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Validated All-in-One™ qPCR Primer for WNT5A(NM_003392.4) 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 98%, 98% and 87% amino acid identity to the mouse, rat and the xenopus Wnt5A protein, respectively. The experiments performed in Xenopus laevis embryos identified that human frizzled-5 (hFz5) is the receptor for the Wnt5A ligand and the Wnt5A/hFz5 signaling mediates axis induction. [provided by RefSeq].
Gene References into function
- Frequent up-regulation of WNT5A mRNA in primary gastric cancer.
- Increased expression of WNT5a is associated with cell motility and invasion of metastatic melanoma
- WNT5a is upregulated by TNF-alpha in tumor cell lines
- Wnt-5a promotes T cell nuclear accumulation of the transcription factor NFAT in the presence of cyclosporin A.
- These results suggest that the TAK1-NLK MAPK cascade is activated by the noncanonical Wnt-5a/Ca(2+) pathway and antagonizes canonical Wnt/beta-catenin signaling.
- Results suggest that disabled-2 functions as a negative regulator of canonical Wnt signaling by stabilizing the beta-catenin degradation complex.
- Down-regulation of Wnt-4 and up-regulation of Wnt-5a are possible markers of the malignant phenotype of human squamous cell carcinoma.
- Altered mRNA expression is associated with prostate cancer recurrence.
- Their different spatial expression patterns suggest that Wnt4 and Wnt5a proteins are not functionally linked to type II collagen and type X collagen synthesis in in vitro chondrogenic models of mesenchyme stem cells
- Wnt-5a is involved in the response of malignant neuroblasts to retinoic acid.
- Wnt-5a serves as an antagonist to the canonical Wnt-signaling pathway with tumor suppressor activity in differentiated thyroid carcinomas.
- Over-expression of Wnt5a in transgenic mice disrupts epithelial-response to FGF10 and regulates Shh signaling.
- function of Wnt 5a as either a suppressor or promoter of malignant progression seems to be modulated by intercellular interactions
- WNT5A and FZD5 regulate the microbially induced interleukin-12 response of antigen-presenting cells and interferon-gamma production by mycobacterial antigen-stimulated T cells
- NFAT1, a transcription factor connected with breast cancer metastasis, is activated by Wnt-5a through a Ca2+ signaling pathway in human breast epithelial cells which was simultaneously counteracted by a Wnt-5a-induced Yes/Cdc42 signaling pathway.
- The Embryonic Lethal Abnormal Vision-like protein HuR, inhibited translation of Wnt-5a when bound to highly conserved AU-rich sequences in the 3'-untranslated region of the Wnt-5a mRNA.
- The aberrant expression of WNT5A suggest that the Wnt signaling pathway may be abnormally regulated in nasopharyngeal carcinoma (NPC), which provides insight into the molecular mechanisms of NPC.
- Screening for Wnt5a-regulated genes in cultured endothelial cells identified several encoding angiogenic regulators, including matrix metalloproteinase-1, an interstitial collagenase, and Tie-2, a receptor for angiopoietins.
- WNT5A is an important target of CUTL1 and mediator of invasiveness and tumor progression in pancreatic cancer.
- Wnt5A can signal via protein kinase C (PKC), so the role of PKC in Wnt5A-mediated motility and epithelial to mesenchymal transition was also assessed using PKC inhibition and activation studies
- Wnt3A/5A can function as mesenchymal regulatory factors by providing instructive cues for the recruitment, maintenance, and differentiation of mesenchymal stem cells.
- Our findings demonstrate that APC status plays a key role as a determinant of Wnt5a secretion and suggest that CaSR-mediated secretion of Wnt5a will inhibit defective Wnt signaling in APC-truncated cells in an autocrine manner.
- Hypomethylation of wingless-related MMTV integration site 5A (WNT5A), S100 calcium-binding protein P (S100P) and cysteine-rich protein 1(CRIP1) was confirmed in the cancer cells by bisulfite sequencing.
- Ability of phenylmethimazole (C10) to decrease growth and migration of papillary thyroid cancer cells may be related to its suppressive effect on TLR3 and Wnt5a signaling.
- 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.
- Data indicate that Wnt5a signaling is an important regulator in the proliferation of glioma cells.
- did not detect submicroscopic deletion or duplication nor sequence alteration in either CACNA2D3 or WNT5A in ZLS-affected individuals
- Wnt5a and Wnt11 expression in EPC cells was induced by coculture with rat neonatal cardiomyocyte and was blocked by gamma-secretase inhibition.
- Our findings suggest non-canonical Wnt signalling plays a role in regulating endothelial cell growth and possibly in angiogenesis.
- These data show activation of the Wnt/beta-catenin-signalling pathway in uveal melanoma and suggest that components of this pathway might be useful prognostic markers as well as attractive therapeutic targets to treat this disease.
- WNT5A, a putative tumour suppressor gene in ALL, is silenced by methylation in this disease and that this epigenetic event is associated with upregulation of CYCLIN D1 expression and confers poor prognosis in patients with ALL.
- WNT5A is frequently inactivated in CRC by tumor-specific methylation, and thus, is a potential biomarker.
- MT1-MMP-induced phenotypic changes were dependent upon up-regulation of Wnt5a, which has been implicated in epithelial-to-mesenchymal transition.
- Wnt5A is critically involved in inflammatory macrophage signaling in sepsis and is a target for antiinflammatory mediators like APC or antagonists like sFRP1.
- findings show cell-autonomous mechanisms allow Wnt5a to control cell orientation, polarity, and directional movement in response to positional cues from chemokine gradients
- Wnt5a expressed in atherosclerotic lesions colocalizes with TLR-4.
- 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
- negative correlation between expression of Wnt-5a & hepatitis B virus x gene(HBx) mutations in hepatocellular carcinoma(HCC); it is concluded that HBx mutants may participate in development & progression of HCC, at least in part through the Wnt-5a pathwa
- No mutation found in Zimmermann-Laband syndrome
- 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
- Data show that Wnt5a is highly expressed during osteoblastic differentiation, and that clusters of genes regulating cell cycle, cell proliferation and cell growth, and gene transcription are altered with absence of Wnt5a expression.
- Expression of Wnt5a plasmid but not Wnt1 or Wnt3a increased caudal homeodomain factor CDX2 transcripts and protein in HT-29 adenocarcinoma cells. Wnt5a increased activity of a sucrase-isomaltase (SI) promoter in Caco-2BBE cells.
- Cytoplasmic WNT5A increases with melanoma progression and strong expression is associated with poor outcome.
- LRP1 stimulates a canonical Wnt5a signaling pathway that prevents cholesterol accumulation.
- These data suggest that the epigenetic remodeling of the WNT5A promoter is correlated with its transcriptional activation and this upregulation likely participates in arsenical-induced malignant transformation.
- Amino acid limitation in colon cancer cells induces phosphorylation of ERK1/2, which then down-regulates WNT5a expression.
- Staining of a melanoma tissue array also highlighted the inverse relationship between MART-1 and Wnt5A expression.
- pathways related to Wnt5a have an important role in ovarian malignant neoplasia.
- Wnt-5a signaling acts to re-establish ERalpha expression in ERalpha-negative breast cancer cells.
