|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for DSG2(NM_001943.4) 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
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.
Gene References into function
- Desmoglein 2 was highly expressed by the least differentiated cells of the cutaneous epithelium, including the hair follicle bulge of the fetus and adult, bulb matrix cells, and basal layer of the outer root sheath.
- Nine heterozygous DSG2 mutations (5 missense, 2 insertion-deletions, 1 nonsense, and 1 splice site mutation) were detected in subjects with ARVC.
- mutations in DSG2 contribute to the development ofarrhythmogenic right ventricular dysplasia/cardiomyopathy
- Data demonstrate that UV-induced desmoglein-2 down-regulation is mediated via reactive oxygen species which are generated through EGF receptor activation and Rac2/NADPH oxidase activation.
- Mutations in DSG2 display a high degree of penetrance. Disease expression was of variable severity with left ventricular involvement a prominent feature.
- long term treatment with epidermal growth factor (EGF) leads to a marked increase in the levels of ADAM17, which also increases the shedding of several substrates of ADAM17, including the desmosomal cadherin Dsg-2
- desmoglein 2 is a novel solitary surface glycoprotein in malignant melanoma cells
- Dsg2 was targeted by caspases in cell lines undergoing staurosporine-induced apoptosis. The proteolytic processing of full-length Dsg2 released a 70-kDa fragment into the cytosol.
- Dsg2 regulates intestinal epithelial cell apoptosis driven by cysteine proteases during physiological differentiation and inflammation
- Mutations in the desmosome genes were identified in four of the five patients (three with a DSG2 mutation and one with a DSP mutation). Five gene mutations were noted in four patients and all mutations were novel (one patient had a DSG2 double mutation).
- DSG2-V55M polymorphism is identified as a novel risk variant for dilated cardiomyopathy.
- Monoclonal antibodies against the proregion of the desmosomal cadherin, human desmoglein-2.
- Desmoglein 2 has been demonstrated in a sizable subset of nevi and primary melanomas.
- Results show that epidermal growth factor receptor inhibition stabilizes desmoglein 2 at intercellular junctions by interfering with its accumulation in an internalized cytoplasmic pool.
- levels of Dsg1 & Dsg2 are reduced in pancreatic tumors; expression of kallikrein 7 in BxPC-3 cells resulted in increase in shedding of soluble Dsg2
