Wnt signaling in kidney disease (WP4150)
This pathway is modeled after Figure 5 of the article "Glomerulocystic kidney disease" (Bissler, et al. 2010). The gene product Wnt signals two different paths titled canonical and non-canonical. The non-canonical path is mediated by the membrane bound protein Disheveled (Dvl) which then controls the planar cell Polarity. The canonical path on the other hand is mediated by the cytoplasmic protein Disheveled (Dvl) and then is effected through b-catenin transcription. The complex of Nphp2 and Nphp3 seem to help facilitate the process by controlling the Wnt signaling. Bergmann, et al. (2008) showed that Nphp3 deficiency in Xenopus resulted to planar cell polarity defects. Proteins on this pathway have targeted assays available via the [https://assays.cancer.gov/available_assays?wp_id=WP4150 CPTAC Assay Portal].
Authors
Martina Summer-Kutmon , Kristina Hanspers , Maintenance bot , and Eric WeitzCited In
Organism
Homo sapiensCommunities
Diseases Renal Genomics PathwaysAnnotations
Disease Ontology: kidney disease
Pathway Ontology: signaling pathway Wnt signaling pathway Wnt signaling, the planar cell polarity pathway
Participants
References
- Bergmann C, Fliegauf M, Brüchle NO, Frank V, Olbrich H, Kirschner J, et al. Loss of nephrocystin-3 function can cause embryonic lethality, Meckel-Gruber-like syndrome, situs inversus, and renal-hepatic-pancreatic dysplasia. Am J Hum Genet. 2008 Apr;82(4):959–70. PubMed Europe PMC Scholia
- Bissler JJ, Siroky BJ, Yin H. Glomerulocystic kidney disease. Pediatr Nephrol. 2010 Oct;25(10):2049–56; quiz 2056–9. PubMed Europe PMC Scholia