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Newsworthy Events
Nolan GP. 2008. Featured Scientist Interview by ScienceWatch.com. Tracking Trends and Performance in Basic Research. April 2008 Lee AW, Sharp ER, O'Mahony A, Rosenberg MG, Israelski DM, Nolan GP , Nixon DF. 2008. Single cell, phosphoepitope-specific analysis demonstrates cell type- and pathway-specific dysregulation of Jak/STAT and MAPK signaling associated with in vivo HIV-1 infection. J Virol. Jan 23; [Epub ahead of print] Krutzik PO, Crane JM, Clutter MR, Nolan GP. 2008. High-content single-cell drug screening with phosphospecific flow cytometry. Nat Chem Biol. Feb;4(2):132-42. Epub 2007 Dec 23. Shachaf CM, Perez OD, Youssef S, Fan AC, Elchuri S, Goldstein MJ, Shirer AE, Sharpe O, Chen J, Mitchell DJ, Chang M, Nolan GP, Steinman L and Felsher DW. 2007. Inhibition of HMGcoA reductase by atorvastatin prevents and reverses MYC-induced lymphomagenesis. Blood. Oct 1;110(7):2674-84. Epub 2007 Jul 10. |
Proteomics of Blood Components in Autoimmune DiseaseThis Proteomics Center represents an interdisciplinary effort to explore and converge results from 4 different platform technologies that analyze intracellular and secreted blood cell proteins related to systemic autoimmune disease processes. A main component of the Center is the development of relational software and statistical analysis regimens that will allow the comparison and correlation of different datasets generated by these diverse technologies. Each platform employs equipment that is familiar to nearly all academic research centers, including fluorescence activated cell sorters (FACS), robotic microarray printers and scanners, and microfabrication design for capillary electrophoresis equipment. We are applying this approach to tractable animal models of two distinct autoimmune diseases, systemic lupus erythematosus (SLE, a disease mediated predominantly by B lymphocytes) and rheumatoid arthritis (RA, a disease mediated predominantly by T lymphocytes). Later years of the proposal will focus on the study of biological specimens derived from human patients as clinical samples that are clinically relevant manifestations of autoimmune disease represented by the disease models.
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