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anti-Human Desmoglein 2 Anticorps:
anti-Mouse (Murine) Desmoglein 2 Anticorps:
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Human Monoclonal Desmoglein 2 Primary Antibody pour IHC (fro), IP - ABIN2473331
: [The 5th consensus conference on intensive care and emergency medicine. Diagnosis of nosocomial pneumopathies in intensive care. 13 October 1989, Bicêtre]. dans La Revue du praticien 1990
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Human Monoclonal Desmoglein 2 Primary Antibody pour IHC (fro), WB - ABIN2191994
Wahl, Sacco, McGranahan-Sadler, Sauppé, Wheelock, Johnson: Plakoglobin domains that define its association with the desmosomal cadherins and the classical cadherins: identification of unique and shared domains. dans Journal of cell science 1996
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Cow (Bovine) Polyclonal Desmoglein 2 Primary Antibody pour IHC, WB - ABIN2782147
Cirillo, Lanza, De Rosa, Cammarota, La Gatta, Gombos, Lanza: The most widespread desmosomal cadherin, desmoglein 2, is a novel target of caspase 3-mediated apoptotic machinery. dans Journal of cellular biochemistry 2008
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Human Monoclonal Desmoglein 2 Primary Antibody pour ICC, IF - ABIN1742581
Keim, Johnson, Wheelock, Wahl: Generation and characterization of monoclonal antibodies against the proregion of human desmoglein-2. dans Hybridoma (2005) 2008
Human Monoclonal Desmoglein 2 Primary Antibody pour EIA, IHC (fro) - ABIN112136
Franke, Nuber, Schmidt, Schäfer: Desmosomes--dual junctional principles of intra- and supracellular order in epithelial differentiation and tissue formation. dans Verhandlungen der Deutschen Gesellschaft für Pathologie 1995
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Both zfDsc and zfDsgalpha were present as maternal and zygotic transcripts whereas zfDsgbeta was first expressed from 8 hours post-fertilisation.
In the present study, we used a candidate gene approach to investigate the associations between rs397729601 (a 2-base pair indel polymorphism) mapping to the 3'UTR of DSG2 with the risk of sudden cardiac death. We concluded that rs397729601 may affect the expression of DSG2 through miR-933-3p regulation, contributing to SCD susceptibility.
We identified, for the first time, a homozygous founder variant of DSG2 in East Asia, which was at surprisingly high frequency of 8.47% among Chinese ARVC patients with a full penetrance. This result suggested an urgent demand of genetic counseling for the probands and their relatives with heterozygous variant.
The prevalence of the majority of non-pathological genetic variations is similar in the Latvian ARVD-C patients and the European population. Possibly, pathogenic variations were found only in 10% of our registry patients, which could mean that PKP2 and DSG2 are not the most commonly affected genes in the Latvian population.
Carriers of DSG2p.F531C showed various phenotypes.
Study reports the structure of human adenovirus type 3 fibre knob (HAd3K) in complex with one and two molecules of the DSG2 receptor.
The authors demonstrate that Ecad interacts with isoform 2 of Dsg via a conserved Leu-175 on the Ecad cis binding interface and facilitates desmosome assembly.
Data provides evidence that Dsg2 regulates barrier properties in enterocytes via modulating the p38MAPK signaling cascade.
A homozygous mutation of DSG2 p.F531C was identified as the pathogenic mutation in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) involving both ventricles, as a result of widened and impaired intercalated discs, interrupted myocardial fibers, and abnormally hyperplastic interstitial fibers, collagen fibers, and adipocytes.
DSG2 as a key regulator of vasculogenic mimicry (VM) activity in human melanoma and suggest this molecule might be therapeutically targeted to reduce tumor blood supply and metastatic spread.
Data suggest that Dsg2 stimulates cell growth and migration by positively regulating EGFR level and signaling through a c-Src and Cav1-dependent mechanism using lipid rafts as signal modulatory platforms.
identified DSG2 expression in distinct progenitor cell subpopulations and show that, independent from its classical function as a component of desmosomes, this cadherin also plays a critical role in the vasculature
Data show that fetal pMSCs (mesenchymal stromal cells) expressing the highest levels of desmoglein 2, desmocollin 3 and plakophilin 2, followed by maternal pMSCs, while bmMSCs expressed the lowest levels.
Expression of the desmosomal protein Desmoglein-2 was reduced in pediatric dilated cardiomyopathy pediatric patients.
This study defines a mechanism by which Dsg2 expression in cancer cells can modulate the tumor microenvironment, a step critical for tumor progression.
Silencing of Dsg2 but not Dsc2 resulted in loss of cell cohesion and enhanced migration, and invasion of pancreatic adenocarcinoma cells.
The homozygous desmoglein 2 variant c.1003A;G co-segregated with Arrhythmogenic right ventricular cardiomyopathy, indicating autosomal recessive inheritance and complete penetrance.
these data suggest that palmitoylation of Dsg2 regulates protein transport to the plasma membrane. Modulation of the palmitoylation status of desmosomal cadherins can affect desmosome dynamics.
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 regulation involving Dsg2
Currently, 13 genes have been associated with the disease but nearly 40 % of clinically diagnosed cases remain without a genetic diagnosis.
This study demonstrates that Dsg2 induces epidermal activation of various signaling cascades and accelerates cutaneous wound healing, in part, through urokinase-type plasminogen activator receptor-related signaling cascades
hape and number of desmosomes as well as the expression of Dsg2 and the desmosomal plaque protein desmoplakin (Dsp) were investigated by electron microscopy and immunohistochemistry in 12 oestrous-dated mice.
these results demonstrate that Dsg2, but not desmocollin 2 is required for the integrity of the intestinal epithelial barrier in vivo
generated a Dsg2 loss-of-function strain (Dsg2 (lo/lo)) and observed that, in response to reduced levels of Dsg2: (i) CD31(+) endothelial cells in the pancreas are hypertrophic and exhibit altered morphology, (ii) bone marrow-derived endothelial colony formation is impaired, (iii) ex vivo vascular sprouting from aortic rings is reduced, and (iv) vessel formation in vitro and in vivo is attenuated
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 expression. Dsg2-mediated hyperproliferation, MEK/Erk1/2 activation, and accelerated squamous tumor development are enhanced on the Ptc1+/lacZ background.
Data demonstrate that desmoglein-2 plays a critical role in cardiomyocyte cohesion and function.
Data demonstrate that partner desmosomal cadherins Dsg2 and Dsc2 play opposing roles in controlling colonic carcinoma cell proliferation through differential effects on EGFR signaling.
Dsg2 compensates for Dsg3 depletion with regard to cell cohesion, but does not regulate p38 MAPK 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