Nuclear PTEN enhances the maturation of a microRNA regulon to limit MyD88-dependent susceptibility to sepsis

Sepsis-induced organ damage is caused by systemic inflammatory response syndrome (SIRS), which results in substantial comorbidities. Therefore, it is of medical importance to identify molecular brakes that can be exploited to dampen inflammation and prevent the development of SIRS. We investigated t...

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Veröffentlicht in:	Science signaling 2018-05, Vol.11 (528)
Hauptverfasser:	Sisti, Flavia, Wang, Soujuan, Brandt, Stephanie L, Glosson-Byers, Nicole, Mayo, Lindsey D, Son, Young Min, Sturgeon, Sarah, Filgueiras, Luciano, Jancar, Sonia, Wong, Hector, Dela Cruz, Charles S, Andrews, Nathaniel, Alves-Filho, Jose Carlos, Cunha, Fernando Q, Serezani, C Henrique
Format:	Artikel
Sprache:	eng
Schlagworte:	Abundance Animals Brake presses Cell Nucleus - genetics Cell Nucleus - metabolism Cytokines Cytoplasm Damage prevention Embryo fibroblasts Embryos Female Fibroblasts Gene Expression Profiling Hazards Homology Humans Immune system Inflammation Inflammation - genetics Inflammation - metabolism Inflammatory response Leukocytes Localization Lungs Macrophages - metabolism Male Maturation Medical importance Mice Mice, Inbred C57BL Mice, Knockout Microorganisms MicroRNAs MicroRNAs - genetics miRNA Mortality mRNA MyD88 protein Myeloid Differentiation Factor 88 - chemistry Myeloid Differentiation Factor 88 - genetics Myeloid Differentiation Factor 88 - metabolism Nuclear transport Peptides - pharmacology Phosphatase Protein phosphatase Proteins PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism PTEN protein Receptors Regulon - genetics Ribonucleic acid RNA RNA Interference Sepsis Sepsis - genetics Sepsis - metabolism Sepsis - prevention & control Surgery Systemic inflammatory response syndrome Tensin Toll-like receptors Translocation
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