| http://purl.uniprot.org/citations/17520698 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17520698 | http://www.w3.org/2000/01/rdf-schema#comment | "Previous work from our laboratory has shown that human ether à go-go (hEAG) K(+) channels are crucial for breast cancer cell proliferation and cell cycle progression. In this study, we investigated the regulation of hEAG channels by an insulin-like growth factor-1 (IGF-1), which is known to stimulate cell proliferation. Acute applications of IGF-1 increased K(+) current-density and hyperpolarized MCF-7 cells. The effects of IGF-1 were inhibited by hEAG inhibitors. Moreover, IGF-1 increased mRNA expression of hEAG in a time-dependent manner in parallel with an enhancement of cell proliferation. The MCF-7 cell proliferation induced by IGF-1 is inhibited pharmacologically by Astemizole or Quinidine or more specifically using siRNA against hEAG channel. Either mitogen-activated protein kinase (MAPK) or phosphatidylinositol 3-kinase (PI3K) are known to mediate IGF-1 cell proliferative signals through the activation of extracellular signal-regulated kinase 1/2 (Erk 1/2) and Akt, respectively. In MCF-7 cells, IGF-1 rapidly stimulated Akt phosphorylation, whereas IGF-1 had little stimulating effect on Erk 1/2 which seems to be constitutively activated. The application of wortmannin was found to block the effects of IGF-1 on K(+) current. Moreover, the inhibition of Akt phosphorylation by the application of wortmannin or by a specific reduction of Akt kinase activity reduced the hEAG mRNA levels. Taken together, our results show, for the first time, that IGF-1 increases both the activity and the expression of hEAG channels through an Akt-dependent pathway. Since a hEAG channel is necessary for cell proliferation, its regulation by IGF-1 may thus play an important role in IGF-1 signaling to promote a mitogenic effect in breast cancer cells."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcp.21065"xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/author | "Guerineau F."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/author | "Guenin S."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/author | "Gouilleux F."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/author | "Lassoued K."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/author | "Borowiec A.S."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/author | "Roudbaraki M."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/author | "Ouadid-Ahidouch H."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/author | "Harir N."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/author | "Hague F."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/name | "J Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/pages | "690-701"xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/title | "IGF-1 activates hEAG K(+) channels through an Akt-dependent signaling pathway in breast cancer cells: role in cell proliferation."xsd:string |
| http://purl.uniprot.org/citations/17520698 | http://purl.uniprot.org/core/volume | "212"xsd:string |
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