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ABSTRACT:
PROVIDER: PRJNA975135 | ENA |
REPOSITORIES: ENA
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1Boyce Thompson Institute and Department of Chemistry and Chemical Biology, Cornell University, Ithaca, New York 14853, United States
2Department of Molecular Biosciences, Northwestern University, Evanston, IL 60208, United States
3Current address: Chemistry Department, College of Environmental Science and Forestry, State University of New York, Syracuse, New York 13210, United States
4Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853, United States
Correspondence to fs31@cornell.edu
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1) Nutritional Immunology and Molecular Medicine Laboratory, Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, Virginia, United States of America, 2) Center for Modeling Immunity to Enteric Pathogens, Virginia Tech, Blacksburg, Virginia, United States of America, 3) Division of Infectious Disease and International Health, Center for Global Health, University of Virginia, Charlottesville, Virginia, United States of America, 4) Medical Informatics and Systems Division, Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, Virginia, United States of America, 5) Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia, United States of America
E-mail: jbassaga@vt.edu
This model represents the interaction between Cdiff, miRNA146b, NCOA4, PPARg, IL10 and IL17. Simulation studies show an aberrant expression of miRNA146b with increasing concentrations of Cdiff over time, which results in decreased PPARg activation due to NCOA4 inhibition. As a final result, PPARg is unable to modulate effector and regulatory responses, since results show an upregulation of IL17 expression and downregulation of IL10 production.
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