Inactivation of Kv2.1 Potassium Channels
We report here several unusual features of inactivation of the rat Kv2.1 delayed rectifier potassium channel, expressed in Xenopus oocytes. The voltage dependence of inactivation was U-shaped, with maximum inactivation near 0 mV. During a maintained depolarization, development of inactivation was sl...
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| Veröffentlicht in: | Biophysical journal 1998-04, Vol.74 (4), p.1779-1789 |
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| creator | Klemic, Kathryn G. Shieh, Char-Chang Kirsch, Glenn E. Jones, Stephen W. |
| description | We report here several unusual features of inactivation of the rat Kv2.1 delayed rectifier potassium channel, expressed in
Xenopus oocytes. The voltage dependence of inactivation was U-shaped, with maximum inactivation near 0
mV. During a maintained depolarization, development of inactivation was slow and only weakly voltage dependent (
τ
=
4
s at 0
mV;
τ
=
7
s at +80
mV). However, recovery from inactivation was strongly voltage dependent (e-fold for 20
mV) and could be rapid (
τ
=
0.27
s at −140
mV). Kv2.1 showed cumulative inactivation, where inactivation built up during a train of brief depolarizations. A single maintained depolarization produced more steady-state inactivation than a train of pulses, but there could actually be more inactivation with the repeated pulses during the first few seconds. We term this phenomenon “excessive cumulative inactivation.” These results can be explained by an allosteric model, in which inactivation is favored by activation of voltage sensors, but the open state of the channel is resistant to inactivation. |
| doi_str_mv | 10.1016/S0006-3495(98)77888-9 |
| format | Article |
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Xenopus oocytes. The voltage dependence of inactivation was U-shaped, with maximum inactivation near 0
mV. During a maintained depolarization, development of inactivation was slow and only weakly voltage dependent (
τ
=
4
s at 0
mV;
τ
=
7
s at +80
mV). However, recovery from inactivation was strongly voltage dependent (e-fold for 20
mV) and could be rapid (
τ
=
0.27
s at −140
mV). Kv2.1 showed cumulative inactivation, where inactivation built up during a train of brief depolarizations. A single maintained depolarization produced more steady-state inactivation than a train of pulses, but there could actually be more inactivation with the repeated pulses during the first few seconds. We term this phenomenon “excessive cumulative inactivation.” These results can be explained by an allosteric model, in which inactivation is favored by activation of voltage sensors, but the open state of the channel is resistant to inactivation.</description><identifier>ISSN: 0006-3495</identifier><identifier>EISSN: 1542-0086</identifier><identifier>DOI: 10.1016/S0006-3495(98)77888-9</identifier><identifier>PMID: 9545040</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Allosteric Regulation ; Animals ; Biophysical Phenomena ; Biophysics ; Delayed Rectifier Potassium Channels ; Female ; In Vitro Techniques ; Kinetics ; Membrane Potentials ; Models, Biological ; Oocytes - metabolism ; Patch-Clamp Techniques ; Potassium Channel Blockers ; Potassium Channels ; Potassium Channels, Voltage-Gated ; Rats ; Recombinant Proteins - antagonists & inhibitors ; Shab Potassium Channels ; Xenopus</subject><ispartof>Biophysical journal, 1998-04, Vol.74 (4), p.1779-1789</ispartof><rights>1998 The Biophysical Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c462t-4547779b08dc71639fa6c6d667336868e576c8f40fd8d8ed1831131ca2c71d8d3</citedby><cites>FETCH-LOGICAL-c462t-4547779b08dc71639fa6c6d667336868e576c8f40fd8d8ed1831131ca2c71d8d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1299522/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-3495(98)77888-9$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,3548,27922,27923,45993,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9545040$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Klemic, Kathryn G.</creatorcontrib><creatorcontrib>Shieh, Char-Chang</creatorcontrib><creatorcontrib>Kirsch, Glenn E.</creatorcontrib><creatorcontrib>Jones, Stephen W.</creatorcontrib><title>Inactivation of Kv2.1 Potassium Channels</title><title>Biophysical journal</title><addtitle>Biophys J</addtitle><description>We report here several unusual features of inactivation of the rat Kv2.1 delayed rectifier potassium channel, expressed in
Xenopus oocytes. The voltage dependence of inactivation was U-shaped, with maximum inactivation near 0
mV. During a maintained depolarization, development of inactivation was slow and only weakly voltage dependent (
τ
=
4
s at 0
mV;
τ
=
7
s at +80
mV). However, recovery from inactivation was strongly voltage dependent (e-fold for 20
mV) and could be rapid (
τ
=
0.27
s at −140
