charybdotoxin/breast neoplasms

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Ionic signals in T47D human breast cancer cells.

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Increasing evidence that ion channels play a key role in the modulation of cellular mitogenesis led us to investigate the membranes of T47D human breast cancer cells to identify the ion currents present. We report here the results of voltage-clamp studies in the whole-cell configuration on isolated,

Cell-cycle-dependent expression of the large Ca2+-activated K+ channels in breast cancer cells.

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In a previous work, we have reported that the ionic nature of the outward current recorded in MCF-7 cells was that of a K+ current. In this study, we have identified a Ca2+-activated K+ channel not yet described in MCF-7 human breast cancer cells. In cells arrested in the early G1 (depolarized

The effect of a hyposmotic shock and purinergic agonists on K+(Rb+) efflux from cultured human breast cancer cells.

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The effect of a hyposmotic shock and extracellular ATP on the efflux of K(+)(Rb(+)) from human breast cancer cell lines (MDA-MB-231 and MCF-7) has been examined. A hyposmotic shock increased the fractional efflux of K(+)(Rb(+)) from MDA-MB-231 cells via a pathway which was unaffected by Cl(-)

The antiestrogen tamoxifen activates BK channels and stimulates proliferation of MCF-7 breast cancer cells.

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In the present study, we investigated the effect of the antiestrogen compound tamoxifen on BK channels by the use of the patch-clamp technique. The perfusion of 10 nM tamoxifen significantly increased the magnitude of a voltage-dependent K+ current by 22.6 +/- 10.6% (n = 23). The effect of tamoxifen

Inhibition of ATP-sensitive potassium channels causes reversible cell-cycle arrest of human breast cancer cells in tissue culture.

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The purpose of this study was to determine if potassium channel activity is required for the proliferation of MCF-7 human mammary carcinoma cells. We examined the sensitivities of proliferation and progress through the cell cycle to each of nine potassium channel antagonists. Five of the potassium

17-beta-estradiol activates maxi-K channels through a non-genomic pathway in human breast cancer cells.

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We have investigated the acute effects of 17-beta-estradiol (E2) on K+ channels in MCF-7 breast epithelial cancer cells. E2 induced a rapid and irreversible augmentation of the K+ current for all membrane potentials superior to -25 mV. The effect of E2 was sensitive to Iberiotoxin, Charybdotoxin and

KV1.1 K(+) channels identification in human breast carcinoma cells: involvement in cell proliferation.

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Electrophysiological, immunocytochemical, and RT-PCR methods were used to identify a K(+) conductance not yet described in MCF-7 human breast cancer cells. A voltage-dependent and TEA-sensitive K(+) current was the most commonly observed in these cells. The noninactivating K(+) current (I(K)) was

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