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.

Pharmacologic inhibition of DNA methylation restrains the growth of urothelial carcinoma by subtype conversion through heightened stromal Hedgehog pathway activity.

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 dependence of Nematostella germ cell specification on zygotic Hedgehog pathway activity supports the hypothesis that the eumetazoan common ancestor segregated its germline by inductive signals rather than maternal determinants.

GLI3 represses Hedgehog target gene expression by regulating histone modifications at a subset of tissue-specific GLI-bound enhancers.

Hedgehog-pathway activation in adjacent epithelial and stromal cells, but not in epithelial or stromal cells alone, enables the generation of functional de novo hair follicles in unwounded adult mouse skin.

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

DYRK2 regulator governs the mammalian ciliogenesis to maintain proper embryogenesis via activation of the Hh signaling during development in vivo.

Sonic Hedgehog is transported inside cytonemes with co-receptors that promote contact-mediated signal delivery to initiate rapid, receptor-dependent responses in recipient cells.

Hedgehog acts as a morphogen by regulating proteolytic processing and activation of full-length Ci/Gli transcriptional effectors but can pattern Drosophila wing discs normally in the absence of regulated proteolytic processing.