Ono completed his fellowship at Harvard and then held faculty positions at Johns Hopkins University, Harvard University, University College London (UCL), and Emory University. He was GlaxoSmithKline Chair of Biomedical Science and Head of the Department of Immunology at the UCL Institute of Ophthalmology and honorary staff member at Moorfields Eye Hospital NHS Foundation Trust. From March 2006 until September 2008, he served as Vice Provost for Academic Initiatives and Deputy to the Provost at Emory University in Atlanta. He was promoted to Senior Vice Provost for Undergraduate Education and Academic Affairs in September 2008 and also served as Professor of Ophthalmology, Medicine, Pediatrics and Biology. In September 2010, he became Senior Vice President and Provost for Academic Affairs at the University of Cincinnati.
Professor Ono has studied on ocular surface inflammation and the immune basis of age-related macular degeneration. His early work focused on the association of certain MHC haplotypes with susceptibility and resistance to type 1 diabetes. Using a number of recombinant and congenic rat strains, the work mapped susceptibility genes in the BB rat to the class II MHC loci. His work also showed that class I and II MHC gene products are expressed at higher levels or de novo on the insulin-producing beta cells of the islets of Langerhans. He focused much of his research in the next decade on the regulation of MHC gene expression. He showed that the different class II MHC isotypes are differentially expressed and showed that the X2-box cis-element controls this differential expression. His work also showed that the bZIP transcription factor: XBP1 forms a hetero-dimer with c-Fos. This has turned out to be relevant to the developmental control of B cell differentiation. His lab also discovered the NFX1 transcription factor and cloned both the human and murine cDNAs. This factor can bind DNA, RNA and protein via a reiterated RING finger motifs in the central domain of the polypeptide. The protein appears to have important roles in neuronal development and mRNA transport. NFX1 is also a probable E3 ubiquitin-protein ligase. These enzymes are of interest as they have been shown to participate in 3 metabolic pathways: ubiquitin mediated proteolysis, parkinson's disease, and huntington's disease. His lab also demonstrated that the non- histone chromosomal protein HMGA is required for the induction of multiple genes, including MHC genes, interferon-gamma and rhodopsin. They mapped the interaction of HMGA1a and the paired homeodomain motif within Crx and showed that these interactions help recruit such transcriptional activators to the promoter/enhancer.
Using transgenic mouse technology, they also showed (concurrently and independently of Alfredo Fusco), that fusion proteins between HMGA2 and other C terminal peptides (following chromosomal translocation) can drive the development of lipomas and generate obese mice. Further contributions in the field include the mapping of the HMGA2 promoter/enhancer.
More recently, his laboratory determined the role of beta-chemokines in mast cell-dependent inflammation in the ocular surface. The work showed that chemokines not only contribute to leukocyte recruitment, but can cooperate with other mast cell activation signals to trigger mast cell degranulation. Finally, his lab showed that certain autoantibodies might contribute to the pathogenesis or exacerbation of AMD and other rapid onset retinal degenerative diseases and may constitute useful biomarkers for the screening for AMD and its progression.
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