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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2003-1-28
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pubmed:databankReference |
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pubmed:abstractText |
The role of K(+) channel activity during cell cycle progression has become a research topic of considerable interest. Blocking of K(+) channels inhibits the proliferation of many cell types, although the mechanism of this inhibition is unclear. There is speculation that K(+) channels differentially regulate the electrical potential of the plasma membrane (V(m)) during proliferation. We have demonstrated that in tumor cells the value of V(m) is clamped to rather depolarized values by K(+) channels belonging to the HERG family. We report here that tumor cell lines preferentially express the herg1 gene and a truncated, N-deleted form that corresponds to herg1b. This alternative transcript is also expressed in human primary acute myeloid leukemias. Both HERG1 and HERG1B proteins are expressed on the plasma membrane of tumor cells and can form heterotetramers. The expression of HERG protein isoforms is strongly cell cycle-dependent, accounting for variations in HERG currents along the mitotic cycle. Moreover, the blocking of HERG channels dramatically impairs cell growth of HERG-bearing tumor cells. These results suggest that modulated expression of different K(+) channels is the molecular basis of a novel mechanism regulating neoplastic cell proliferation.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cation Transport Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/ERG protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/ERG1 potassium channel,
http://linkedlifedata.com/resource/pubmed/chemical/Ether-A-Go-Go Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/KCNH6 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Voltage-Gated,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Isoforms,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
31
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pubmed:volume |
278
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2947-55
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pubmed:dateRevised |
2008-10-28
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pubmed:meshHeading |
pubmed-meshheading:12431979-Base Sequence,
pubmed-meshheading:12431979-Cation Transport Proteins,
pubmed-meshheading:12431979-Cell Cycle,
pubmed-meshheading:12431979-Cell Division,
pubmed-meshheading:12431979-DNA Primers,
pubmed-meshheading:12431979-DNA-Binding Proteins,
pubmed-meshheading:12431979-Ether-A-Go-Go Potassium Channels,
pubmed-meshheading:12431979-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:12431979-Humans,
pubmed-meshheading:12431979-Molecular Sequence Data,
pubmed-meshheading:12431979-Neuroblastoma,
pubmed-meshheading:12431979-Potassium Channels,
pubmed-meshheading:12431979-Potassium Channels, Voltage-Gated,
pubmed-meshheading:12431979-Protein Isoforms,
pubmed-meshheading:12431979-Recombinant Proteins,
pubmed-meshheading:12431979-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:12431979-Sequence Deletion,
pubmed-meshheading:12431979-Trans-Activators,
pubmed-meshheading:12431979-Transcription, Genetic,
pubmed-meshheading:12431979-Transfection,
pubmed-meshheading:12431979-Tretinoin,
pubmed-meshheading:12431979-Tumor Cells, Cultured
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pubmed:year |
2003
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pubmed:articleTitle |
Cell cycle-dependent expression of HERG1 and HERG1B isoforms in tumor cells.
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pubmed:affiliation |
Department of Experimental Pathology and Oncology, University of Firenze, Viale G. B. Morgagni 50, 50134 Firenze, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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