DAAM1
Protein-coding gene in the species Homo sapiens
From Wikipedia, the free encyclopedia
Dishevelled-associated activator of morphogenesis 1 is a protein that in humans is encoded by the DAAM1 gene.[5][6][7] Evidence of alternative splicing has been observed for this gene but the full-length nature of these variants has not been determined.
| DAAM1 | |||||||||||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| |||||||||||||||||||||||||||||||||||||||||||||||||||
| Identifiers | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Aliases | DAAM1, dishevelled associated activator of morphogenesis 1 | ||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM: 606626; MGI: 1914596; HomoloGene: 36635; GeneCards: DAAM1; OMA:DAAM1 - orthologs | ||||||||||||||||||||||||||||||||||||||||||||||||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||
| Wikidata | |||||||||||||||||||||||||||||||||||||||||||||||||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||
Function
Cell motility, adhesion, and cytokinesis, and other functions of the cell cortex are mediated by the reorganization of the actin cytoskeleton and recent evidence suggests a role for formin homology (FH) proteins in these processes. The protein encoded by this gene contains FH domains and belongs to a novel FH protein subfamily implicated in cell polarity. Wnt/Fz signaling activates the small GTPase Rho, a key regulator of cytoskeleton architecture, to control cell polarity and movement during development. Activation requires Dvl-Rho complex formation, an assembly mediated by this gene product, which is thought to function as a scaffolding protein.[7]
Clinical significance
The deletion of a single copy of this gene has been associated with congenital heart defects.[8]