Receptor for Wnt proteins. Most of frizzled receptors are coupled to the beta-catenin canonical signaling pathway, which leads to the activation of disheveled proteins, inhibition of GSK-3 kinase, nuclear accumulation of beta-catenin and activation of Wnt target genes (PubMed:25759469). A second signaling pathway involving PKC and calcium fluxes has been seen for some family members, but it is not yet clear if it represents a distinct pathway or if it can be integrated in the canonical pathway, as PKC seems to be required for Wnt-mediated inactivation of GSK-3 kinase. Both pathways seem to involve interactions with G-proteins. May be involved in transduction and intercellular transmission of polarity information during tissue morphogenesis and/or in differentiated tissues. (Microbial infection) Acts as a receptor for C.difficile toxin TcdB in the colonic epithelium (PubMed:27680706, PubMed:29748286). TcdB occupies the binding site for Wnt-adducted palmitoleate in frizzled receptors and TcdB-binding prevents Wnt-binding and downstream Wnt signaling (PubMed:29748286). (Microbial infection) Interacts with C.difficile toxin TcdB; frizzled receptors constitute the major host receptors for TcdB in the colonic epithelium. Widely expressed. In the adult, mainly found in heart, placenta, skeletal muscle, lung, kidney, pancreas, prostate, testis, ovary and colon. In the fetus, expressed in brain, lung and kidney. Low levels in fetal liver. Lys-Thr-X-X-X-Trp motif interacts with the PDZ domain of Dvl (Disheveled) family members and is involved in the activation of the Wnt/beta-catenin signaling pathway. The FZ domain is involved in binding with Wnt ligands. Ubiquitinated by ZNRF3, leading to its degradation by the proteasome. The disease is caused by variants affecting the gene represented in this entry. Defects in FZD2 have been found in patients with Robinow syndrome-like features including short-limb dwarfism, broad thumbs and craniofacial abnormalities. Belongs to the G-protein coupled receptor Fz/Smo family.