DVL3 Antibodies

Segment polarity protein dishevelled homolog DVL-3 (DVL3)

Involved in the signal transduction pathway mediated by multiple Wnt genes. .

Gene Information

Human
Gene Name:	DVL3
Uniprot:	Q92997
Entrez:	1857

Family

Belongs to:
DSH family

Alternative Names

dishevelled 3 (homologous to Drosophila dsh); dishevelled, dsh homolog 3 (Drosophila); Dishevelled3; Dishevelled-3; DSH homolog 3; DVL3; KIAA0208dishevelled-3; segment polarity protein dishevelled homolog DVL-3

Molecular Weight

Mass (kDA):
78.055 kDA

Genomic Context

Human
Location:	3q27.1
Sequence:	3; NC_000003.12 (184155311..184173614)

Subcellular Localizations

Cytoplasm.

Diseases

• Malignant Neoplasms
• Neoplasms
• Carcinoma
• Malignant Squamous Cell Neoplasm
• Esophageal Neoplasms
• Malignant Paraganglionic Neoplasm
• Malignant Neoplasm Of Lung
• Cytogenetic Abnormality
• Malignant Neoplasm Of Stomach
• Neoplasm Metastasis
• Carcinogenesis
• Nervousness
• Ulcer

• Tumor Angiogenesis
• Cell Invasion
• Tissue Adhesions
• Crest Syndrome
• Malignant Neoplasm Of Breast
• Strabismus
• Mammary Neoplasms

Interacting Proteins

• ADAP1
• BAHD1
• CEP164
• CSNK1D
• CSNK1E

• CSNK2A1
• Dab2
• DVL1
• FAM13C
• KLF3

• KLHL12
• LRRFIP2
• LRRK2
• NOL12
• NXF1

• PITX1
• PRICKLE1
• PRPF3
• RWDD2B
• SIRT1

• STOM
• TNFAIP8L1
• UTP3
• YTHDC1
• ZBTB48

• ZNF408
• ZNF774

Pathways

• Convergent Extension
• Cell Growth
• Fertilization
• Cell Cycle
• Localization
• Neural Tube Closure
• Cell Proliferation
• Methylation
• Tube Closure
• Angiogenesis
• Tissue Homeostasis
• Transport
• Cell Adhesion

• Cell Migration
• Brain Development
• Lung Development
• Neurogenesis
• Endothelial Cell Proliferation
• Blastocyst Hatching
• Axon Guidance

PTMs

• Phosphorylation
• Methylation
• Cleavage

• Acetylation
• Prenylation
• Ubiquitination

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/DVL3

Best Uses Of The DVL3 Marker

DVL3 regulates Wnt/b–catenin signaling. This is why it is important for understanding the extent and causes of adipogenesis. Scientists may submit data for species, applications, special samples, and other purposes. These results could be eligible for product credits. This marker has many benefits for scientists all over the world. Scientists can submit their results to get product credits and special access.

DVL3 regulates the extent of adipogenesis

DVL3 regulates the degree of adipogenesis in adipocytes. It regulates the expression of genes involved in terminal differentiation. This gene has been implicated in severe obesity, and it may be one of the major drivers of this disease. It also controls the expression of two other genes essential for adipocyte differentiation, Dact1 and PPARg.

XOR regulates PPARg activation and contributes to ROS production, which both inhibit adipogenesis. It also colocalizes on milk-fat globules with the lipid binding protein adipophilin. XOR is required for fat-droplet release in mice. Nevertheless, it is not clear whether XOR is required for adipogenesis.

DVL3 is another factor that influences the amount of adipogenesis. This protein is essential for adipogenesis. Many diseases including diabetes, hypertension, and insulin resistance have been linked back to DVL3. The process also involves the creation of WNTs (Wingless type MMTV integration sites), a specialized family secreted glycoproteins that regulate cell fate and behavior.

In addition, miR-204-5p induces post-transcriptional silencing of DVL3, a key negative regulator of adipogenesis. It also regulates Wnt/bcatenin signaling at hADSCs. These genes could be targeted for therapeutics in metabolic diseases such as obesity and diabetes.

Osteoporosis has been linked with DVL3's regulation of adipogenesis. It regulates adipogenesis, PPARg, and FABP. Its function in adipogenesis is unknown, but it is implicated with Wnt signaling.

