| First Author | Kriz V | Year | 2007 |
| Journal | Dev Dyn | Volume | 236 |
| Issue | 9 | Pages | 2485-92 |
| PubMed ID | 17676633 | Mgi Jnum | J:124188 |
| Mgi Id | MGI:3721013 | Doi | 10.1002/dvdy.21257 |
| Citation | Kriz V, et al. (2007) Shb null allele is inherited with a transmission ratio distortion and causes reduced viability in utero. Dev Dyn 236(9):2485-92 |
| abstractText | SHB is an Src homology 2 domain-containing adapter protein that has been found to be involved in numerous cellular responses. We have generated an Shb knockout mouse. No Shb(-/-) pups or embryos were obtained on the C57Bl6 background, indicating an early defect as a consequence of Shb- gene inactivation on this genetic background. Breeding heterozygotes for Shb gene inactivation (Shb(+/-)) on a mixed genetic background (FVB/C57Bl6/129Sv) reveals a distorted transmission ratio of the null allele with reduced numbers of Shb(+/+) and Shb(-/-) animals, but increased number of Shb(+/-) animals. The Shb(-) allele is associated with various forms of malformations, explaining the relative reduction in the number of Shb(-/-) offspring. Shb(-/-) animals that were born were viable, fertile, and showed no obvious defects. However, Shb(+/-) female mice ovulated preferentially Shb(-) oocytes explaining the reduced frequency of Shb(+/+) mice. Our study suggests a role of SHB during reproduction and development. Developmental Dynamics 236:2485-2492, 2007. (c) 2007 Wiley-Liss, Inc. |
