| First Author | Thomsen N | Year | 2011 |
| Journal | Genesis | Volume | 49 |
| Issue | 8 | Pages | 681-8 |
| PubMed ID | 21786402 | Mgi Jnum | J:168970 |
| Mgi Id | MGI:4939467 | Doi | 10.1002/dvg.20735 |
| Citation | Thomsen N, et al. (2011) Mouse strains for the ubiquitous or conditional overexpression of the Flii gene. Genesis 49(8):681-8 |
| abstractText | The gelsolin related actin binding protein, Flii, is able to regulate wound healing; mice with decreased Flii expression show improved wound healing whereas mice with elevated Flii expression exhibit impaired wound healing. In both mice and humans Flii expression increases with age and amelioration of FLII activity represents a possible therapeutic strategy for improved wound healing in humans. Despite analysis of Flii function in a variety of organisms we know little of the molecular mechanisms underlying Flii action. Two new murine alleles of Flii have been produced to drive constitutive or tissue-specific expression of Flii. Each strain is able to rescue the embryonic lethality associated with a Flii null allele and to impair wound healing. These strains provide valuable resources for ongoing investigation of Flii function in a variety of biological processes. |
