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Kir 4.1 channel expression in neuroblastoma×glioma hybrid NG108-15 cell line

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Abstract

To study a possible involvement of inwardly rectifying K+ 4.1 (Kir 4.1) channels in neural cell development, RT-PCR, immunocytochemistry and whole-cell patch-clamp techniques were used to assess expression of Kir 4.1 channels in proliferating and differentiated NG108-15 cells. RT-PCR revealed co-expression of Kir 4.1 and rat ether-a-go-go-related gene (R-ERG) mRNAs in both proliferating and differentiated cells. The relative Kir 4.1 mRNA concentration increased markedly as cells progressed from undifferentiated to differentiated cells. Kir 4.1-immunoreactivity was barely detectable in undifferentiated cells, but clearly detected in differentiated cells, indicating that Kir 4.1 gene and protein expressions are developmentally regulated. However, corresponding Kir 4.1 current could not be detected in differentiated cells using whole-cell patch-clamp recording. The `silent' channel/receptor, often found in tumor cells, may carry genetic defects, which prevent functional expression of the channel. NG108-15 may serve as unique model for studying the relationship between the expression of an ion channel gene and the electrophysiological phenotype it encodes.

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Acknowledgements

The authors gratefully thank Dr. Kenton Swartz of NINDS, NIH for his comments. The opinions and assertions contained herein are the private ones of the authors and are not to be construed as official or reflecting the views of the Department of the Navy.

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