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XB-ART-2290
Cell Mol Life Sci 2005 Feb 01;624:461-70. doi: 10.1007/s00018-004-4456-6.
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Cofilin activity during insulin-like growth factor I-stimulated neuroblastoma cell motility.

Meyer G , Kim B , van Golen C , Feldman EL .


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Insulin-like growth factor I (IGF-I) is a potent stimulator of neuroblastoma cell motility. Cell motility requires lamellipodium extension at the leading edge of the cell through organized actin polymerization, and IGF-I stimulates lamellipodial elaboration in human neuroblastoma cells. Rac is a Rho GTPase that stimulates lamellipodial formation via the regulation of actin polymerization. In this study, we show that IGF-I-stimulated phosphatidylinositol 3-kinase (PI-3K) activity promotes rac activation and subsequent activation of the down- stream effectors LIM kinase and cofilin. Overexpression of wild-type LIM kinase and wild-type Xenopus ADF/cofilin (XAC) suppresses IGF-I-stimulated motility in SH-SY5Y cells, while expression of dominant negative LIM kinase and constitutively active XAC increases SH-SY5Y motility in the absence of IGF-I stimulation. These results suggest that regulation by cofilin of actin depolymerization is important in the process of neuroblastoma cell motility, and IGF-I regulates cofilin activity in part through PI-3K, rac, and LIM kinase.

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Species referenced: Xenopus
Genes referenced: actl6a akt1 dstn ins rac1 rho

References [+] :
Abhayaratna, Characteristics of left ventricular diastolic dysfunction in the community: an echocardiographic survey. 2006, Pubmed