期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2002
卷号：99
期号：14
页码：9352-9357
DOI：10.1073/pnas.102291599
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：The G12 subfamily of heterotrimeric G-proteins consists of two members, G12 and G13. Gene-targeting studies have revealed a role for G13 in blood vessel development. Mice lacking the subunit of G13 die around embryonic day 10 as the result of an angiogenic defect. On the other hand, the physiological role of G12 is still unclear. To address this issue, we generated G12-deficient mice. In contrast to the G13-deficient mice, G12-deficient mice are viable, fertile, and do not show apparent abnormalities. However, G12 does not seem to be entirely redundant, because in the offspring generated from G12{+/-} G13{+/-} intercrosses, at least one intact G12 allele is required for the survival of animals with only one G13 allele. In addition, G12 and G13 showed a difference in mediating cell migratory response to lysophosphatidic acid in embryonic fibroblast cells. Furthermore, mice lacking both G12 and Gq die in utero at about embryonic day 13. These data indicate that the G12-mediated signaling pathway functionally interacts not only with the G13- but also with the Gq/11-mediated signaling systems.
