| First Author | Umans L | Year | 2003 |
| Journal | Genesis | Volume | 37 |
| Issue | 1 | Pages | 5-11 |
| PubMed ID | 14502571 | Mgi Jnum | J:86157 |
| Mgi Id | MGI:2678887 | Doi | 10.1002/gene.10219 |
| Citation | Umans L, et al. (2003) Generation of a floxed allele of Smad5 for cre-mediated conditional knockout in the mouse. Genesis 37(1):5-11 |
| abstractText | Smad5 is a member of the Smad family of intracellular mediators of BMP signals and in endothelial cells of TGF-beta signals. We and others previously showed that loss of Smad5 in the mouse results in embryonic lethality (between E9.5-E11.5) due to multiple embryonic and extraembryonic defects. To circumvent the early embryonic lethality and to allow tissue- and time-specific Smad5 inactivation, we created a conditional Smad5 allele in the mouse. Floxed Smad5 (Smad5(flE2,Neo/flE2,Neo)) mice were generated in which both exon2 and the Neo-cassette were flanked by loxP sites. Here we demonstrate that embryos with ubiquitous Cre-mediated deletion of Smad5 (Smad5(flDeltaE2/flDeltaE2)) phenocopy the conventional Smad5 knockout mice. Smad5(flE2/flE2) mice are now available and will be a valuable tool to analyze the role of Smad5 beyond its crucial early embryonic function throughout development and postnatal life. |
