DACT1

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.

dapper, antagonist of beta-catenin, homolog 1 (Xenopus laevis)

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.

By similarity5 Publications

Embryonic hindgut morphogenesis Source: UniProtKB
Negative regulation of beta-catenin-TCF complex assembly Source: ParkinsonsUK-UCL
Negative regulation of canonical Wnt signaling pathway Source: ParkinsonsUK-UCL
Negative regulation of G1/S transition of mitotic cell cycle Source: UniProtKB
Negative regulation of JNK cascade Source: UniProtKB
Negative regulation of protein binding Source: ParkinsonsUK-UCL
Negative regulation of transcription by RNA polymerase II Source: UniProtKB
Negative regulation of Wnt signaling pathway Source: UniProtKB
Neural tube development Source: ParkinsonsUK-UCL
Positive regulation of canonical Wnt signaling pathway Source: UniProtKB
Positive regulation of cellular protein catabolic process Source: ParkinsonsUK-UCL
Positive regulation of protein binding Source: ParkinsonsUK-UCL
Positive regulation of protein catabolic process Source: MGI
Positive regulation of Wnt signaling pathway Source: UniProtKB
Regulation of canonical Wnt signaling pathway Source: UniProtKB
Regulation of protein stability Source: UniProtKB
Regulation of Wnt signaling pathway, planar cell polarity pathway Source: UniProtKB
Wnt signaling pathway Source: UniProtKB-KW

Nucleus; Cytoplasm; Synapse. Shuttles between the nucleus and the cytoplasm. Seems to be nuclear in the absence of Wnt signaling and to translocate to the cytoplasm in its presence.

Neural tube defects (NTD):
Congenital malformations of the central nervous system and adjacent structures related to defective neural tube closure during the first trimester of pregnancy. Failure of neural tube closure can occur at any level of the embryonic axis. Common NTD forms include anencephaly, myelomeningocele and spina bifida, which result from the failure of fusion in the cranial and spinal region of the neural tube. NTDs have a multifactorial etiology encompassing both genetic and environmental components.
Townes-Brocks syndrome 2 (TBS2):
A form of Townes-Brocks syndrome, a rare autosomal dominant disease characterized by the triad of imperforate anus, dysplastic ears, and thumb malformations. Minor features of the condition include hearing loss, foot malformations, renal impairment with or without renal malformations, genitourinary malformations, and congenital heart disease.