Aliases for WNT5A Gene
External Ids for WNT5A Gene
Previous GeneCards Identifiers for WNT5A Gene
The WNT gene family consists of structurally related genes which encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene encodes a member of the WNT family that signals through both the canonical and non-canonical WNT pathways. This protein is a ligand for the seven transmembrane receptor frizzled-5 and the tyrosine kinase orphan receptor 2. This protein plays an essential role in regulating developmental pathways during embryogenesis. This protein may also play a role in oncogenesis. Mutations in this gene are the cause of autosomal dominant Robinow syndrome. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Jan 2012]
GeneCards Summary for WNT5A Gene
WNT5A (Wnt Family Member 5A) is a Protein Coding gene. Diseases associated with WNT5A include Robinow Syndrome, Autosomal Dominant 1 and Autosomal Dominant Robinow Syndrome. Among its related pathways are Validated targets of C-MYC transcriptional repression and Wnt Signaling Pathways: beta-Catenin-independent Wnt/Ca2+ Signaling and Other Non-canonical Wnt Signaling Pathways. GO annotations related to this gene include transcription factor activity, sequence-specific DNA binding and protein domain specific binding. An important paralog of this gene is WNT5B.
UniProtKB/Swiss-Prot for WNT5A Gene
Ligand for members of the frizzled family of seven transmembrane receptors. Can activate or inhibit canonical Wnt signaling, depending on receptor context. In the presence of FZD4, activates beta-catenin signaling. In the presence of ROR2, inhibits the canonical Wnt pathway by promoting beta-catenin degradation through a GSK3-independent pathway which involves down-regulation of beta-catenin-induced reporter gene expression. Suppression of the canonical pathway allows chondrogenesis to occur and inhibits tumor formation. Stimulates cell migration. Decreases proliferation, migration, invasiveness and clonogenicity of carcinoma cells and may act as a tumor suppressor. Mediates motility of melanoma cells. Required during embryogenesis for extension of the primary anterior-posterior axis and for outgrowth of limbs and the genital tubercle. Inhibits type II collagen expression in chondrocytes.