A cysteine-rich domain within the Smoothened receptor may represent a novel therapeutic target for cancers caused by abnormal functioning of the Hedgehog signaling pathway.

Cholesterol regulates cell-cell communication by activating the Hedgehog pathway, a central signaling system in development, regeneration and cancer.

Hedgehog leads to Smoothened accumulation by favoring its recycling and high Hedgehog levels promote a basolateral enrichment of Smoothened via its phosphorylation by the protein kinase Fused.

Ptch1/2 can lower the sensitivity of Smo to activation by Shh via the secretion of a sterol precursor.

The patched hedgehog receptor inhibits the transmembrane transducer smoothened by reducing the accessibility of cholesterol locally at the membrane of the primary cilium.

Cholesterol accessibility in the plasma membrane can be controlled by proteins and function as a signaling messenger in cell-cell communication pathways.

Membrane recruitment of BBSome is coupled to a conformational change, and interaction of the BBSome with GPCR cargoes depends on the GPCRs releasing their amphipathic helix 8 from the membrane.

The Hedgehog signalling pathway is a master regulator of lipid metabolic processes and their zonation in the adult liver of mice and humans.

Unlike in early embryonic development, injured spinal cord and muscle in Xenopus laevis larvae recruit non-canonical Hedgehog signaling essential for their regeneration, while repressing Gli transcriptional activity.