DACT2 Gene - Dapper Dishevelled Antagonist of Beta-Catenin 2
A key regulator of Wnt signaling and tumor suppression
Gene Information Card
| Symbol | DACT2 |
|---|---|
| Full Name | Dapper Dishevelled Antagonist of Beta-Catenin 2 |
| Gene Type | protein-coding |
| Chromosomal Location | 6q27 |
| NCBI Gene ID | 168002 ncbi.nlm.nih.gov/gene/168002 |
| Ensembl ID | ENSG00000164463 |
| UniProt ID | Q5T6F2 |
| OMIM ID | 608966 |
| HGNC ID | 21269 |
| Aliases | DAPPER2, DPR2, THYEX3 |
Description
DACT2 (Dapper Dishevelled Antagonist of Beta-Catenin 2) is a protein-coding gene that encodes a member of the DACT (Dapper) family. The protein functions as a negative regulator of the Wnt signaling pathway by interacting with Dishevelled (DVL) and promoting its degradation, thereby inhibiting beta-catenin-mediated transcription. DACT2 is frequently silenced by promoter hypermethylation in various cancers, suggesting a tumor suppressor role.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Colorectal Cancer | Promoter hypermethylation leads to DACT2 silencing, resulting in aberrant Wnt activation | PMID: 22198284 |
| Gastric Cancer | DACT2 downregulation via methylation correlates with poor prognosis and metastasis | PMID: 23233744 |
| Hepatocellular Carcinoma | Loss of DACT2 expression promotes beta-catenin nuclear accumulation and tumor growth | PMID: 23708659 |
| Breast Cancer | DACT2 methylation is associated with aggressive tumor subtypes | PMID: 25964282 |
| Lung Cancer | DACT2 acts as a tumor suppressor; reduced expression linked to metastasis | PMID: 24662952 |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Placenta | 12.5 | Medium |
| Kidney | 8.2 | Low |
| Liver | 6.1 | Low |
| Lung | 5.4 | Low |
| Colon | 4.8 | Low |
| Breast | 3.2 | Not detected |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| HEK 293 | 10.1 | Embryonic kidney, moderate expression |
| HepG2 | 7.3 | Hepatocellular carcinoma, low expression |
| A549 | 4.5 | Lung carcinoma, low expression |
| MCF7 | 2.1 | Breast cancer, very low expression |
| HCT116 | 1.8 | Colorectal carcinoma, very low expression |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.1A>G | Missense | <0.1% | Likely benign |
| c.256C>T | Nonsense | <0.1% | Predicted loss of function |
| c.789_790insA | Frameshift | <0.1% | Loss of function |
| c.1024G>A | Missense | <0.1% | Unknown significance |
Mutation functional classification
Loss of Function (LOF)
Nonsense and frameshift mutations in DACT2 are predicted to truncate the protein, impairing its ability to antagonize Dishevelled and leading to unchecked Wnt signaling.
Gain of Function (GOF)
No gain-of-function mutations have been reported for DACT2.
Dominant Negative (DN)
No dominant-negative mutations have been characterized for DACT2.
View complete mutation data：
Gene Ontology (GO)
| • negative regulation of canonical Wnt signaling pathway | • protein binding |
| • cytoplasm | • nucleus |
| • signal transduction |
Pathways
• Wnt signaling pathway
• Beta-catenin destruction complex
Protein Summary
The DACT2 protein is a cytoplasmic and nuclear protein that binds to Dishevelled (DVL) and promotes its degradation via the ubiquitin-proteasome pathway. By reducing DVL levels, DACT2 inhibits the stabilization and nuclear translocation of beta-catenin, thereby suppressing Wnt target gene transcription. DACT2 is often epigenetically silenced in cancers, leading to constitutive Wnt pathway activation.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| DACT2 Knockout HEK293 Cell Line | EDJ-KQ12315 | Human | 168002 | Details Get a Quote |
| DACT2 Knockout HeLa Cell Line | EDJ-KQ58909 | Human | 168002 | Details Get a Quote |
| DACT2 Knockout A-549 Cell Line | EDJ-KQ67397 | Human | 168002 | Details Get a Quote |
| DACT2 Knockout HCT 116 Cell Line | EDJ-KQ75791 | Human | 168002 | Details Get a Quote |
