期刊
SCIENCE
卷 320, 期 5884, 页码 1777-1781出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1157983
关键词
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资金
- Howard Hughes Medical Institute Funding Source: Medline
- NCI NIH HHS [R01 CA113656-02, R01 CA113656-03, R01 CA113656, 5R01 CA113656-02] Funding Source: Medline
- NHLBI NIH HHS [R01 HL070631, HL16037, R01 HL016037, HL70631, R01 HL070631-04, R01 HL016037-35] Funding Source: Medline
- NIAID NIH HHS [T32 AI007217, 5T32 AI007217-25, T32 AI007217-25, T32 AI007217-26] Funding Source: Medline
beta-arrestins have important roles in the regulation of seven- transmembrane receptors ( 7TMRs). Smoothened ( Smo) is a 7TMR that mediates effects of Hedgehog on developmental processes and whose dysregulation may cause tumorigenesis. beta-Arrestins are required for endocytosis of Smo and signaling to Gli transcription factors. In mammalian cells, Smo- dependent signaling requires translocation to primary cilia. We demonstrated that beta- arrestins mediate the activity- dependent interaction of Smo and the kinesin motor protein Kif3A. This multimeric complex localized to primary cilia and was disrupted in cells transfected with beta- arrestin small interfering RNA. beta- Arrestin 1 or beta- arrestin 2 depletion prevented the localization of Smo to primary cilia and the Smo- dependent activation of Gli. These results suggest roles for beta- arrestins in mediating the intracellular transport of a 7TMR to its obligate subcellular location for signaling.
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