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Desmosomes are cell-cell junctions between epithelial, myocardial, and certain other cell types. Additionally we are shipping Desmoglein 2 Antibodies (171) and Desmoglein 2 Kits (10) and many more products for this protein.
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Both Dsg2 mRNA and protein were highly expressed in non-small cell lung cancer (NSCLC) tissues and associated with NSCLC size, but not with overall survival of patients.
a novel pathway of CSTA (show CSTA Proteins) regulation involving Dsg2
DSG2 and DSG3 (show DSG3 Proteins) might be potential diagnostic markers for squamous cell carcinoma of the lung.
In endometrial luminal epithelium, cadherin 6 (show CDH6 Proteins), desmoglein 2 and plexin b2 (show PLXNB2 Proteins) were surprisingly found in the apical as well as the lateral membrane domain; their knock-down compromised epithelial integrity.
a low DSG2 expression phenotype is a useful prognostic biomarker of tumor aggressiveness and may serve as an aid in identifying patients with clinically significant prostate cancer.
Six variants of uncertain clinical significance in the PKP2, JUP (show JUP Proteins), and DSG2 genes showed a deleterious effect on mRNA splicing, indicating these are ARVD (show TGFB3 Proteins)/C-related pathogenic splice site mutations.
This structure reveals that the ectodomain of Dsg2 is flexible even in the calcium-bound state and, on average, is shorter than the type 1 cadherin crystal structures.
Data demonstrate that partner desmosomal cadherins Dsg2 and Dsc2 (show DSC2 Proteins) play opposing roles in controlling colonic carcinoma cell proliferation through differential effects on EGFR (show EGFR Proteins) signaling.
Desmoglein 2 expression attenuates migration of melanoma cells, mediated by downregulation of secretogranin II (show SCG2 Proteins).
Reduced cardiac desmoglein-2 and desmocollin-2 (show DSC2 Proteins) levels appear to be specifically associated with Arrhythmogenic right ventricular Dysplasia/cardiomyopathy, independent of underlying mutations.
Data suggest that loss of desmoglein 2 (Dsg2) compromises adhesion, and that this is a major pathogenic mechanism in DSG2-related and probably other desmosome-related arrhythmogenic cardiomyopathy (AC).
Dsg2 modulates Gli1 (show GLI1 Proteins) expression. Dsg2-mediated hyperproliferation, MEK (show MDK Proteins)/Erk1/2 activation, and accelerated squamous tumor development are enhanced on the Ptc1 (show PTCH1 Proteins)+/lacZ (show GLB1 Proteins) background.
Data demonstrate that desmoglein-2 plays a critical role in cardiomyocyte cohesion and function.
Dsg2 compensates for Dsg3 (show DSG3 Proteins) depletion with regard to cell cohesion, but does not regulate p38 MAPK (show MAPK14 Proteins) signaling.
In vivo interaction between Dsg2 and Na(V)1.5 provides a molecular pathway for the observed electrical disturbances during the early arrhythmogenic right ventricular cardiomyopathy.
Mutant desmoglein 2 cannot support the increased requirements placed on intercalated disc adhesion during postnatal heart development. This induces cardiomyocyte death, aseptic inflammation and fibrotic replacement.
ventricular arrhythmias that has been linked to mutations in desmosomal proteins including desmoglein 2
Myocyte necrosis underlies progressive myocardial dystrophy in N271S-dsg2-related arrhythmogenic right ventricular cardiomyopathy.
Desmosomes are cell-cell junctions between epithelial, myocardial, and certain other cell types. This gene product is a calcium-binding transmembrane glycoprotein component of desmosomes in vertebrate epithelial cells. Currently, three desmoglein subfamily members have been identified and all are members of the cadherin cell adhesion molecule superfamily. These desmoglein gene family members are located in a cluster on chromosome 18. This second family member is expressed in colon, colon carcinoma, and other simple and stratified epithelial-derived cell lines. Mutations in this gene have been associated with arrhythmogenic right ventricular dysplasia, familial, 10.
, Dsg alpha
, desmocollin a
, cadherin family member 5