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Anti-Desmoglein 2/DSG2 Antibody Picoband™ (monoclonal, 2B4D1)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC |
|---|---|
| Primary Accession | Q14126 |
| Host | Mouse |
| Isotype | IgG1 |
| Reactivity | Human |
| Clonality | Monoclonal |
| Format | Lyophilized |
| Description | Anti-Desmoglein 2/DSG2 Antibody Picoband™ (monoclonal, 2B4D1) . Tested in IHC, WB applications. This antibody reacts with Human. |
| Reconstitution | Adding 0.2 ml of distilled water will yield a concentration of 500 µg/ml. |
| Gene ID | 1829 |
|---|---|
| Other Names | Desmoglein-2, Cadherin family member 5, HDGC, DSG2, CDHF5 |
| Calculated MW | 160 kDa |
| Application Details | Western blot, 0.25-0.5 µg/ml, Human Immunohistochemistry(Paraffin-embedded Section), 2-5 µg/ml, Human |
| Contents | Each vial contains 4 mg Trehalose, 0.9 mg NaCl and 0.2 mg Na2HPO4. |
| Clone Names | Clone: 2B4D1 |
| Immunogen | E.coli-derived human Desmoglein 2/DSG2 recombinant protein (Position: L24-E1020). |
| Purification | Immunogen affinity purified. |
| Storage | At -20°C for one year from date of receipt. After reconstitution, at 4°C for one month. It can also be aliquotted and stored frozen at -20°C for six months. Avoid repeated freezing and thawing. |
| Name | DSG2 |
|---|---|
| Synonyms | CDHF5 |
| Function | A component of desmosome cell-cell junctions which are required for positive regulation of cellular adhesion (PubMed:38395410). Involved in the interaction of plaque proteins and intermediate filaments mediating cell-cell adhesion. Required for proliferation and viability of embryonic stem cells in the blastocyst, thereby crucial for progression of post-implantation embryonic development (By similarity). Maintains pluripotency by regulating epithelial to mesenchymal transition/mesenchymal to epithelial transition (EMT/MET) via interacting with and sequestering CTNNB1 to sites of cell-cell contact, thereby reducing translocation of CTNNB1 to the nucleus and subsequent transcription of CTNNB1/TCF-target genes (PubMed:29910125). Promotes pluripotency and the multi-lineage differentiation potential of hematopoietic stem cells (PubMed:27338829). Plays a role in endothelial cell sprouting and elongation via mediating the junctional-association of cortical actin fibers and CDH5 (PubMed:27338829). Plays a role in limiting inflammatory infiltration and the apoptotic response to injury in kidney tubular epithelial cells, potentially via its role in maintaining cell-cell adhesion and the epithelial barrier (PubMed:38395410). |
| Cellular Location | Cell membrane; Single-pass type I membrane protein. Cell junction, desmosome. Cytoplasm |
| Tissue Location | Expressed in undifferentiated pluripotent stem cells, expression decreases during differentiation (at protein level) (PubMed:29910125). Expressed in hematopoietic stem cells and circulating endothelial progenitor cells, expression decreases upon increasing cell lineage commitment (at protein level) (PubMed:27338829). Expressed on common myeloid progenitors, pro- myelocytes, pro-erythrocytes and B-cell linage progenitors (at protein level). Expression in mature cell types in the bone marrow and mature leukocyte populations is absent (PubMed:27338829). Expressed by foreskin fibroblasts, expression peaks during the early stage of differentiation reprogramming (at protein level) (PubMed:29910125) Expressed by endothelial cells in both arterioles and venules in the cervix (at protein level) (PubMed:27338829). Expressed in kidney tubular epithelial cells (PubMed:38395410) |
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Provided below are standard protocols that you may find useful for product applications.
Background
Desmoglein-2 is a protein that in humans is encoded by the DSG2 gene. 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 DSG2 display a high degree of penetrance. Disease expression was of variable severity with LV involvement a prominent feature. The low prevalence of classical ECG changes highlights the need to expand current diagnostic criteria to take account of LV disease, childhood disease expression, and incomplete penetrance.
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