a protein in the WNT/planar cell polarity (PCP) signaling pathway. Dvl2-deficient mice indicate that Dvl2 is essential for normal cardiac morphogenesis, somite segmentation and neural tube closure. Transduces the Wnt signal by interacting with the cytoplasmic Axin complex. Dvl and Axin each contain a DIX domains, which mediate their dynamic polymerization. The Dvl-Axin interaction is essential for Wnt signaling. Interacts through its PDZ domain with the C-terminal regions of VANGL1 and VANGL2. Interacts with Dixin and Rac. There is functional redundancy between Dvl1 and Dvl2 in some phenotypes. Note: This description may include information from UniProtKB.
Protein type: Motility/polarity/chemotaxis; Adaptor/scaffold
Cellular Component: clathrin-coated vesicle; apical part of cell; cytoplasm; plasma membrane; cell cortex; cytosol; nucleus
Molecular Function: identical protein binding; protein domain specific binding; protein binding; signal transducer activity; protein self-association; frizzled binding
Biological Process: transcription from RNA polymerase II promoter; heart morphogenesis; positive regulation of JNK activity; Wnt receptor signaling pathway; convergent extension involved in neural plate elongation; Wnt receptor signaling pathway, planar cell polarity pathway; positive regulation of transcription, DNA-dependent; heart development; Wnt receptor signaling pathway through beta-catenin; cell migration in hindbrain; segment specification; convergent extension; neural tube closure; positive regulation of transcription factor activity; positive regulation of protein amino acid phosphorylation
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.