Vascular System Defects and Impaired Cell Chemokinesis as a Result of Gα 13 Deficiency
Copyright policy )Vascular System Defects and Impaired Cell Chemokinesis as a Result of Gα 13 Deficiency
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.
- California Institute of Technology United States
Male, Heterozygote, Homozygote, 610, Gene Expression, Cell Differentiation, Bradykinin, Embryo, Mammalian, Fibronectins, Mice, Inbred C57BL, Embryonic and Fetal Development, Mice, Blood, Cell Movement, GTP-Binding Proteins, Gene Targeting, Animals, Female, Endothelium, Vascular, Lysophospholipids, Cells, Cultured
Male, Heterozygote, Homozygote, 610, Gene Expression, Cell Differentiation, Bradykinin, Embryo, Mammalian, Fibronectins, Mice, Inbred C57BL, Embryonic and Fetal Development, Mice, Blood, Cell Movement, GTP-Binding Proteins, Gene Targeting, Animals, Female, Endothelium, Vascular, Lysophospholipids, Cells, Cultured
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