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. 2019 May 14;9:132. doi: 10.3389/fcimb.2019.00132

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Copyright © 2019 Menard, Haskins and Denkers.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Model for mir-17-92 inhibition of apoptosis during T. gondii infection. During intracellular infection, T. gondii injects the ROP16 protein into the host cell cytoplasm. In the cytoplasm, ROP16 phosphorylates STAT3. Phosphorylated STAT3 enters the nucleus of the host cell, binds to STAT3 sites in the promoter of the miR-17-92 cluster gene, and upregulates miR-17-92 miRNAs. miR-17-92 cluster miRNAs then bind to the Bim transcript and reduce BIM levels, thereby inhibiting the process of apoptosis. This model is based upon data reported in Cai et al. (2013, 2014).