Article,

Embryonic cardiomyocyte hypoplasia and craniofacial defects in G alpha q/G alpha 11-mutant mice

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EMBO J, 17 (15): 4304-12 (August 1998)Offermanns, S Zhao, L P Gohla, A Sarosi, I Simon, M I Wilkie, T M DK47890/DK/NIDDK NIH HHS/United States Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. England The EMBO journal EMBO J. 1998 Aug 3;17(15):4304-12..

Abstract

Heterotrimeric G proteins of the Gq 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 Gq class of G proteins plays a crucial role in cardiac growth and development.

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