SIRT1 inhibits Wnt signaling through inhibition of sFRP1 or Dact1 genes. These proteins are crucial for the initiation of and progression of adipogenesis. SIRT1 knockdown reduces adipogenesis, and increases Wnt signaling activation. It also affects gene activity in cells without adiponectin.

While adipogenesis may not be fully understood, DVL3 plays an important role in obesity pathophysiology. It involves different transcriptional cascades, signaling pathways, and molecular mechanisms. Most studies on Adipogenesis have been done in vitro without the use of animals. Research into natural anti-obesity products is increasing as obesity becomes more common. These natural products could be used to reduce the amount of tissue mass by inhibiting Adipogenesis.

SIRT1 also inhibits adipogenesis within adipocytes. When SIRT1 is activated, adipocytes express adipogenic markers. These molecules inhibit adipocyte division. They also regulate the production of insulin and PPARg. Thus, SIRT1 plays an important role in regulating adipogenesis. Sirtuins/miRNAs may be useful if you have high levels SIRT1 in your blood.

DVL3 regulates activation of Wnt/b–catenin signals

DVL3, a scaffold protein that has three structurally-conserved domains, regulates Wnt/Bcatenin activity. It contains a domain called the DIX that mediates self-association and leads to the formation of multimerized receptor complexes at the membrane. These complexes are responsible to driving the signaling activity, and providing high local concentrations in binding sites for Wnt signals proteins.

The PDZ Domain located in the central area of Dvl binds a conserved peptide. It is the Fz motif. It has a low affinity that binds this peptide, suggesting other molecular interactions. Although the Dvl PDZ domain can accommodate many Fz-like peptides it is not yet clear what the binding mechanism is.

K34 and K285, which are both conserved lysine residues, play a key role in regulating DVL1's transfer into the nucleus. DVL1 regulates this interaction and can bind promoters of Wnt target gene genes to modulate their expression. These results are the first to demonstrate novel regulatory mechanisms in Wnt's signaling pathway.

A cell cannot activate the canonicalWnt signaling pathway unless it has a Wnt ligand, Fz. When a canonical molecule of Wnt binds with Fz, it recruits Dishevelled(Dvl) into the plasma membrane. Ring finger protein43 inhibits the signaling function of Fz by blocking the pathway. DEP-C is required for the binding motif between Fz & Dvl.

Quantitative realtime PCR was used in order to determine the mRNA expression levels of target genes within the Wnt/B'catenin signaling pathway. The normalization of the results was done using b–actin as the control. The sign "*" represents a significant change in gene expression. Results were reported as mean + SD. p values of 0.01 or 0.05 were considered significant.

Wnt/B–catenin pathway is a broad range of biological processes that play a role in the growth and proliferation of cells. Therefore, it is imperative to identify targeted agents that target Wnt/Bcatenin signalsing. The success of these agents will depend on the safety and effectiveness of these targeted therapies.

This study, in addition to targeting Wnt complex, has important implications on the development anticancer treatments. These pathways are so poorly controlled in many types of cancer, misregulation of them could lead to new anticancer drugs. This research could lead to new ways to treat cancer.

This research shows how aberrant activation o Wnt/b -catenin pathway contributes tumorigenesis as well as resistance to cancer therapies. In colorectal tumors, aberrant activation (Wnt/B)catenin signaling promotes the growth and spread of glioblastoma cells despite the presence or p53-positive cancer stem cell. The success of these treatments depends on the ability to block the Wnt/b–catenin signaling pathway.

DVL3 also has an effect on the centrosomal stage in cell-cycle progression. It regulates cell cycle phases by linking with linker protein. One experiment showed that a mutant of DVL-3 caused a change in cell-cycle phase. This was correlated with the mutation of adjacent DVL-1 genes. Live cells were stained by Vybrantcell violet, a fluorescent light dye.

The DVL3 proteins are involved in the formation a Wnt signalosome. This dynamic signaling complex controls the activity Wnt/b Catenin pathway. In addition, DVL3 negatively regulates the activity of Wnt signaling through receptor-mediated endocytosis. We will continue to study receptor-mediated endocysis in order to gain a better understanding of how Wnt signals are regulated.

Isoquercitrin and palmitoleic acids are two examples of compounds that can inhibit DVL3. These compounds have potent antitumor and translocation inhibitory effects on cancer cells. These compounds have been proven to be effective in preventing the growth of colon cancer cells. The drug nimbolide blocks the Wnt/b–catenin signaling pathway.