Ashkenazi, Avi, et al., Protection Against Endotoxic Shock by a Tumor Necrosis Factor Receptor Immunoadhesin, Medical Sciences (1991) 10535-10539, vol. 88. |
Bicknell, Roy, et al., Mechanisms and Therapeutic Implications of Angiogenesis, Current Opinion in Oncology (1996) 60-65, vol. 8. |
Duncan, Alexander, et al., The binding site for Clq on IgG, Nature (1988) 738-740, vol. 332, No. 21. |
Fisher, Charles J., et al., Treatment of Septic Shock with the Tumor Necrosis Factor Receptor:Fc Fusion Protein, The New England Journal of Medicine (1996) 1697-1702, vol. 334, No. 26. |
Kiefer, Michael, C., et al., Molecular Cloning of a Human Basic Fibroblast Growth Factor Receptor cDNA and Expression of a Biologically Active Extracellular Domain in a Baculovirus System, Growth Factors (1991) 115-127, vol. 5. |
Kim, K. Jin, et al., Inhibition of Vascular Endothelial Growth Factor-Induced Angiogenesis Suppresses Tumour Growth in vivo, Nature (1993) 841-844, vol. 362. |
Lenschow, Deborah, et al., Long-Term Survival of Xenogeneic Pancreatic Islet Grafts Induced by CTLA4lg. Science (1992) 789-792, Vol 257. |
Linsley, Peter, et al., Immunosuppression in vivo by a Soluble Form of the CTLA-4 T Cell Activation Molecule, Science (1992) 792-794, vol. 257. |
Millauer, Birgit, et al., Glioblastoma Growth Inhibited in vivo by a Dominant-Negative Flk-1 Mutant, Nature (1994) 576-579, vol. 367. |
Min, Hye Yeong, et al., Urokinase Receptor Antagonists Inhibit Angiogenesis and Primary Tumor Growth in Syngenic Mice, Cancer Research (1996) 2428-2433, vol. 56. |
Mohler, Kendall, et al., Soluble Tumor Necrosis Factor (TNF) Receptors are Effective Therapeutic Agents in Lethal Endotoxemia and Function Simultaneously as both TNF Carriers and TNF Antagonists, The Journal of Immunology (1993) 1548-1561, vol. 151, No. 3. |
Moreland, Larry W., et al., Treatment of Rheumatoid Arthritis with a Recombinant Human Tumor Necrosis Factor Receptor (p75)-Fe Fusion Protein, The New England Journal of Medicine (1997) 141-147, vol. 337, No. 3. |
Moy, Franklin J., et al., Properly Oriented Heparin—Decasaccharie-Induced Dimers Are the Biologically Active Form of Basic Fibroblast Growth Factor, Biochemistry (1997) 4782-4791, vol. 36, No. 16. |
Pantoliano, Michael W., et al., Multivalent Ligand-Receptor Binding Interactions in the Fibroblast Growth Factor System Produce a Cooperative Growth Factor and Heparin Mechanism for Receptor Dimerization, Biochemistry (1994) 10229-10248, vol. 33, No. 34. |
Werner, Sabine, et al., Differential Splicing in the Extracellular Region of Fibroblast Growth Factor Receptor 1 Generates Receptor Variants with Different Ligand-Binding Specificities, Molecular and Cellular Biology (1992) 82-88, vol. 12, No. 1. |
Xu, Yuanyuan, et al., Residue at Position 331 in the IgG1 and IgG4 CH2 Domains Contributes to Their Differential Ability to Bind and Activate Complement*, (1994) 3469-3474, vol. 269, No. 5. |
Galzie et al. (1997) “Fibroblast Growth Factors and Their Receptors,” Biochem. Cell Biol. 75:669-685. |
Duncan et al., “Localization of the Binding Site for the Human High-Affinity Fc Receptor on IgG”, Nature, (1988) 332(6164):563-564. |