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E-GEOD-66808 - IFN-g Regulates mTORC1, Cellular Metabolism and mRNA Translation to Potentiate Inflammatory Macrophage Activation [miRNA-Seq]

Status
Released on 29 June 2015, last updated on 19 August 2015
Organism
Homo sapiens
Samples (8)
Protocols (4)
Description
IFN-g primes macrophages for enhanced inflammatory activation by TLRs and microbial killing, but little is known about the regulation of cell metabolism or mRNA translation during priming. We found that IFN-g regulates macrophage metabolism and translation in an integrated manner by targeting mTORC1 and MNK pathways that converge on the selective regulator of translation initiation eIF4E. Physiological downregulation of the central metabolic regulator mTORC1 by IFN-g was associated with autophagy and translational suppression of repressors of inflammation such as HES1. Genome-wide ribosome profiling in TLR2-stimulated macrophages revealed that IFN-g selectively modulates the macrophage translatome to promote inflammation, further reprogram metabolic pathways, and modulate protein synthesis. These results add IFN-g-mediated metabolic reprogramming and translational regulation as key components of classical inflammatory macrophage activation. microRNA-seq libraries were generated from mock or IFN-g-primed human macrophages. Cells were stimulated with or without Pam3Cys and harvested at 4 hours Libraries were generated using Illumina Truseq small RNA technology.
Experiment type
RNA-seq of non coding RNA 
Contacts
Xiaodi Su <xis2003@med.cornell.edu>, Charles M Rice, Eugenia G Giannopoulou, Gunnar Rätsch, Hui Liu, Justin R Cross, Lionel B Ivashkiv, Xiaoyu Hu, Yi Zhong, Yingpu Yu
MINSEQE
Exp. designProtocolsVariablesProcessedSeq. reads
Files
Investigation descriptionE-GEOD-66808.idf.txt
Sample and data relationshipE-GEOD-66808.sdrf.txt
Additional data (1)E-GEOD-66808.additional.1.zip
Links