Published January 24, 1997
| public
Journal Article
Vascular System Defects and Impaired Cell Chemokinesis as a Result of Gα_(13) Deficiency
Abstract
Heterotrimeric GTP-binding proteins (G proteins) participate in cellular signaling and regulate a variety of physiological processes. Disruption of the gene encoding the G protein subunit α_(13) (Gα_(13)) in mice impaired the ability of endothelial cells to develop into an organized vascular system, resulting in intrauterine death. In addition, Gα_(13) (−/−) embryonic fibroblasts showed greatly impaired migratory responses to thrombin. These results demonstrate that Gα_(13) participates in the regulation of cell movement in response to specific ligands, as well as in developmental angiogenesis.
Additional Information
© 1997 American Association for the Advancement of Science. Received 9 September 1996; accepted 2 December 1996. We thank J. Edens, Y.-H. Hu, and the La Jolla Cancer Research Foundation for technical assistance; T. Gridley for ES cell line CJ7; and A. Aragay, S. Pease, H. Wang, T. Wieland, and J. T. Yang for helpful suggestions. Supported by NIH grants GM 34236 and AG 12288 (M.I.S.). S.O. was a recipient of a fellowship from the Deutsche Forschungsgemeinschaft and the Guenther Foundation.Additional details
- Alternative title
- Vascular System Defects and Impaired Cell Chemokinesis as a Result of Gα13 Deficiency
- Eprint ID
- 52303
- Resolver ID
- CaltechAUTHORS:20141203-082740702
- NIH
- GM 34236
- NIH
- AG 12288
- Deutsche Forschungsgemeinschaft (DFG)
- Guenther Foundation
- Created
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2014-12-03Created from EPrint's datestamp field
- Updated
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2021-11-10Created from EPrint's last_modified field