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Vascular system defects and impaired cell chemokinesis as a result of Galpha13 deficiency.
- Source :
-
Science (New York, N.Y.) [Science] 1997 Jan 24; Vol. 275 (5299), pp. 533-6. - Publication Year :
- 1997
-
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 alpha13 (Galpha13) in mice impaired the ability of endothelial cells to develop into an organized vascular system, resulting in intrauterine death. In addition, Galpha13 (-/-) embryonic fibroblasts showed greatly impaired migratory responses to thrombin. These results demonstrate that Galpha13 participates in the regulation of cell movement in response to specific ligands, as well as in developmental angiogenesis.
- Subjects :
- Animals
Blood
Bradykinin pharmacology
Cell Differentiation
Cells, Cultured
Embryo, Mammalian metabolism
Embryonic and Fetal Development
Endothelium, Vascular embryology
Female
Fibronectins pharmacology
GTP-Binding Proteins genetics
Gene Expression
Gene Targeting
Heterozygote
Homozygote
Lysophospholipids pharmacology
Male
Mice
Mice, Inbred C57BL
Signal Transduction
Thrombin pharmacology
Cell Movement drug effects
Endothelium, Vascular cytology
GTP-Binding Proteins physiology
Neovascularization, Physiologic
Subjects
Details
- Language :
- English
- ISSN :
- 0036-8075
- Volume :
- 275
- Issue :
- 5299
- Database :
- MEDLINE
- Journal :
- Science (New York, N.Y.)
- Publication Type :
- Academic Journal
- Accession number :
- 8999798
- Full Text :
- https://doi.org/10.1126/science.275.5299.533