| First Author | Offermanns S | Year | 1998 |
| Journal | EMBO J | Volume | 17 |
| Issue | 15 | Pages | 4304-12 |
| PubMed ID | 9687499 | Mgi Jnum | J:49140 |
| Mgi Id | MGI:1276765 | Doi | 10.1093/emboj/17.15.4304 |
| Citation | Offermanns S, et al. (1998) Embryonic cardiomyocyte hypoplasia and craniofacial defects in G alpha q/G alpha 11-mutant mice. EMBO J 17(15):4304-12 |
| abstractText | Heterotrimeric G proteins of the G(q) class have been implicated in signaling pathways regulating cardiac growth under physiological and pathological conditions. Knockout mice carrying inactivating mutations in both of the widely expressed G alpha(q) class genes, G alpha(q) and G alpha(11)(,) demonstrate that at least two active alleles of these genes are required for extrauterine life. Mice carrying only one intact allele [G alpha(q)((-/+)); G alpha(11)((-/-)) or G alpha(q)((-/-)); G alpha(11)((-/+))] died shortly after birth. These mutants showed a high incidence of cardiac malformation. In addition, G alpha(q)((-/-)); G alpha(11)((-/+)) newborns suffered from craniofacial defects. Mice lacking both G alpha(q) and G alpha(11) [G alpha(q)((-/-)); G alpha(11)((-/-))] died at embryonic day 11 due to cardiomyocyte hypoplasia, These data demonstrate overlap in G alpha(q) and G alpha(11) gene functions and indicate that the G(q) class of G proteins plays a crucial role in cardiac growth and development. |
