Author: Wang, Yi; Liu, Li
Title: The Membrane Protein of Severe Acute Respiratory Syndrome Coronavirus Functions as a Novel Cytosolic Pathogen-Associated Molecular Pattern To Promote Beta Interferon Induction via a Toll-Like-Receptor-Related TRAF3-Independent Mechanism Document date: 2016_2_9
ID: uf96jgig_14
Snippet: SARS-CoV M protein may function as a novel intracellular PAMP to induce IFN-⤠production. One critical question remaining to be answered is whether the driving force for M protein-mediated IFN-⤠induction is generated intracellularly or extracellularly. To answer this question directly, the TRAP⥠gene, an endoplasmic reticulum (ER)-associated gene, was cotransfected with M into HeLa cells. Brefeldin A (BFA) was employed in the assay system .....
Document: SARS-CoV M protein may function as a novel intracellular PAMP to induce IFN-⤠production. One critical question remaining to be answered is whether the driving force for M protein-mediated IFN-⤠induction is generated intracellularly or extracellularly. To answer this question directly, the TRAP⥠gene, an endoplasmic reticulum (ER)-associated gene, was cotransfected with M into HeLa cells. Brefeldin A (BFA) was employed in the assay system to block M protein transport from the rough endoplasmic reticulum to the cell surface. Indeed, the addition of BFA effectively increased the retention of M proteins in the ER compartment (Fig. 6A) . Figure 6B shows that addition of BFA also effectively inhibited the secretion of IFN-⤠into the cell culture medium (right panel) but did not inhibit M-mediated IFN-⤠induction at either the mRNA level or the protein level (left panel), indicating that the driving force for M-mediated IFN-⤠induction was indeed derived from intracellular stimulation by M proteins.
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