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Validated All-in-One™ qPCR Primer for CTNND1(NM_001085458.2) Search again
Product ID:
HQP152175
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BCDS2, CAS, CTNND, P120CAS, P120CTN, p120, p120(CAS), p120(CTN)
Gene Description:
catenin delta 1
Target Gene Accession:
NM_001085458.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
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.
Summary
This gene encodes a member of the Armadillo protein family, which function in adhesion between cells and signal transduction. Multiple translation initiation codons and althernative splicing result in many different isoforms being translated. Not all of the full-length natures of the described transcript variants have been determined. [provided by RefSeq].
Gene References into function
- The interaction of VE-cadherin with p120 catenin plays an important role in cellular growth, suggesting that the binding of p120 catenin to cadherins may regulate cell proliferation.
- Overexpression of delta catenin is associated with prostatic adenocarcinoma
- These data reveal a cooperative interaction between p120 catenin and E-cadherin and a novel role for p120 that is likely indispensable in normal cells.
- roles of p120 as a tumor suppressor or metastasis promoter are discussed (review)
- Both p120(ctn)-defective tumor cell contacts and p120(ctn)-mediated growth signals appear to contribute to the aggressive spread of pancreatic cancer.
- study links posttranslational modifications of VEC, beta-catenin, and p120 to the mechanism of thrombin-induced increase in endothelial permeability
- The data reveal a core function of p120 in cadherin complexes, and strongly predict a dose-dependent loss of E-cadherin in tumors that partially or completely down-regulate p120.
- Cellular levels of p120ctn function as a set point mechanism that regulates cadherin expression levels; a major function of p120ctn is to control cadherin internalization and degradation.
- binding of p120ctn to microtubules is inversely related to its ability to regulate Rho GTPases
- differential expression of p120(ctn) and Kaiso mRNA was observed in human coronary artery endothelial cells depending on how laminar shear stress was applied in relation to the wounding process
- Cytoplasmic p120ctn may contribute to the invasive phenotype of E-cadherin-deficient breast cancer cells
- Galpha12-p120ctn interaction acts as a molecular switch, which regulates cadherin-mediated cell-cell adhesion.
- in human lymphoblasts, the silencing of one allele is incomplete
- E-cadherin-deficiency in metastatic cancer may in some cases be due to p120 downregulation [review]
- Catenin p120ctn inhibits association of Kaiso with the matrilysin promoter.
- Overexpression of P-cadherin was strongly associated with cytoplasmic accumulation of one of the catenins, p120ctn, and cadherin switching in pancreatic ductal carcinoma cells.
- trans-interacting nectin inhibits non-trans-interacting E-cadherin endocytosis through afadin, Rap1, and p120ctn
- These results support a model in which the VE-cadherin tail mediates interactions with clathrin-dependent endocytic machinery, and this endocytic processing is inhibited by p120 binding to the cadherin tail.
- Increased expression of delta-catenin is associated with the down-regulation and redistribution of ECAD and p120ctn in prostatic cancer.
- results indicate that p120ctn plays an important role in regulating the formation of E-cadherin and -catenin complex, cell apoptosis, cell cycle and hepatoma cell biological function
- the degradation of E-cadherin in response to expression of R-cadherin is due to competition for p120(ctn)
- Membrane-localization and not cadherin interaction is the main determinant in p120 serine-threonine phosphorylation-dephosphorylation, further, the phospho-status had no effect on p120's role in cadherin complex stabilization or cell-cell adhesion.
- p120 catenin and mesenchymal cadherins are both required for invasiveness of E-cadherin-deficient cells; p120 acts as a rheostat, promoting a sessile cell phenotype associated with E-cadherin or a motile phenotype associated with mesenchymal cadherins.
- the recruitment of PI3K to the E-cadherin/beta-catenin/p120-catenin complex via beta-catenin at the plasma membrane is required for calcium-induced phospholipase C-gamma1 activation and, ultimately, keratinocyte differentiation
- In this review, p120 catenins function in the cytoplasm as versatile scaffolds that confer specificity to the complex regulation of Rho-GTPases and direct the spatio-temporal control of Rho-signalling.
- membranous p120 is maintained in invasive squamous cell carcinomas in tumours suggesting that p120 may be important for the collective invasion of tumours cells in vivo
- identification of Gli-similar 2 (Glis2) as a novel binding protein for p120 catenin
- P120CTN was expressed stongly on the cuboidal cell membrane and cytoplasm of both tumor types. In polygonal cells, expression was decreased and mostly cytoplasmic.
- Helicobacter pylori infected gastric epithelial cells showed altered distribution/phosphorylation of p120ctn.
- Cortactin and p120 are shown to directly interact with each other via the cortactin N-terminal region
- We show that a fraction of N-cadherin in a complex with catenins is associated with cholesterol/sphingolipid-rich membrane microdomains in aggressive melanoma cells in vitro and experimental melanomas in vivo.
- These data suggest that serine/threonine phosphorylation of p120 influences the dynamics of E-cadherin in junctions.
- The expression of p120-catenin isoforms was associated with the genomic and transcriptional phenotype of breast cancer cells.
- findings show that p120ctn is a novel interactor of the desmoglein proteins, and may play a role in desmosome remodeling
- the the increased expression of p120 isoform 1 during tumor progression contributes to the invasive phenotype of cadherin-deficient carcinomas and that the N-terminal domain of p120 is a valid therapeutic target
- Report nuclear targeting of beta-catenin and p120ctn during thrombin-induced endothelial barrier dysfunction.
- p120 expression in solid pseudopapillary tumors (SPTs) is abnormal. Loss of E-cadherin is probably consequent on p120 loss or decrease. Aberrations & other alterations of the E-cadherin gene are unlikely to be responsible for loss of E-cadherin in SPTs.
- Reduced expression of P120 catenin in cholangiocarcinoma correlated with tumor clinicopathologic parameters.
- p120-catenin is a key component of the cadherin-gamma-secretase supercomplex
- VE-cad gap formation is required for leukocyte transmigration and identify p120 as a critical intracellular mediator of this process through its regulation of VE-cad expression at junctions.
- p120 and Kaiso regulate Helicobacter pylori-induced expression of matrix metalloproteinase-7
- PDGFR-mediated phosphorylation at this site is dependent on PKCalpha, a conventional PKC isoform implicated previously in disruption of adherens junctions.
- VE-cadherin levels are not directly related to N-cadherin levels but may be inversely related due to competition for p120.
- p120ctn is a unique positive regulator of the gamma-secretase processing of cadherins and a negative regulator of the amyloid precursor protein processing
- The extracellular accumulation of delta-catenin in urine supporting its potential utility for non-invasive prostate cancer detection.
- p120ctn isoforms 1A and 3A differently regulated the adhesive, proliferative, and invasive properties of lung cancer cells through distinct mechanisms.
- p120-catenin gene knockdown enhances the metastasis of lung cancer cells