol 150:4315-22
Routes, J M; Metz, B A; Cook, J L (1993) Endogenous expression of E1A in human cells enhances the effect of adenovirus E3 on class I major histocompatibility complex antigen expression. J Virol 67:3176-81
Routes, J M (1992) IFN increases class I MHC antigen expression on adenovirus-infected human cells without inducing resistance to natural killer cell killing. J Immunol 149:2372-7