The glucose-sensing transcription factor MondoA regulates zebrafish epiboly via cholesterol biosynthesis genes including the human disease gene Nsdhl, revealing an unknown role for metabolic glucose signalling in vertebrate development.

Melanocortin 1 receptor (MC1-R) deficiency in hepatocytes increases cholesterol levels in the circulation and liver in mice, while selective activation of MC1-R reduces cellular cholesterol content in cultured hepatocytes.

Lovastatin ability to rescue motor deficits and survival in a mouse model of Rett syndrome is strongly influenced by the genetic background.

Genome-scale integration of transposon mutagenesis with a redox biosensor identified a hypothetical transcription factor- Rv0158 required to calibrate the growth, cytoplasmic redox potential, and respiration of Mycobacterium tuberculosis in response to metabolic switching from glucose to fatty acids.

COPII vesicles regulate the metabolism of cholesterol through the selective transport of secretory proteins.

The associations of egg consumption with metabolic markers and of these markers with cardiovascular disease (CVD) risk showed opposite directions, which may partially explain the protective effect of moderate egg consumption on CVD in the Chinese population.

In-depth proteomic analyses of intestinal tissue-resident intraepithelial T lymphocytes reveals how these cells are adapted to the intestinal environment through increased cholesterol and lipid metabolism, tailored metabolic profiles, receptors for interacting with epithelial cells, and tightly regulated signalling pathways.

Cells use two interdigitated biosynthetic pathways that can be regulated independently to produce diverse bioactive sterols.

Trypanosoma cruzi intracellular amastigotes exhibit rapid resistance to azoles, independent of genetic selection, which is dependent on metabolic state and mechanistically distinct from latency.

A phase transition of TIR-1/SARM1 induced by either pathogen or non-pathogen stress potentiates its intrinsic NADase activity, which activates the p38 PMK-1 signaling cascade to induce protective immune defenses in Caenorhabditis elegans intestinal epithelial cells.