For the past decade, the Oklahoma COBRE GM103456 (previously RR020143) """"""""Molecular Mechanisms and Genetics of Autoimmunity"""""""" has been a pivotal resource in transforming the Oklahoma Medical Research Foundation into an institution committed to the mentoring and development of junior investigators to productive independent scientific careers with an emphasis on the genetics of autoimmune diseases. Through its support of 11 junior investigators, 16 pilot projects, and an evolving set of 3-4 cores, this resource has provided the infrastructure to help launch 11 independent research careers and support the subsequent funding of numerous multi-investigator grants (""""""""program grants"""""""") funded by other NIH institutes. Our Administrative Core will serve as a centralized governing resource for the COBRE, provide adminitstrative assistance and oversight to the research and Pilot cores and serve as a liason between the steering committee, external advisory committee, institutional administration and COBRE investigators. The scientific strategic purpose of the continuation of this COBRE is to support research in the genetics and genomics of autoimmune diseases and begin to broaden our scope of COBRE investigators to other disciplines including cancer, cardiovascular diseases and rare disorders.
The Specific Aims ofthe Administrative core are to 1) coordinate, integrate and fiscally manage to financial independence research cores, which meet and extend the scientific opportunities of our COBRE Investigators, 2) evaluate and manage the effectiveness of research cores and pilot projects, 3) implement and expand multidisciplinary enrichment programs and, 4) assist with grant applications, management and compliance issues.
This OMRF COBRE has been very successful in identifying and facilitating the careers of talented junior investigators. The Administrative Core supports this success through compentent management of overall COBRE operations.
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|Hegen, Harald; Adrianto, Indra; Lessard, Christopher J et al. (2016) Cytokine profiles show heterogeneity of interferon-Î² response in multiple sclerosis patients. Neurol Neuroimmunol Neuroinflamm 3:e202|
|Ward, Julie M; Ratliff, Michelle L; Dozmorov, Mikhail G et al. (2016) Expression and methylation data from SLE patient and healthy control blood samples subdivided with respect to ARID3a levels. Data Brief 9:213-9|
|Wang, S; Wen, F; Tessneer, K L et al. (2016) TALEN-mediated enhancer knockout influences TNFAIP3 gene expression and mimics a molecular phenotype associated with systemic lupus erythematosus. Genes Immun 17:165-70|
|Ward, Julie M; Ratliff, Michelle L; Dozmorov, Mikhail G et al. (2016) Human effector B lymphocytes express ARID3a and secrete interferon alpha. J Autoimmun 75:130-140|
|Lareau, Caleb A; Adrianto, Indra; Levin, Albert M et al. (2015) Fine mapping of chromosome 15q25 implicates ZNF592 in neurosarcoidosis patients. Ann Clin Transl Neurol 2:972-7|
|Dozmorov, Mikhail G; Dominguez, Nicolas; Bean, Krista et al. (2015) B-Cell and Monocyte Contribution to Systemic Lupus Erythematosus Identified by Cell-Type-Specific Differential Expression Analysis in RNA-Seq Data. Bioinform Biol Insights 9:11-9|
|Dozmorov, Mikhail G; Adrianto, Indra; Giles, Cory B et al. (2015) Detrimental effects of duplicate reads and low complexity regions on RNA- and ChIP-seq data. BMC Bioinformatics 16 Suppl 13:S10|
|Lareau, Caleb A; White, Bill C; Montgomery, Courtney G et al. (2015) dcVar: a method for identifying common variants that modulate differential correlation structures in gene expression data. Front Genet 6:312|
|Bello, Ghalib A; Adrianto, Indra; Dumancas, Gerard G et al. (2015) Role of NOD2 Pathway Genes in Sarcoidosis Cases with Clinical Characteristics of Blau Syndrome. Am J Respir Crit Care Med 192:1133-5|
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