| Literature DB >> 33140520 |
Syed Muhammad Hamid1, Mevlut Citir2, Erdem Murat Terzi3, Ismail Cimen4, Zehra Yildirim1,5,6, Asli Ekin Dogan1,5,6, Begum Kocaturk7, Umut Inci Onat5,6, Moshe Arditi1,7,8, Christian Weber4,9,10, Alexis Traynor-Kaplan11,12, Carsten Schultz2,13, Ebru Erbay1,8.
Abstract
The ER-bound kinase/endoribonuclease (RNase), inositol-requiring enzyme-1 (IRE1), regulates the phylogenetically most conserved arm of the unfolded protein response (UPR). However, the complex biology and pathology regulated by mammalian IRE1 cannot be fully explained by IRE1's one known, specific RNA target, X box-binding protein-1 (XBP1) or the RNA substrates of IRE1-dependent RNA degradation (RIDD) activity. Investigating other specific substrates of IRE1 kinase and RNase activities may illuminate how it performs these diverse functions in mammalian cells. We report that macrophage IRE1 plays an unprecedented role in regulating phosphatidylinositide-derived signaling lipid metabolites and has profound impact on the downstream signaling mediated by the mammalian target of rapamycin (mTOR). This cross-talk between UPR and mTOR pathways occurs through the unconventional maturation of microRNA (miR) 2137 by IRE1's RNase activity. Furthermore, phosphatidylinositol (3,4,5) phosphate (PI(3,4,5)P3 ) 5-phosphatase-2 (INPPL1) is a direct target of miR-2137, which controls PI(3,4,5)P3 levels in macrophages. The modulation of cellular PI(3,4,5)P3 /PIP2 ratio and anabolic mTOR signaling by the IRE1-induced miR-2137 demonstrates how the ER can provide a critical input into cell growth decisions.Entities:
Keywords: ER stress; hyperlipidemia; mTOR signaling; macrophage; microRNA
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Year: 2020 PMID: 33140520 PMCID: PMC7726810 DOI: 10.15252/embr.202051462
Source DB: PubMed Journal: EMBO Rep ISSN: 1469-221X Impact factor: 9.071