Key negative regulator of Shh signaling, which promotes the processing of GLI3 into GLI3R during neural tube development. Recruited by TULP3 and the IFT-A complex to primary cilia and acts as a regulator of the PKA-dependent basal repression machinery in Shh signaling by increasing cAMP levels, leading to promote the PKA-dependent processing of GLI3 into GLI3R and repress the Shh signaling. In presence of SHH, it is removed from primary cilia and is internalized into recycling endosomes, preventing its activity and allowing activation of the Shh signaling. Its ligand is unknown. Mainly localizes to primary cilium in a TULP3 and IFT-A complex-dependent manner. In presence of SHH, it is removed from primary cilia and is internalized into recycling endosomes and is apparently not degraded. Expressed ubiquitously from 8.5 dpc and is mostly concentrated in the developing nervous system at later stages. By 10.5 dpc, it is mainly expressed in the neural tube. At later embryonic stages (12.5 dpc and 15.5 dpc), it is predominantly expressed in the brain, spinal cord, and dorsal ganglia and weakly expressed in the hindlimb. According to PubMed:18250320, expression is restricted to the lateral neural folds, while PubMed:23332756 detects expression throughout the neural tube. Also expressed at low levels in kidney stroma and retina at 15.5 dpc. An intragenic deletion in Gpr161 is responsible for the vacuolated lens (vl) phenotype that is characterized by neural tube defects and congenital cataracts. The vl mutation aroses spontaneously. About half of vl/vl embryos display lumbar-sacral spina bifida and die before birth, and the other half have closed neural tubes but show thinning of the midline neuroepithelium and epidermis, dilation of the dorsal ventricle, and presence of ectopic neuroepithelial cells in the ventricle. All surviving adults display congenital cataracts (PubMed:18250320). It is not a null mutant allele (PubMed:23332756). Embryonic lethality by 10.5 dpc caused by increased Shh signaling and ventralization throughout the developing neural tube. Defects in Gli3 processing. Belongs to the G-protein coupled receptor 1 family.