First Author | Hot B | Year | 2017 |
Journal | Cell Signal | Volume | 32 |
Pages | 93-103 | PubMed ID | 28126591 |
Mgi Jnum | J:318440 | Mgi Id | MGI:6859643 |
Doi | 10.1016/j.cellsig.2017.01.023 | Citation | Hot B, et al. (2017) FZD10-Galpha13 signalling axis points to a role of FZD10 in CNS angiogenesis. Cell Signal 32:93-103 |
abstractText | Among the 10 Frizzled (FZD) isoforms belonging to the Class F of G protein-coupled receptors (GPCRs), FZD10 remains the most enigmatic. FZD10 shows homology to FZD4 and FZD9 and was previously implicated in both beta-catenin-dependent and -independent signalling. In normal tissue, FZD10 levels are generally very low; however, its upregulation in synovial carcinoma has attracted some attention for therapy. Our findings identify FZD10 as a receptor interacting with and signalling through the heterotrimeric G protein Galpha13 but not Galpha12, Galphai1, GalphaoA, Galphas, or Galphaq. Stimulation with the FZD agonist WNT induced the dissociation of the Galpha13 protein from FZD10, and led to global Galpha12/13-dependent cell changes assessed by dynamic mass redistribution measurements. Furthermore, we show that FZD10 mediates Galpha12/13 activation-dependent induction of YAP/TAZ transcriptional activity. In addition, we show a distinct expression of FZD10 in embryonic CNS endothelial cells at E11.5-E14.5. Given the well-known importance of Galpha13 signalling for the development of the vascular system, the selective expression of FZD10 in brain vascular endothelial cells points at a potential role of FZD10-Galpha13 signalling in CNS angiogenesis. |