Aliases for DACT1 Gene
- Dishevelled-Binding Antagonist Of Beta-Catenin 1 2 3 5
- Hepatocellular Carcinoma Novel Gene 3 Protein 3 4
- Dapper Antagonist Of Catenin 1 3 4
- HDPR1 3 4
- DPR1 3 4
- Dapper, Antagonist Of Beta-Catenin, Homolog 1 (Xenopus Laevis) 2
- Dapper Homolog 1, Antagonist Of Beta-Catenin (Xenopus) 2
- Dapper, Antagonist Of Beta-Catenin, Homolog 1 3
External Ids for DACT1 Gene
Previous GeneCards Identifiers for DACT1 Gene
The protein encoded by this gene belongs to the dapper family, characterized by the presence of PDZ-binding motif at the C-terminus. It interacts with, and positively regulates dishevelled-mediated signaling pathways during development. Depletion of this mRNA from xenopus embryos resulted in loss of notochord and head structures, and mice lacking this gene died shortly after birth from severe posterior malformations. Alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Jan 2012]
GeneCards Summary for DACT1 Gene
DACT1 (Dishevelled-Binding Antagonist Of Beta-Catenin 1) is a Protein Coding gene. Diseases associated with DACT1 include Occipital Encephalocele and Craniorachischisis. Among its related pathways are Signaling by Wnt and CDK-mediated phosphorylation and removal of Cdc6. GO annotations related to this gene include beta-catenin binding and protein kinase A binding. An important paralog of this gene is DACT2.
UniProtKB/Swiss-Prot for DACT1 Gene
Involved in regulation of intracellular signaling pathways during development. Specifically thought to play a role in canonical and/or non-canonical Wnt signaling pathways through interaction with DSH (Dishevelled) family proteins. The activation/inhibition of Wnt signaling may depend on the phosphorylation status. Proposed to regulate the degradation of CTNNB1/beta-catenin, thereby modulating the transcriptional activation of target genes of the Wnt signaling pathway. Its function in stabilizing CTNNB1 may involve inhibition of GSK3B activity. Promotes the membrane localization of CTNNB1. The cytoplasmic form can induce DVL2 degradation via a lysosome-dependent mechanism; the function is inhibited by PKA-induced binding to 14-3-3 proteins, such as YWHAB. Seems to be involved in morphogenesis at the primitive streak by regulating VANGL2 and DVL2; the function seems to be independent of canonical Wnt signaling and rather involves the non-canonical Wnt/planar cell polarity (PCP) pathway (By similarity). The nuclear form may prevent the formation of LEF1:CTNNB1 complex and recruit HDAC1 to LEF1 at target gene promoters to repress transcription thus antagonizing Wnt signaling. May be involved in positive regulation of fat cell differentiation. During neuronal differentiation may be involved in excitatory synapse organization, and dendrite formation and establishment of spines.