| First Author | Dahlhoff M | Year | 2013 |
| Journal | Exp Cell Res | Volume | 319 |
| Issue | 4 | Pages | 529-35 |
| PubMed ID | 23142483 | Mgi Jnum | J:194427 |
| Mgi Id | MGI:5473756 | Doi | 10.1016/j.yexcr.2012.11.001 |
| Citation | Dahlhoff M, et al. (2013) Genetic deletion of the EGFR ligand epigen does not affect mouse embryonic development and tissue homeostasis. Exp Cell Res 319(4):529-35 |
| abstractText | The epidermal growth factor receptor (EGFR) is a tyrosine kinase receptor with manifold functions during development, tissue homeostasis and disease. EGFR activation, the formation of homodimers or heterodimers (with the related ERBB2-4 receptors) and downstream signaling is initiated by the binding of a family of structurally related growth factors, the EGFR ligands. Genetic deletion experiments clarified the biological function of all family members except for the last characterized ligand, epigen. We employed gene targeting in mouse embryonic stem cells to generate mice lacking epigen expression. Loss of epigen did not affect mouse development, fertility, or organ physiology. Quantitative RT-PCR analysis revealed increased expression of betacellulin and EGF in a few organs of epigen-deficient mice, suggesting a functional compensation by these ligands. In conclusion, we completed the genetic analysis of EGFR ligands and show that epigen has non-essential functions or functions that can be compensated by other EGFR ligands during growth and tissue homeostasis. |
