DACT3

Official Full Name

dishevelled binding antagonist of beta catenin 3

Organism

Homo sapiens

Gene ID

147906

Background

Predicted to enable delta-catenin binding activity; protein kinase A binding activity; and protein kinase C binding activity. Involved in negative regulation of canonical Wnt signaling pathway and negative regulation of cell growth. Predicted to be active in cytoplasm. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

RRR1; DAPPER3

Cat.No.	Product Name	Price
CSC-DC004012	Panoply™ Human DACT3 Knockdown Stable Cell Line	Inquiry
CSC-SC004012	Panoply™ Human DACT3 Over-expressing Stable Cell Line	Inquiry

Cat.No.	Product Name	Price
AD04571Z	Human DACT3 adenoviral particles	Inquiry
LV10275L	human DACT3 (NM_145056) lentivirus particles	Inquiry

Cat.No.	Product Name	Price
SHG220915	shRNA set against Mouse Dact3(NM_001081655.1)	Inquiry
SHH274397	shRNA set against Human DACT3 (NM_145056.2)	Inquiry
SHH274401	shRNA set against Mouse DACT3 (NM_001081655.1)	Inquiry

Cat.No.	Product Name	Price
CDCR053366	Human DACT3 ORF clone (NM_145056.2)	Inquiry
CDFG008866	Human DACT3 cDNA Clone(NM_145056.2)	Inquiry
MiUTR1M-03680	DACT3 miRNA 3'UTR clone	Inquiry
MiUTR3H-11659	DACT3 miRNA 3'UTR clone	Inquiry
CDCB182141	Rabbit DACT3 ORF clone (XM_008250797.1)	Inquiry
CDCH384891	Rat DACT3 ORF clone(NM_001191947.1)	Inquiry
CDCR053372	Mouse Dact3 ORF clone (NM_001081655.1)	Inquiry
CDCS416980	Human DACT3 ORF Clone (BC034052)	Inquiry

Detailed Information

Dishevelled-Binding Antagonist of Beta-Catenin 3 (DACT3) is a vital component of the Wnt signaling pathway, a highly conserved pathway essential for embryonic development, tissue homeostasis, and cancer progression. DACT3 exhibits a distinct domain composition, including regions that interact with Dishevelled (Dvl) proteins and beta-catenin, pivotal players in the Wnt signaling cascade. DACT3 acts as a negative regulator of the Wnt/beta-catenin pathway, modulating cellular responses to Wnt ligands. It influences cell adhesion, migration, and proliferation, thereby impacting tissue morphogenesis and organ development.

The Structure of DACT3

DACT3 is a pivotal protein in the regulation of cell signaling and development. The primary structure of DACT3 consists of a series of structural domains that provide it with unique functional properties. The N-terminal domain is responsible for binding to disheveled proteins, whereas the C-terminal domain interacts withβ-catenin, thereby inhibiting its transcriptional activity. This dual binding capacity enables DACT3 to act as a molecular switch that regulates the balance between Wnt signaling activation and inhibition. A significant feature of DACT3's structure is its highly flexible nature, which allows for dynamic interactions with multiple partners within the cell. This mobility is facilitated by the presence of several short peptide motifs, called beta-propeller domains, which provide a scaffold for the assembly of diverse signaling complexes. The structure of DACT3 also includes a series of conserved loops and hydrophobic regions that contribute to its stability and interaction with other cellular components. These structural features enable DACT3 to function as a adaptor protein, facilitating the assembly of multiprotein complexes and the modulation of signal transduction pathways. DACT3 enables it to act as a regulatory hub within the cell, controlling essential signaling pathways that govern cell fate, proliferation, and differentiation.

DACT3 Affects Cell Migration and Proliferation

DACT3 gene plays a crucial role in regulating cell migration and proliferation. Cell migration is a vital process in embryonic development, tissue repair, and immune responses, while cell proliferation is essential for growth and tissue homeostasis. DACT3 influences these processes by modulating the activity of the Wnt/β-catenin signaling pathway, which is a key regulator of cell fate decisions and cellular behaviors.In cells, DACT3 functions as a natural antagonist of the Wnt/β-catenin pathway. It binds to dishevelled proteins, which are crucial components of the pathway. This interaction leads to the inhibition of β-catenin signaling, resulting in downstream effects on cell migration and proliferation. Studies have shown that increased DACT3 expression inhibits cell migration and proliferation, while reduced DACT3 expression promotes these processes.The mechanism underlying DACT3's influence on cell migration and proliferation involves the regulation of key signaling molecules and transcription factors. DACT3 inhibits the nuclear translocation of β-catenin, which prevents the activation of genes involved in cell migration and proliferation. As a result, cells with high DACT3 expression have reduced migratory and proliferative capabilities.

DACT3 Critical Pathway in Cancer

DACT3 gene has recently emerged as a promising candidate in the field of cancer research. One of the key underlying mechanisms involves the abnormal activation of the Wnt/β-catenin signaling pathway, which plays a vital role in cell proliferation, differentiation, and apoptosis. DACT3 is a natural antagonist of the Wnt/β-catenin pathway, and its expression is often reduced in various types of cancers, leading to abnormal signaling and tumorigenesis. Increased expression of DACT3 can effectively inhibit tumor growth and metastasis in vitro and in vivo. Mechanistically, DACT3 functions by binding to dishevelled proteins, which are crucial components of the Wnt/β-catenin signaling pathway. This interaction blocks the activation ofβ-catenin, thereby inhibiting tumor promotion and progression. The evaluation of DACT3 as a potential prognostic and diagnostic marker is under investigation, as its expression levels in cancer tissues may predict patient outcomes.

References:

Qu X, Liu B, Wang L, Liu L, Zhao W, Liu C, Ding J, Zhao S, Xu B, Yu H, Zhang X, Chai J. Loss of cancer-associated fibroblast-derived exosomal DACT3-AS1 promotes malignant transformation and ferroptosis-mediated oxaliplatin resistance in gastric cancer. Drug Resist Updat. 2023 May;68:100936. doi: 10.1016/j.drup.2023.100936. Epub 2023 Jan 31. PMID: 36764075.
Wang L, Li B, Bo X, Yi X, Xiao X, Zheng Q. Hypoxia-induced LncRNA DACT3-AS1 upregulates PKM2 to promote metastasis in hepatocellular carcinoma through the HDAC2/FOXA3 pathway. Exp Mol Med. 2022 Jun;54(6):848-860. doi: 10.1038/s12276-022-00767-3. Epub 2022 Jun 28. PMID: 35764883; PMCID: PMC9256752.

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