Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 24, Issue 20, Pages 8907-8916Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.24.20.8907-8916.2004
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Funding
- NCI NIH HHS [CA092479, R01 CA092479, CA084239, CA009385, T32 CA009385, U01 CA084239] Funding Source: Medline
- NICHD NIH HHS [HD33994, U54 HD033994, HD12304, P30 HD033994, R37 HD012304, R01 HD039896, HD039896] Funding Source: Medline
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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.
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