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Junction plakoglobin

gamma Catenin, JUP
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Armadillo, DSP, Desmoglein 2, HAD, AGE
Papers on gamma Catenin
Diagnostic value of cyclin-dependent kinase/cyclin-dependent kinase inhibitor expression ratios as biomarkers of locoregional and hematogenous dissemination risks in oral squamous cell carcinoma.
New
Takagi et al., Niigata, Japan. In Mol Clin Oncol, Sep 2015
UNASSIGNED: The aim of the present study was to investigate the diagnostic value of cell cycle-related genes in oral squamous cell carcinoma (OSCC) by examining the expression of the following genes in 77 OSCC tissues by quantitative polymerase chain reaction: Cyclin genes (CCNA1, CCND1, CCND2 and CCNE1), cyclin-dependent kinase (CDK) genes (CDK1, CDK2 and CDK4), CDK inhibitor genes (CDKN2A, CDKN1A, CDKN1B and CDKN1C), and integrin and associated genes that we previously reported (ITGA3, ITGB4, CD9 and JUP).
Comprehensive analysis of desmosomal gene mutations in Han Chinese patients with arrhythmogenic right ventricular cardiomyopathy.
New
Yang et al., Nanjing, China. In Eur J Med Genet, Apr 2015
Five desmosomal genes (PKP2, DSG2, DSP, DSC2 and JUP) were sequenced directly from genomic DNA.
Normalization of Naxos plakoglobin levels restores cardiac function in mice.
New
Chen et al., In J Clin Invest, Apr 2015
A subset of patients with AC have the autosomal recessive cardiocutaneous disorder Naxos disease, which is caused by a 2-base pair deletion in the plakoglobin-encoding gene JUP that results in a truncated protein with reduced expression.
Assessment of HaloPlex amplification for sequence capture and massively parallel sequencing of arrhythmogenic right ventricular cardiomyopathy-associated genes.
Jonasson et al., Linköping, Sweden. In J Mol Diagn, 2015
We used SureDesign to prepare a HaloPlex enrichment system for sequencing of DES, DSC2, DSG2, DSP, JUP, PKP2, RYR2, TGFB3, TMEM43, and TTN from patients with ARVC using a MiSeq instrument.
BALL-SNP: combining genetic and structural information to identify candidate non-synonymous single nucleotide polymorphisms.
Keller et al., Saarbrücken, Germany. In Genome Med, 2014
Here, the analysis highlighted accumulation of variations in the genes JUP, VCL, and SMYD2.
Genetic Analysis of Arrhythmogenic Diseases in the Era of NGS: The Complexity of Clinical Decision-Making in Brugada Syndrome.
Brugada et al., Girona, Spain. In Plos One, 2014
Twenty-eight genes were resequenced: AKAP9, ANK2, CACNA1C, CACNB2, CASQ2, CAV3, DSC2, DSG2, DSP, GPD1L, HCN4, JUP, KCNE1, KCNE2, KCNE3, KCNH2, KCNJ2, KCNJ5, KCNQ1, NOS1AP, PKP2, RYR2, SCN1B, SCN3B, SCN4B, SCN5A, SNTA1, and TMEM43.
Identification of network-based biomarkers of cardioembolic stroke using a systems biology approach with time series data.
Chen et al., In Bmc Syst Biol, 2014
Genes, including UBC, CUL3, APP, NEDD8, JUP, and SIRT7, showed high associations with time after a stroke, and Ingenuity Pathway Analysis results showed that these post-stroke time series-associated genes were related to molecular and cellular functions of cell death, cell survival, the cell cycle, cellular development, cellular movement, and cell-to-cell signaling and interactions.
Clinical and functional characterization of a novel mutation in lamin a/c gene in a multigenerational family with arrhythmogenic cardiac laminopathy.
Favale et al., Bari, Italy. In Plos One, 2014
Mutation screening of LMNA and ARVC-related genes PKP2, DSP, DSG2, DSC2, JUP, and CTNNA3 was performed.
Increased frequency of de novo copy number variants in congenital heart disease by integrative analysis of single nucleotide polymorphism array and exome sequence data.
Chung et al., Philadelphia, United States. In Circ Res, 2014
encompassing CYFIP1, NIPA1, and NIPA2 and single de novo CNVs encompassing DUSP1, JUN, JUP, MED15, MED9, PTPRE SREBF1, TOP2A, and ZEB2, genes that interact with established CHD proteins NKX2-5 and GATA4.
Heterogeneous and abnormal localization of desmosomal proteins in oral intraepithelial neoplasms.
