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Slit3 regulates cell motility through Rac/Cdc42 activation in lipopolysaccharide‐stimulated macrophages
Author(s) -
Tanno Toshihiko,
Fujiwara Ayumi,
Sakaguchi Kunihiko,
Tanaka Katsuhiro,
Takenaka Shigeo,
Tsuyama Shingo
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.02.001
Subject(s) - microbiology and biotechnology , motility , cdc42 , gene silencing , chemistry , hek 293 cells , rna interference , signal transduction , biology , receptor , biochemistry , rna , gene
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.