| First Author | Lee D | Year | 2004 |
| Journal | Mol Cell Biol | Volume | 24 |
| Issue | 20 | Pages | 8907-16 |
| PubMed ID | 15456865 | Mgi Jnum | J:93327 |
| Mgi Id | MGI:3056859 | Doi | 10.1128/MCB.24.20.8907-8916.2004 |
| Citation | Lee D, et al. (2004) Epiregulin is not essential for development of intestinal tumors but is required for protection from intestinal damage. Mol Cell Biol 24(20):8907-16 |
| abstractText | Epiregulin, an epidermal growth factor family member, acts as a local signal mediator and shows dual biological activity, stimulating the proliferation of fibroblasts, hepatocytes, smooth muscle cells, and keratinocytes while inhibiting the growth of several tumor-derived epithelial cell lines. The epiregulin gene (Ereg) is located on mouse chromosome 5 adjacent to three other epidermal growth factor family members, epigen, amphiregulin, and betacellulin. Gene targeting was used to insert a lacZ reporter into the mouse Ereg locus and to ablate its function. Although epiregulin is broadly expressed and regulated both spatially and temporally, Ereg null mice show no overt developmental defects, reproductive abnormalities, or altered liver regeneration. Additionally, in contrast to previous hypotheses, Ereg deficiency does not alter intestinal cancer susceptibility, as assayed in the Apc(Min) model, despite showing robust expression in developing tumors. However, Ereg null mice are highly susceptible to cancer-predisposing intestinal damage caused by oral administration of dextran sulfate sodium. |
