Dicer protein levels elevated by mild hyperthermia promote a pro-survival phenotype.

Cellular exposure to mild stress (39.5°C - 41.5°C) induces thermotolerance, rendering cells resistant to a subsequent heat shock (>42°C) insult.

Mechanisms underlying the inhibition of interferon signaling by viruses.

A hallmark of the antiviral response is the induction of interferons. First discovered in 1957 by Issac and Lindeman, interferons are noted for their ability to interfere with viral replication. Interferons act via autocrine and paracrine pathways to induce an antiviral state in infected cells and in neighboring cells containing interferon receptors.

Dicer in immune cell development and function.

Dicer is an enzyme of the RNase III endoribonuclease family, which is crucial for RNA interference (RNAi) in eukaryotes. Dicer is a component of the protein machinery (the RNA Induced Silencing Complex [RISC]) which is involved in catalyzing the formation of mature microRNAs from their precursors in the process of microRNA biogenesis. RISC-associated microRNAs bind to specific sequences in the 3' untranslated region of cognate mRNAs largely through complementary base pairing, resulting in either translational inhibition and/or the degradation of a specific mRNA pool.

Mild hyperthermia enhances the expression and induces oscillations in the Dicer protein.

Purpose: To investigate whether mild heat stress at 39.5°C altered Dicer protein and miRNA expression patterns in several cell types.

Methods: Multiple human and mouse cell types were cultured during the course of 9 h at temperatures from 37°C to 39.