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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1997-9-30
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pubmed:abstractText |
1. Electrophysiological (single-channel patch clamp) and molecular biological experiments (reverse transcriptase-polymerase chain reaction) were performed to attempt to identify the O2-sensitive K+ channel in rat phaeochromocytoma (PC12) cells. 2. Four types of K+ channels were recorded in PC12 cells: a small-conductance K+ channel (14 pS), a calcium-activated K+ channel (KCa; 102 pS) and two K+ channels with similar conductance (20 pS). These last two channels differed in their time-dependent inactivation: one was a slow-inactivating channel, while the other belonged to the family of fast transient K+ channels. 3. The slow-inactivating 20 pS K+ channel was inhibited by hypoxia. Exposure to hypoxia produced a 50% reduction in channel activity (number of active channels in the patch x open probability). Hypoxia had no effect on the 20 pS transient K+ channels, whereas reduced O2 stimulated the KCa channels. 4. The genes encoding the alpha-subunits of slow-inactivating K+ channels for two members of the Shaker subfamily of K+ channels (Kv1.2 and Kv1.3) together with the Kv2.1, Kv3.1 and Kv3.2 channel genes were identified in PC12 cells. 5. The expression of the Shaker Kv1.2, but none of the other K+ channel genes, increased in cells exposed to prolonged hypoxia (18 h). The same cells were more responsive to a subsequent exposure to hypoxia (35% inhibition of K+ current measured in whole-cell voltage clamp) compared with the cells maintained in normoxia (19% inhibition). 6. These results indicate that the O2-sensitive K+ channel in PC12 cells is a 20 pS slow-inactivating K+ channel that is upregulated by hypoxia. This channel appears to belong to the Shaker subfamily of voltage-gated K+ channels.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-1331289,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-1377421,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-1383932,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-1438587,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-1557388,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-1879548,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-2414437,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-2449514,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-2555158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-2599109,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-2770868,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-6270629,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-7517498,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-7539843,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-7559551,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-7788870,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-7788871,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-7788875,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-7891161,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-7903970,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-8276901,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-8593702,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-8770007,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9263911-8888521
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
502 ( Pt 2)
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
293-305
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:9263911-Adrenal Gland Neoplasms,
pubmed-meshheading:9263911-Animals,
pubmed-meshheading:9263911-Cell Hypoxia,
pubmed-meshheading:9263911-Electric Conductivity,
pubmed-meshheading:9263911-Gene Expression,
pubmed-meshheading:9263911-Membrane Potentials,
pubmed-meshheading:9263911-Oxygen,
pubmed-meshheading:9263911-PC12 Cells,
pubmed-meshheading:9263911-Patch-Clamp Techniques,
pubmed-meshheading:9263911-Pheochromocytoma,
pubmed-meshheading:9263911-Polymerase Chain Reaction,
pubmed-meshheading:9263911-Potassium Channel Blockers,
pubmed-meshheading:9263911-Potassium Channels,
pubmed-meshheading:9263911-Rats
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pubmed:year |
1997
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pubmed:articleTitle |
Selective inhibition of a slow-inactivating voltage-dependent K+ channel in rat PC12 cells by hypoxia.
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pubmed:affiliation |
Department of Molecular and Cellular Physiology, College of Medicine, University of Cincinnati, OH 45267-0576, USA. conforl@ucbeh.san.uc.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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