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Validated All-in-One™ qPCR Primer for JUP(NM_002230.3) 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
This gene encodes a major cytoplasmic protein which is the only known constituent common to submembranous plaques of both desmosomes and intermediate junctions. This protein forms distinct complexes with cadherins and desmosomal cadherins and is a member of the catenin family since it contains a distinct repeating amino acid motif called the armadillo repeat. Mutation in this gene has been associated with Naxos disease. Alternative splicing occurs in this gene; however, not all transcripts have been fully described.
Gene References into function
- Arrhythmogenic right ventricular cardiomyopathy caused by a deletion in plakoglobin (Naxos disease). Review.
- stimulation of beta-catenin and suppression of gamma-catenin expression, occur within endometrial carcinomas with squamous differentiation
- function as an inhibitor of beta-catenin/TCF-dependent gene transcription and role as a potentially novel tumor suppressor protein in a subset of human NSCLC cancers
- heregulin/neuregulin-1 induces binding of MUC1 and gamma-catenin and targeting of the MUC1-gamma-catenin complex to the nucleolus
- phosphorylation of Tyr549 and the increased binding of plakoglobin to components of adherens junctions can contribute to the upregulation of the transcriptional activity of the beta-catenin-Tcf-4 complex observed in many epithelial tumor cells
- plakoglobin can activate the Wnt signaling cascade directly without interaction of beta-catenin, and that plakoglobin has multiple functions as a transcriptional activator and a cell adhesion molecule like beta-catenin
- plakoglobin is a new target gene governed by HDAC, and it acts as an oncogene in HT1080 cells
- show that the AML-associated translocation products (AATPs) directly activate the gamma-catenin promoter, which plays a crucial role in increasing the self-renewal of HSCs upon expression of AATPs
- Methylation of the gamma-catenin gene is associated with renal cell carcinoma
- The gamma-catenin mutation related to Bcl-2 overexpression has a significant effect on the pathogenesis of hormone refractory prostate cancer.
- Loss of expression indicated a reduced survival rate in nodal-negative squamous cell carcinomas of the mouth floor
- results show that plakoglobin acts as a tumour suppressor gene in bladder carcinoma cells and the silencing of plakoglobin gene expression in late-stage bladder cancer is a primary event in tumour progression
- Presenilin-1association with plakoglobin enhances the interaction of this molecule with Tcf-4 and prevents its binding to DNA.
- plakoglobin is differentially expressed in alveolar and embryonal rhabdomyosarcoma and its expression depends on the methylation and acetylation status of the gene
- A dominant mutation in the gene encoding plakoglobin in a German family with Arrhythmogenic right ventricular cardiomyopathy but no cutaneous abnormalities, is reported.
- the autocrine hGH-stimulated increases in DNMT3A and DNMT3B expression mediate repression of plakoglobin gene transcription by direct hypermethylation of its promoter and consequent phenotypic conversion of mammary carcinoma cells
- Overexpression of gamma-catenin caused an increase in PTTG and c-Myc protein levels, which are likely to accelerate chromosomal instability and uncontrolled proliferation, respectively, in the affected cells.
- Abnormal plakoglobin expression may be involved in the formation of some cases of Paget's of the vulva and the breast.
- In Wilm's tumors,there was an absence of strong correlation between the loss of gamma-catenin and unfavorable outcome.
