The transcriptional and translational landscape of HCoV-OC43 infection.

The coronavirus HCoV-OC43 circulates continuously in the human population and is a frequent cause of the common cold. Here, we generated a high-resolution atlas of the transcriptional and translational landscape of OC43 during a time course following infection of human lung fibroblasts. Using ribosome profiling, we quantified the relative expression of the canonical open reading frames (ORFs) and identified previously unannotated ORFs.

Persistent organic pollutants disrupt the oxidant/antioxidant balance of INS-1E pancreatic β-cells causing their physiological dysfunctions.

Background: Persistent organic pollutants (POPs) have emerged as potent diabetogenic agents, but their mechanisms of action remain poorly identified.

Objectives: In this study, we aim to determine the mechanisms regulating the damaging effects of POPs in pancreatic β-cells, which have a central role in the development of diabetes.

Methods: We treated INS-1E pancreatic β-cells with PCB-153, p,p'-DDE, PCB-126, or TCDD at doses ranging from 1 × 10to 5 × 10M.

Mice lacking intestinal Nr1i2 have normal intestinal homeostasis under steady-state conditions and are not hypersensitive to inflammation under lipopolysaccharide treatment.

Nr1i2, a nuclear receptor known for its key function in xenobiotic detoxification, has emerged as a potential regulator of intestinal homeostasis and inflammation. However, the role of Nr1i2 in different intestinal segments remains poorly known. Moreover, in vivo investigations on intestinal Nr1i2 have essentially been performed in whole-body Nr1i2 knockout (Nr1i2 ) mice where the deletion of Nr1i2 in all tissues may affect the intestinal phenotype.

A posttranscriptional pathway regulates cell wall mRNA expression in budding yeast.

The fungal cell wall provides protection and structure and is an important target for antifungal compounds. A mitogen-activated protein (MAP) kinase cascade termed the cell wall integrity (CWI) pathway regulates transcriptional responses to cell wall damage. Here, we describe a posttranscriptional pathway that plays an important complementary role.

FK506-Binding Protein 2 Participates in Proinsulin Folding.

Apart from chaperoning, disulfide bond formation, and downstream processing, the molecular sequence of proinsulin folding is not completely understood. Proinsulin requires proline isomerization for correct folding. Since FK506-binding protein 2 (FKBP2) is an ER-resident proline isomerase, we hypothesized that FKBP2 contributes to proinsulin folding.