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. 2019 Jul 2;10:1451. doi: 10.3389/fimmu.2019.01451

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Copyright © 2019 Watson, Dai, Zheng, Nakano, Giannou, Menk, Stolz, Delgoffe and Thomson.

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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Proposed mechanism by which TORC2 may restrain TORC1 activity in DC via the transcriptional suppression of upstream TORC1 activators. Based on our observations, TORC2 activity may lead to transcriptional suppression of integrin (ItgA2 and FAK) and cytokine receptor (IL-7R) and JAK1 signaling in conjunction with PIK3AP upstream of Akt/mTORC1 activity, and ultimately the metabolic regulators SREBP1 and Pparγ downstream of TORC1 activity (upregulated genes labeled in red). Itga2b, integrin alpha II b; FAK, focal adhesion kinase (Ptk2, protein kinase 2), Hcst, hematopoietic cell signal transducer; Pparγ, peroxisome proliferator-activated receptor gamma; Sregf1, sterol regulatory element transcription factor 1.