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Detailed biochemical and metabolic analysis of the inflammatory response in human endothelial cells reveals that inflammation directly regulates cholesterol homeostasis.

Activation of Wnt/β-catenin signaling in endothelial progenitors derived from human pluripotent stem cells partially induces the specialized blood–brain barrier phenotype while the same treatment in matured endothelial cells is less efficacious.

After myocardial infarction, gut microbiota affects platelet aggregation rate by regulating the absorption and metabolism of ticagrelor.

The transcriptional adapter protein NCOR1 that links chromatin-modifying enzymes with gene-specific transcription factors controls naive and effector regulatory T cell states.

The structures of ABCA4 in two conformations provide a framework to understand its transport mechanism.

CRISPR/Cas9 genome-wide screens using sterol-sensitive endogenous HMG-CoA reductase (HMGCR) reporter identify the sterol-responsive RNF145 and gp78 as independently responsible for sterol-accelerated degradation of HMGCR, the rate-limiting enzyme of cholesterol biosynthesis.

In vitro culture of brain endothelial cells leads to a rapid loss of the blood-brain barrier transcriptional and accessible chromatin landscapes that is resistant to the effects of beta-catenin stabilization.

SREBP-2 directly regulates genes involved in cholesterol homeostasis and indirectly regulates fatty acid synthesis through the production of a ligand responsible for the activation of LXR and SREBP-1c.

Dysfunctions of myelin peroxisomes cause a lysosomal storage-like disorder associated with alterations in glial and axonal membranes, which is the likely cause of nerve impairment in peroxisomal disorders.

The E3 ubiquitin ligase RNF145 is shown to contribute to crosstalk between the LXR and SREBP-2 pathways in the regulation of cholesterol homeostasis.