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: apical part of cell; clathrin-coated endocytic vesicle; cytoplasm; cytoplasmic vesicle; cytosol; nucleus; plasma membrane
Molecular Function: frizzled binding; identical protein binding; protein binding; protein binding, bridging; protein domain specific binding; protein kinase binding; protein self-association; Rac GTPase binding
Biological Process: convergent extension involved in neural plate elongation; heart development; neural tube closure; positive regulation of GTPase activity; positive regulation of JNK activity; positive regulation of protein amino acid phosphorylation; positive regulation of transcription factor activity; positive regulation of transcription, DNA-dependent; protein oligomerization; segment specification; transcription from RNA polymerase II promoter; Wnt receptor signaling pathway; Wnt receptor signaling pathway through beta-catenin; Wnt receptor signaling pathway, planar cell polarity pathway
LTP: 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.