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Validated All-in-One™ qPCR Primer for WNT3A(NM_033131.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
The WNT gene family consists of structurally related genes which encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene is a member of the WNT gene family. It encodes a protein which shows 96% amino acid identity to mouse Wnt3A protein, and 84% to human WNT3 protein, another WNT gene product. This gene is clustered with WNT14 gene, another family member, in chromosome 1q42 region. [provided by RefSeq].
Gene References into function
- Regulation of WNT3 and WNT3A mRNAs in human cancer cell lines NT2, MCF-7, and MKN45
- Clustered with WNT14 on 1q42.
- wnt3a-beta catenin signaling regulates LEF-1 gene expression
- CKI epsilon-dependent phosphorylation of Dvl enhances the formation of a complex of Dvl-1 with Frat-1 and this complex leads to the activation of Wnt-3a-induced accumulation of beta-catenin
- These results suggest that Wnt responsiveness is a stage-specific phenomenon in B-cell development and that the morphological changes associated with Wnt signaling may play a role in the motility and metastatic potential of myeloma cells.
- Results suggest that disabled-2 functions as a negative regulator of canonical Wnt signaling by stabilizing the beta-catenin degradation complex.
- Wnt3a may stimulate a cellular phosphatase to dephosphorylate and activate CKIepsilon
- Wnt/beta-catenin pathway activation by Wnt3a raised beta-catenin in monocytes & decreased migration thru a dermal microvascular endothelial cell layer. This was associated with specific monocyte adherence to endothelial cells after Wnt3a exposure.
- BMP-2 antagonizes Wnt-3a signaling in osteoblast progenitors by promoting an interaction between Smad1 and Dvl-1 that restricts beta-catenin activation
- ILK activity can modulate acute Wnt3a mediated beta-catenin phosphorylation, stabilization and nuclear activation in a PI3K-independent manner.
- Wnt-LRP5 signalling may play a role in the adaptation of bone to mechanical load in humans, and may explain some gender-related differences in bone mass
- Over-expression of the Wnt3a gene significantly enhances the ability of fibroblast feeder cells to support the undifferentiated growth of 3 different human embryonic stem cell lines.
- Wnt3A/5A can function as mesenchymal regulatory factors by providing instructive cues for the recruitment, maintenance, and differentiation of mesenchymal stem cells.
- Wnt3A treatment significantly activated human hepatic stellate cells, while this was inhibited in secreted frizzled-related protein 1 (sFRP1) overexpressing cells.
- These results suggest that Wnt signaling crosstalk and functional antagonism with the LRP5 co-receptor are key signaling regulators of mesenchymal stem cells maintenance and differentiation.
- Blockade of Wnt3a stimulation of IP(5) generation blocks beta-catenin accumulation
- Results identify a novel feedback mechanism by which Wnt, including Wnt3a, negatively regulates LRP6 at the mRNA level.
- These findings demonstrate a requirement of Wnt signaling for maintenance, proliferation, and survival of NP when cultured in neurosphere conditions.
- Wnt3a markedly reduced the forskolin-induced expression of RANKL, a target gene of PTH/cAMP/PKA.
- Our results suggest that Wnt/beta-catenin signaling plays important roles in human fetal skin development and homeostasis, which also provide new insights on the molecular mechanisms of oncogenesis in human epidermis.
- bone marrow sera from 21 multiple myeloma patients significantly suppressed Wnt3a-induced OPG expression and enhanced RANKL expression in osteoblasts in a DKK1-dependent manner
- effect of Wnt3a on bone disease and growth of multiple myeloma cells in vitro and in vivo
- study demonstrated that Wnt3a & Wnt5a can promote proliferation of HEK293 cells & inhibit serum starvation-induced apoptosis, which implies Wnt3a & Wnt5a can maintain survival of HEK293 cells under stress
- FGF antagonizes Wnt signaling by inhibiting Wnt-induced transcription and suggest that multiple mechanisms, including downregulation of TCFs and Wnt receptors, contribute to this effect.
- glutamine synthetase has a role in control of glutamate signalling through Wnt3A and steroid pathways in osteoblastic cells
- both Wnt5a and Wnt3a bound Ror2, only Wnt5a induced Ror2 homo-dimerization and tyrosine phosphorylation in U2OS human osteoblastic cells.
- Wnt3a and Wnt5a have roles in inducing BMP-4 and 6 expression in prostate cancer osteoblast differentiation
- essential role of Wnt3a in hepatocyte differentiation from hESCs; Wnt3a facilitates clonal plating of hESCs exhibiting functional hepatic differentiation
- the frequent loss of stromal TGF-beta type II receptor expression in prostate cancer can relieve the paracrine suppression of Wnt3a expression
- These findings suggest that WNT3A can mediate transcriptional changes in melanoma cells in a manner reminiscent of the known role of Wnt/beta-catenin signaling in normal melanocyte development.
