Lipid efflux by the retinal pigment epithelium is crucial for proper retinal integrity and function, and its impairment may contribute to diseases like age-related macular degeneration.

Tyrosine phosphorylation of the intracellular domain of LRP1 serves as a molecular switch to regulate cellular cholesterol homeostasis through nuclear hormone receptor-mediated regulation of the cellular cholesterol exporter ABCA1.

The cholesterol-sensing nuclear receptor LXR regulates inflammatory responses by altering the lipid composition of cell membranes.

In vivo genetic lineage-tracing reveals the developmental trajectory of neurogliaform cells, the main effectors of a powerful inhibitory motif in the neocortex.

The fibronectin synergy site is only required in vivo when forces exceed or αvβ3 integrin levels fall below certain thresholds.

Biochemical and genetic experiments show that Ebf and Lhx2 cooperate to specify olfactory receptor enhancers, which cooperate to drive olfactory receptor expression.

E3 ubiquitin ligase Bre1-induced H2B monoubiquitination is epigenetically important for recruiting replication factor Mcm10 and cohesion establishment factors Ctf4, Ctf18 and Eco1 to early replication origins to establish sister chromatid cohesion.

NFATc2 maintains the drug-induced TIC phenotypes through trans-activating SOX2/ALDH1A1 expression and scavenging stress from ROS.

The activation of beige adipocyte thermogenesis by cold temperatures and β3-adrenergic receptor agonists induce beige adipocyte formation, function and perdurance.

Ablation of the Cdkn1c cell cycle inhibitor leads to defective muscle stem cell dynamics and myogenic potential, while progressive cytoplasmic to nuclear cellular localization of the Cdkn1c protein regulates growth arrest.