| First Author | Imaizumi T | Year | 1999 |
| Journal | Biochem Biophys Res Commun | Volume | 266 |
| Issue | 2 | Pages | 569-74 |
| PubMed ID | 10600543 | Mgi Jnum | J:59071 |
| Mgi Id | MGI:1350865 | Doi | 10.1006/bbrc.1999.1869 |
| Citation | Imaizumi T, et al. (1999) Mutant mice lacking Crk-II caused by the gene trap insertional mutagenesis: Crk-II is not essential for embryonic development. Biochem Biophys Res Commun 266(2):569-74 |
| abstractText | Crk family adapter proteins including Crk-II, Crk-I, and Crk-L consist mostly of SH2 and SH3 domains. Through the interactions between SH2 domain and phosphotyrosine residues and/or between SH3 domain and proline-rich motifs, they are involved in a variety of signaling cascades. Despite their essential roles in the signal transductions, knock-out mice of these molecules have not been reported yet. We performed the gene trap insertional mutagenesis with a trap vector, pU-Hachi, and generated a mutant mice line, Ayu 8104, in which the trap vector was inserted into the c-crk gene. Homozygous Ayu 8104 mice lacked Crk-II and Crk-I transcripts but expressed the truncated Crk proteins retaining one SH2 and one SH3 domain. Since the structure of the truncated proteins was similar to that of Crk-I, the insertion was considered to cause Crk-II-specific disruption. Homozygous mutant mice, however, did not exhibit any obvious abnormalities, suggesting that Crk-family adapters, Crk-II, Crk-I, and Crk-L would redundantly function in the signaling cascades and Crk-II was not apparently essential for embryonic development. Copyright 1999 Academic Press. |