Hasegawa et al., Oral, Kazakhstan. In J Oral Sci, 2014
All samples were stained using antibodies against desmoglein 1 (DSG1), desmocollin 3 (DSC3), junction plakoglobin (JUP) and serine peptidase inhibitor Kazal type 5 (SPINK5) domain.
TMEM43 mutation p.S358L alters intercalated disc protein expression and reduces conduction velocity in arrhythmogenic right ventricular cardiomyopathy.
Hamilton et al., Toronto, Canada. In Plos One, 2013
Junctional Plakoglobin (JUP) and α-catenin proteins were redistributed to the cytoplasm with decreased localization to cell-cell junctions.
Beyond cell adhesion: the role of armadillo proteins in the heart.
Review
Radice et al., Philadelphia, United States. In Cell Signal, 2013
Plakoglobin (PG, γ-Catenin, JUP), a member of the armadillo protein family and close homolog of β-catenin, functions to link cell surface cadherin molecules with the cytoskeleton.
High motility of triple-negative breast cancer cells is due to repression of plakoglobin gene by metastasis modulator protein SLUG.
GeneRIF
Chaudhuri et al., Nashville, United States. In J Biol Chem, 2012
This study thus implicates SLUG-induced repression of plakoglobin as a motility determinant in highly disseminating breast cancer.
Mutations with pathogenic potential in proteins located in or at the composite junctions of the intercalated disk connecting mammalian cardiomyocytes: a reference thesaurus for arrhythmogenic cardiomyopathies and for Naxos and Carvajal diseases.
Review
Pieperhoff et al., Heidelberg, Germany. In Cell Tissue Res, 2012
As the pertinent literature is still in an expanding phase and is obviously becoming important for various groups of researchers in basic cell and molecular biology, developmental biology, histology, physiology, cardiology, pathology and genetics, the relevant references so far recognized have been collected and are presented here in the following order: desmocollin-2 (Dsc2, DSC2), desmoglein-2 (Dsg2, DSG2), desmoplakin (DP, DSP), plakoglobin (PG, JUP), plakophilin-2 (Pkp2, PKP2) and some non-desmosomal proteins such as transmembrane protein 43 (TMEM43), ryanodine receptor 2 (RYR2), desmin, lamins A and C, striatin, titin and transforming growth factor-β3 (TGFβ3), followed by a collection of animal models and of reviews, commentaries, collections and comparative studies.
Lack of plakoglobin in epidermis leads to keratoderma.
GeneRIF
Shou et al., Indianapolis, United States. In J Biol Chem, 2012
Lack of plakoglobin in epidermis leads to keratoderma.
Gastro-oesophageal reflux disease is associated with up-regulation of desmosomal components in oesophageal mucosa.
GeneRIF
Malfertheiner et al., Magdeburg, Germany. In Histopathology, 2012
Induced gene expression levels of plakoglobin, desmoglein-1 and desmoglein-2 correlated significantly with dilatation of intercellular spaces and basal cell hyperplasia in esophageal mucosa of patients with gastro-oesophageal reflux disease.
Arrhythmogenic right ventricular cardiomyopathy/dysplasia: a review and update.
Review
Erbel et al., Essen, Germany. In Clin Res Cardiol, 2011
Dysfunctional desmosomes resulting in defective cell adhesion proteins, such as plakoglobin (JUP), desmoplakin (DSP), plakophilin-2 (PKP-2), and desmoglein-2 (DSG-2) consequently cause loss of electrical coupling between cardiac myocytes, leading to myocyte cell death, fibrofatty replacement and arrhythmias.
Cell-cell contact preserves cell viability via plakoglobin.
GeneRIF
Huang et al., New York City, United States. In Plos One, 2010
the junctional protein plakoglobin is a key regulator of cell-cell contact,which may be a fundamental control mechanism governing cell viability
SOX4 interacts with plakoglobin in a Wnt3a-dependent manner in prostate cancer cells.
GeneRIF
Moreno et al., Atlanta, United States. In Bmc Cell Biol, 2010
The junction plakoglobin (JUP) interacts with SOX4 in both the cytosol and the nucleus and the interaction between SOX4 and plakoglobin is significantly increased when prostate and breast cancer cells are stimulated with WNT3A.
Molecular genetics of arrhythmogenic right ventricular cardiomyopathy: emerging horizon?
Review
Jongbloed et al., Groningen, Netherlands. In Curr Opin Cardiol, 2007
Mutations in genes encoding desmosomal proteins such as PKP2, DSP, JUP, DSC2 and DSG2 underlie arrhythmogenic right ventricular cardiomyopathy, which can therefore be considered a desmosome cardiomyopathy.
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