Cavin-3 is a tumor suppressor protein that inhibits Akt signaling, suppresses Warburg metabolism, promotes apoptosis, and protects against cachexia.

Caveolae and Bin1 form tubulation platforms.

β₃-AR signalling via cGMP in cardiomyocytes is regulated via phosphodiesterase 2 and 5 degradation, it is potentially cardioprotective, but dysregulated in heart failure through signal redistribution and higher phosphodiesterase activity.

Cells repair damage to their outer membranes not by patching them as previously thought, but by using proteins called caveolins to remove the damaged regions by endocytosis.

Mice lacking the membrane-shaping protein syndapin III show severe reduction of caveolae reminiscent of human caveolinopathies but maintain plasma membrane-associated caveolar coats proteins and thereby unveil physiological impairments associated with lack of invaginated caveolae.

The association of caveolin with the potassium channel Kv1.3 fine-tunes cell survival and apoptosis.

Caveolae regulate integrin mechanosensing by establishing a force threshold for activation and recycling.

PTRF (Cavin-1) mediates metabolism-regulated ribosomal transcription in mature adipocytes, independent of its role in caveolae formation.

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.

Wound-specific notochord sheath cell subpopulations associate with notochord repair and adult vertebrae formation.