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| Content Provider | PubMed Central |
|---|---|
| Author | Gu, Jennifer L. Müller, Stefan Mancino, Valeria Offermanns, Stefan Simon, Melvin I. |
| Copyright Year | 2002 |
| Abstract | The G12 subfamily of heterotrimeric G-proteinsconsists of two members, G12 and G13.Gene-targeting studies have revealed a role for G13 inblood vessel development. Mice lacking the α subunit ofG13 die around embryonic day 10 as the result of anangiogenic defect. On the other hand, the physiological role ofG12 is still unclear. To address this issue, we generatedGα12-deficient mice. In contrast to theGα13-deficient mice, Gα12-deficient miceare viable, fertile, and do not show apparent abnormalities. However,Gα12 does not seem to be entirely redundant, because inthe offspring generated from Gα12± Gα13±intercrosses, at least one intact Gα12 allele is requiredfor the survival of animals with only one Gα13 allele. Inaddition, Gα12 and Gα13 showed a differencein mediating cell migratory response to lysophosphatidic acid inembryonic fibroblast cells. Furthermore, mice lacking bothGα12 and Gαq die in utero atabout embryonic day 13. These data indicate that theGα12-mediated signaling pathway functionally interactsnot only with the Gα13- but also with theGαq/11-mediated signaling systems. |
| Related Links | http://dx.doi.org/10.1073/pnas.102291599 |
| Ending Page | 9357 |
| Page Count | 6 |
| Starting Page | 9352 |
| File Format | |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 14 |
| Volume Number | 99 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2002-07-09 |
| Access Restriction | Open |
| Rights Holder | National Academy of Sciences |
| Subject Keyword | General Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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