DSC2 — Desmocollin 2
DSC2 belongs to a gene co-expression module in 3 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
DSC2's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| Goblet cells | Epithelial Junction Integrity migration & adhesion | ACTR2, ANXA2, CTNNA1, GLUL, PERP, SERPINB1, TNFSF10 | View in SCUBA |
| Hematopoietic progenitor cells | T-cell Progenitor Lymphcyte development | GATA3, HOXB5, LAG3, MDK, OPTN, PTMS, SELENOP, SKAP1 +2 more | |
| Neutrophils | Freshly infiltrated neutrophils Developmental | CCR3, FSTL4, GABRR2, GRAMD1C, HPGD, ITPK1, KIF27, MAK +3 more |
About the gene
| Synonyms | CDHF2, DSC3 |
|---|---|
| Chromosome | 18: 31058840-31102522 |
| Predicted location | Membrane |
| Essential gene | No |
| Protein class | Disease related genes, Human disease related genes, Plasma proteins, Predicted membrane proteins |
| Biological process | Cell adhesion |
Function
A component of desmosome cell-cell junctions which are required for positive regulation of cellular adhesion. Promotes timely incorporation of DSG2 into desmosome intercellular junctions and promotes interaction of desmosome cell junctions with intermediate filament cytokeratin, via modulation of DSP phosphorylation. Plays an important role in desmosome-mediated maintenance of intestinal epithelial cell intercellular adhesion strength and barrier function. Positively regulates wound healing of intestinal mucosa via promotion of epithelial cell migration, and also plays a role in mechanotransduction of force between intestinal epithelial cells and extracellular matrix. May contribute to epidermal cell positioning (stratification) by mediating differential adhesiveness between cells that express different isoforms. May promote p38MAPK signaling activation that facilitates keratinocyte migration (By similarity).
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.