Robert Opoka

ORCID: 0000-0002-8879-0099
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • Wnt/β-catenin signaling in development and cancer
  • Congenital heart defects research
  • Diabetes and associated disorders
  • Epigenetics and DNA Methylation
  • CAR-T cell therapy research
  • T-cell and B-cell Immunology
  • Pluripotent Stem Cells Research
  • Hippo pathway signaling and YAP/TAZ
  • Developmental Biology and Gene Regulation
  • Pancreatic function and diabetes
  • Cancer-related gene regulation
  • Kruppel-like factors research
  • Immunotherapy and Immune Responses
  • Genetic Syndromes and Imprinting
  • Nuclear Receptors and Signaling

Cincinnati Children's Hospital Medical Center
2004-2019

Diabetes Research Center
2010

Center of Molecular Immunology (Cuba)
2010

University of Cincinnati
2004-2007

The canonical Wnt pathway is necessary for gut epithelial cell proliferation, and aberrant activation of this causes intestinal neoplasia. We report a novel mechanism by which the Sox family transcription factors regulate signaling pathway. found that some proteins antagonize while others enhance β-catenin/T-cell factor (TCF) activity. Sox17, expressed in normal epithelium but exhibits reduced expression neoplasia, antagonistic to signaling. When overexpressed SW480 colon carcinoma cells,...

10.1128/mcb.02179-06 article EN Molecular and Cellular Biology 2007-09-18

Little is known about how the endoderm germ layer patterned along anterior-posterior (A-P) axis before formation of a gut tube (embryonic day [e] 7.5-8.5 in mouse), largely due to paucity molecular markers endoderm. In particular, there are few genes that mark posterior domains give rise midgut and hindgut. We have identified 8 expressed discrete gastrula stage (e7.5), suggesting significant level pattern exists tube. Three Tmprss2, NM_029639, Dsp presumptive domain overlying node, for which...

10.1002/dvdy.21204 article EN Developmental Dynamics 2007-06-18

Abstract In type 1 diabetes, the breach of central and peripheral tolerance results in autoreactive T cells that destroy insulin-producing, pancreatic β cells. this study, we identify a critical subpopulation dendritic responsible for mediating both cross-presentation islet Ags to CD8+ direct presentation cell CD4+ These cells, termed merocytic (mcDCs), are more numerous NOD mouse and, when Ag-loaded, rescue from anergy deletion while stimulating islet-reactive When purified lymph nodes...

10.4049/jimmunol.1001398 article EN The Journal of Immunology 2010-07-19

Type 1 diabetes (T1D) is a chronic multi-factorial disorder characterized by the immune-mediated destruction of insulin-producing pancreatic beta cells. Variations at large number genes influence susceptibility to spontaneous autoimmune T1D in non-obese diabetic (NOD) mice, one most frequently studied animal models for human disease. The genetic analysis these mice allowed identification many insulin-dependent (Idd) loci and candidate genes, them being Cd101. CD101 heavily glycosylated...

10.1371/journal.pgen.1008178 article EN cc-by PLoS Genetics 2019-06-14

TCR ligation is critical for the selection, activation, and integrin expression of T lymphocytes. Here, we explored role adaptor protein slp-76 on iNKT-cell biology. Compared to B6 controls, slp-76(ace/ace) mice carrying a missense mutation (Thr428Ile) within SH2-domain showed an increase in iNKT cells thymus lymph nodes, but decrease spleens livers, along with reduced ADAP cytokine response. A comparable reduction was observed livers ADAP-deficient mice. Like ADAP(-/-) cells, were...

10.1002/eji.201646331 article EN European Journal of Immunology 2016-06-28
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