Essential for hedgehog signaling regulation: acts as both a negative and positive regulator of sonic hedgehog (Shh) and Indian hedgehog (Ihh) pathways, acting downstream of SMO, through both SUFU-dependent and -independent mechanisms. Involved in the regulation of microtubular dynamics. Required for proper organization of the ciliary tip and control of ciliary localization of SUFU-GLI2 complexes. Required for localization of GLI3 to cilia in response to Shh. Negatively regulates Shh signaling by preventing inappropriate activation of the transcriptional activator GLI2 in the absence of ligand. Positively regulates Shh signaling by preventing the processing of the transcription factor GLI3 into its repressor form. In keratinocytes, promotes the dissociation of SUFU-GLI2 complexes, GLI2 nuclear translocation and Shh signaling activation. Involved in the regulation of epidermal differentiation and chondrocyte development. Can form homodimers and interacts with microtubules (PubMed:24952464). Interacts with GLI1 and SMO (By similarity). Interacts with GLI2, GLI3 and SUFU (PubMed:19549984). Interacts with NPHP1 (By similarity). Interacts with SMO and DLG5 (via PDZ4 or guanylate kinase-like domain) (PubMed:25644602). Localizes to the cilium tip. Expressed in heart, lung, liver, kidney, testis, spleen and cerebellum. Polyubiquitinated by UBR3. Mutations appear to be the cause of the matariki (maki) phenotype, characterized by expanded motor neuron domain in the 10.5 dpc neural tube. Motor neurons are increased in number and expand dorsally. Mutants die at the end of gestation, when other phenotypes characteristic of elevated Shh signaling are apparent, including preaxial polydactyly. Knockout mice have defects in developmental patterning and die at birth with severe malformations, including exencephaly and polydactyly. Belongs to the TRAFAC class myosin-kinesin ATPase superfamily. Kinesin family.