Oncogenic potential of EAG K(+) channels.

Article Details

Citation

Pardo LA, del Camino D, Sanchez A, Alves F, Bruggemann A, Beckh S, Stuhmer W

Oncogenic potential of EAG K(+) channels.

EMBO J. 1999 Oct 15;18(20):5540-7.

PubMed ID
10523298 [ View in PubMed
]
Abstract

We have investigated the possible implication of the cell cycle-regulated K(+) channel ether a go-go (EAG) in cell proliferation and transformation. We show that transfection of EAG into mammalian cells confers a transformed phenotype. In addition, human EAG mRNA is detected in several somatic cancer cell lines, despite being preferentially expressed in brain among normal tissues. Inhibition of EAG expression in several of these cancer cell lines causes a significant reduction of cell proliferation. Moreover, the expression of EAG favours tumour progression when transfected cells are injected into immune-depressed mice. These data provide evidence for the oncogenic potential of EAG.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Potassium voltage-gated channel subfamily H member 1O95259Details