mV). Kv2.1 showed cumulative inactivation, where inactivation built up during a train of brief depolarizations. A single maintained depolarization produced more steady-state inactivation than a train of pulses, but there could actually be more inactivation with the repeated pulses during the first few seconds. We term this phenomenon “excessive cumulative inactivation.” These results can be explained by an allosteric model, in which inactivation is favored by activation of voltage sensors, but the open state of the channel is resistant to inactivation.</description><subject>Allosteric Regulation</subject><subject>Animals</subject><subject>Biophysical Phenomena</subject><subject>Biophysics</subject><subject>Delayed Rectifier Potassium Channels</subject><subject>Female</subject><subject>In Vitro Techniques</subject><subject>Kinetics</subject><subject>Membrane Potentials</subject><subject>Models, Biological</subject><subject>Oocytes - metabolism</subject><subject>Patch-Clamp Techniques</subject><subject>Potassium Channel Blockers</subject><subject>Potassium Channels</subject><subject>Potassium Channels, Voltage-Gated</subject><subject>Rats</subject><subject>Recombinant Proteins - antagonists & inhibitors</subject><subject>Shab Potassium Channels</subject><subject>Xenopus</subject><issn>0006-3495</issn><issn>1542-0086</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkFtLwzAUx4Moc14-wqBPMh86kzTXF0WGl-FAQX0OWZK6SNvMpi347e0uDH3y6cD5X87hB8AIwQmCiF29QghZmhFJx1Jcci6ESOUBGCJKcAqhYIdguLccg5MYPyFEmEI0AANJCYUEDsF4VmnT-E43PlRJyJOnDk9Q8hIaHaNvy2S61FXlingGjnJdRHe-m6fg_f7ubfqYzp8fZtPbeWoIw01KKOGcywUU1nDEMplrZphljGcZE0w4ypkROYG5FVY4i0SGUIaMxr29X2Wn4Hrbu2oXpbPGVU2tC7WqfanrbxW0V3-Vyi_VR-gUwlJSjPuCi11BHb5aFxtV-mhcUejKhTYqLrkkQqDeSLdGU4cYa5fvjyCo1ojVBrFa81NSqA1iJfvc6PeH-9SOaa_fbPWemuu8q1U03lXGWV870ygb_D8XfgAW6opm</recordid><startdate>19980401</startdate><enddate>19980401</enddate><creator>Klemic, Kathryn G.</creator><creator>Shieh, Char-Chang</creator><creator>Kirsch, Glenn E.</creator><creator>Jones, Stephen W.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19980401</creationdate><title>Inactivation of Kv2.1 Potassium Channels</title><author>Klemic, Kathryn G. ; Shieh, Char-Chang ; Kirsch, Glenn E. ; Jones, Stephen W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c462t-4547779b08dc71639fa6c6d667336868e576c8f40fd8d8ed1831131ca2c71d8d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Allosteric Regulation</topic><topic>Animals</topic><topic>Biophysical Phenomena</topic><topic>Biophysics</topic><topic>Delayed Rectifier Potassium Channels</topic><topic>Female</topic><topic>In Vitro Techniques</topic><topic>Kinetics</topic><topic>Membrane Potentials</topic><topic>Models, Biological</topic><topic>Oocytes - metabolism</topic><topic>Patch-Clamp Techniques</topic><topic>Potassium Channel Blockers</topic><topic>Potassium Channels</topic><topic>Potassium Channels, Voltage-Gated</topic><topic>Rats</topic><topic>Recombinant Proteins - antagonists & inhibitors</topic><topic>Shab Potassium Channels</topic><topic>Xenopus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Klemic, Kathryn G.</creatorcontrib><creatorcontrib>Shieh, Char-Chang</creatorcontrib><creatorcontrib>Kirsch, Glenn E.</creatorcontrib><creatorcontrib>Jones, Stephen W.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biophysical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Klemic, Kathryn G.</au><au>Shieh, Char-Chang</au><au>Kirsch, Glenn E.</au><au>Jones, Stephen W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inactivation of Kv2.1 Potassium Channels</atitle><jtitle>Biophysical journal</jtitle><addtitle>Biophys J</addtitle><date>1998-04-01</date><risdate>1998</risdate><volume>74</volume><issue>4</issue><spage>1779</spage><epage>1789</epage><pages>1779-1789</pages><issn>0006-3495</issn><eissn>1542-0086</eissn><abstract>We report here several unusual features of inactivation of the rat Kv2.1 delayed rectifier potassium channel, expressed in
Xenopus oocytes. The voltage dependence of inactivation was U-shaped, with maximum inactivation near 0
mV. During a maintained depolarization, development of inactivation was slow and only weakly voltage dependent (
τ
=
4
s at 0
mV;
τ
=
7
s at +80
mV). However, recovery from inactivation was strongly voltage dependent (e-fold for 20
mV) and could be rapid (
τ
=
0.27
s at −140
mV). Kv2.1 showed cumulative inactivation, where inactivation built up during a train of brief depolarizations. A single maintained depolarization produced more steady-state inactivation than a train of pulses, but there could actually be more inactivation with the repeated pulses during the first few seconds. We term this phenomenon “excessive cumulative inactivation.” These results can be explained by an allosteric model, in which inactivation is favored by activation of voltage sensors, but the open state of the channel is resistant to inactivation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>9545040</pmid><doi>10.1016/S0006-3495(98)77888-9</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Biophysical journal, 1998-04, Vol.74 (4), p.1779-1789 |
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| language | eng |
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| source | PubMed Central (Open Access); MEDLINE; Elsevier ScienceDirect Journals Complete; Cell Press Free Archives; EZB Electronic Journals Library |
| subjects | Allosteric Regulation Animals Biophysical Phenomena Biophysics Delayed Rectifier Potassium Channels Female In Vitro Techniques Kinetics Membrane Potentials Models, Biological Oocytes - metabolism Patch-Clamp Techniques Potassium Channel Blockers Potassium Channels Potassium Channels, Voltage-Gated Rats Recombinant Proteins - antagonists & inhibitors Shab Potassium Channels Xenopus |
| title | Inactivation of Kv2.1 Potassium Channels |
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