Slit3 regulates cell motility through Rac/Cdc42 activation in lipopolysaccharide-stimulated macrophages
| Autor: | Ayumi Fujiwara, Shigeo Takenaka, Toshihiko Tanno, Shingo Tsuyama, Katsuhiro Tanaka, Kunihiko Sakaguchi |
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| Rok vydání: | 2007 |
| Předmět: |
Lipopolysaccharides
Biophysics Motility Lipopolysaccharide Cell motility CDC42 Biology Biochemistry Cell Line SLIT3 Mice Cell Movement Slit3 Structural Biology RNA interference Genetics SLIT2 Animals Gene silencing RNA Messenger cdc42 GTP-Binding Protein GTPase Molecular Biology Cells Cultured DNA Primers Base Sequence Macrophages Membrane Proteins Cell Biology Molecular biology rac GTP-Binding Proteins Cell biology Cell culture embryonic structures Intracellular Subcellular Fractions |
| Zdroj: | FEBS Letters. 581:1022-1026 |
| ISSN: | 0014-5793 |
| DOI: | 10.1016/j.febslet.2007.02.001 |
| Popis: | Three slit genes, slit1 to slit3, have been cloned to date. Slit1 and slit2 act as chemorepellent factors for axon guidance. Slit3 is involved in the formation of the diaphragm and kidney during embryogenesis. However, its molecular function remains unclear. We found that slit3 expression was induced by lipopolysaccharide (LPS)-stimulation in macrophages and that it was localized in the mitochondria and along the plasma membrane. Silencing of slit3 expression by RNA interference reduced cell motility and Rac/Cdc42 activation. These results suggest that slit3 functions as an intracellular signaling molecule for cell motility as part of the LPS-induced signaling cascade. |
| Databáze: | OpenAIRE |
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