The first specific aim of this project is to provide COBRE Investigators and collaborators access to state of the art high throughput genetic analysis platforms, other sophisticated equipment, and experimental capabilities. Genetic discoveries and emerging technologies are radically changing biomedical research and the methods by which our COBRE investigators unravel the complex genomic architecture of autoimmune diseases. The Genomics Core serves as the central resource for COBRE investigators to access cuttingedge genomic technologies that allow their research programs to develop and test their hypotheses, therefore, the Genomics Core is highly significant and vital to the success of our Center investigators. The second specific aim of this project is to transition the Genomics Core from a COBRE-subsidized facility to a self-sustaining business entity supported by users both internal to OMRF as well as external. The capabilities of the Genomics Core make it particularly attractive to those researchers planning research projects that incorporate genomics. As such, researchers have utilized and can be expected to continue utilizing the Core as a simple fee-for-service unit or in a sub-contractual setting in funded grants. With our services in high demand from both COBRE and external investigators, the Core is poised to pursue multiple lines of funding through various mechanisms in our move towards overall financial self-sufficiency in Phase III. Furthermore, with the embrace of exome and whole genome sequencing of human patients, the Core could expand its local impact and open an entirely new revenue stream by providing medical diagnostic tests in addition to our central focus of supporting research. It is anticipated that the expansion into clinical genomics, coupled with increasing grant support from other mechanisms, will lead to the Core becoming completely self-sufficient at the end of 5 years.

Public Health Relevance

Genomics technologies, such as second-generation sequencing and high-throughput genotyping, form the backbone of cutting edge biomedical innovation in complex and autoimmune diseases. The Genomics Core facilitates and makes available these technologies to investigators. As more researchers turn to these experimental designs, the usage ofthe Core will increase to the point of self-sufficient funding.

National Institute of Health (NIH)
National Institute of General Medical Sciences (NIGMS)
Center Core Grants (P30)
Project #
Application #
Study Section
Special Emphasis Panel (ZGM1-TWD-C (3C))
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Oklahoma Medical Research Foundation
Oklahoma City
United States
Zip Code
Leehan, Kerry M; Pezant, Nathan P; Rasmussen, Astrid et al. (2018) Minor salivary gland fibrosis in Sjögren's syndrome is elevated, associated with focus score and not solely a consequence of aging. Clin Exp Rheumatol 36 Suppl 112:80-88
Celada, Lindsay J; Kropski, Jonathan A; Herazo-Maya, Jose D et al. (2018) PD-1 up-regulation on CD4+ T cells promotes pulmonary fibrosis through STAT3-mediated IL-17A and TGF-?1 production. Sci Transl Med 10:
Pelikan, Richard C; Kelly, Jennifer A; Fu, Yao et al. (2018) Enhancer histone-QTLs are enriched on autoimmune risk haplotypes and influence gene expression within chromatin networks. Nat Commun 9:2905
Patel, Zubin; Lu, Xiaoming; Miller, Daniel et al. (2018) A plausibly causal functional lupus-associated risk variant in the STAT1-STAT4 locus. Hum Mol Genet :
Fu, Yao; Tessneer, Kandice L; Li, Chuang et al. (2018) From association to mechanism in complex disease genetics: the role of the 3D genome. Arthritis Res Ther 20:216
Bagavant, Harini; Dunkleberger, Micah L; Wolska, Nina et al. (2018) Antibodies to periodontogenic bacteria are associated with higher disease activity in lupus patients. Clin Exp Rheumatol :
Wang, Chih-Chuan; Ortiz-González, Xilma R; Yum, Sabrina W et al. (2018) ?IV Spectrinopathies Cause Profound Intellectual Disability, Congenital Hypotonia, and Motor Axonal Neuropathy. Am J Hum Genet 102:1158-1168
Wang, Hong-Cheng; Qian, Liangyue; Zhao, Ying et al. (2017) Downregulation of E Protein Activity Augments an ILC2 Differentiation Program in the Thymus. J Immunol 198:3149-3156
Lareau, C A; DeWeese, C F; Adrianto, I et al. (2017) Polygenic risk assessment reveals pleiotropy between sarcoidosis and inflammatory disorders in the context of genetic ancestry. Genes Immun 18:88-94
Braun, Daniela A; Rao, Jia; Mollet, Geraldine et al. (2017) Mutations in KEOPS-complex genes cause nephrotic syndrome with primary microcephaly. Nat Genet 49:1529-1538

Showing the most recent 10 out of 32 publications