Mark K. Devries

TL;DR: In this article, the authors utilized acetyl-peptide arrays and metabolomic analyses to identify substrates of the mitochondrial deacetylase Sirt3, and found that under low energy input, sirt3 modulates mitochondria by promoting amino acid catabolism and β-oxidation.

TL;DR: It is discovered that expression of human cadherin-related family member 3 (CDHR3), a transmembrane protein with yet unknown biological function, enables RV-C binding and replication in normally unsusceptible host cells, and suggests that rs6967330 mutation could be a risk factor for RV- C wheezing illnesses.

TL;DR: Evidence is provided that SIRT6-dependent histone deacetylation produces O-acetyl-ADP-ribose but at a rate ∼1,000 times slower than other highly active sirtuins, which implies a unique activating mechanism and/or the possibility that Sirt6 could act as an NAD+ metabolite sensor.

TL;DR: Allergic asthmatic children have impaired innate immune responses to HRV that correlate with increased FcεRI expression on pDCs and are reduced by Fc�RI cross-linking, which likely increase susceptibility to HRv-induced wheezing and asthma exacerbations.

TL;DR: This study suggests that SNPs regulating GSDMB expression in airway epithelial cells have a major role in childhood-onset asthma, whereasSNPs regulating the expression levels of 17q12-21 genes in resting blood cells are not central asthma risk.