Proteolysis of lipidated N-terminal peptides that tether Hedgehog morphogens to the surface of source cells is absolutely required for their coupled release and bioactivation in vivo in Drosophila melanogaster.

The seemingly simple, constitutive response of the patched/Ptch1 gene to Hedgehog signaling is in fact regulated by large batteries of context-specific Hedgehog-responsive enhancers in both fly and mouse, allowing tissue-specific tuning of the Hedgehog pathway in animal development and evolution.

Dispatched cleavage, mediated by Furin, regulates Dispatched membrane trafficking and release of Sonic Hedgehog ligand.

Direct interaction between Hedgehog-sending and Hedgehog-receiving cytonemes is a fundamental mechanism for morphogen transfer and gradient establishment.

Hedgehog signaling plays a role in regulating glia gene expression in planarians, pointing to a candidate ancestral and broadly used role for the Hedgehog pathway.

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

Targeted activation of Hedgehog signalling via Gli2 facilitated the reduction of high-fat-diet-induced obesity and improvement of whole-body glucose tolerance and insulin sensitivity in adult mice.

The Drosophila equivalent of Substance P signaling modulates nociceptive sensitization by regulating Hedgehog signaling within nociceptive sensory neurons.

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.

Methylation of Gli3 by Set7 enhances the activation of Hedgehog signaling and contributes to tumor growth and metastasis in vitro and in vivo.