Mitochondrial ATP-sensitive potassium channel activity and hypoxic preconditioning are independent of an inwardly rectifying potassium channel subunit in C. elegans
Hypoxic preconditioning (HP) is an evolutionarily-conserved mechanism that protects an organism against stress. The mitochondrial ATP-sensitive K + channel (mK ATP ) plays an essential role in the protective signaling, but remains molecularly undefined. Several lines of evidence suggest that mK ATP...
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| Veröffentlicht in: | FEBS letters 2012-01, Vol.586 (4), p.428-434 |
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| container_title | FEBS letters |
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| creator | Wojtovich, Andrew P. DiStefano, Peter Sherman, Teresa Brookes, Paul S. Nehrke, Keith |
| description | Hypoxic preconditioning (HP) is an evolutionarily-conserved mechanism that protects an organism against stress. The mitochondrial ATP-sensitive K
+
channel (mK
ATP
) plays an essential role in the protective signaling, but remains molecularly undefined. Several lines of evidence suggest that mK
ATP
may arise from an inward rectifying K
+
channel (Kir). The genetic model organism
C. elegans
exhibits HP and displays mK
ATP
activity. Here, we investigate the tissue expression profile of the three
C. elegans
Kir genes and demonstrate that mutant strains where the irk genes have been deleted either individually or in combination can be protected by HP and exhibit robust mK
ATP
channel activity in purified mitochondria. These data suggest that the mK
ATP
in
C. elegans
does not arise from a Kir derived channel. |
| doi_str_mv | 10.1016/j.febslet.2012.01.021 |
| format | Article |
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+
channel (mK
ATP
) plays an essential role in the protective signaling, but remains molecularly undefined. Several lines of evidence suggest that mK
ATP
may arise from an inward rectifying K
+
channel (Kir). The genetic model organism
C. elegans
exhibits HP and displays mK
ATP
activity. Here, we investigate the tissue expression profile of the three
C. elegans
Kir genes and demonstrate that mutant strains where the irk genes have been deleted either individually or in combination can be protected by HP and exhibit robust mK
ATP
channel activity in purified mitochondria. These data suggest that the mK
ATP
in
C. elegans
does not arise from a Kir derived channel.</description><identifier>ISSN: 0014-5793</identifier><identifier>EISSN: 1873-3468</identifier><identifier>DOI: 10.1016/j.febslet.2012.01.021</identifier><identifier>PMID: 22281198</identifier><language>eng</language><ispartof>FEBS letters, 2012-01, Vol.586 (4), p.428-434</ispartof><rights>2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids></links><search><creatorcontrib>Wojtovich, Andrew P.</creatorcontrib><creatorcontrib>DiStefano, Peter</creatorcontrib><creatorcontrib>Sherman, Teresa</creatorcontrib><creatorcontrib>Brookes, Paul S.</creatorcontrib><creatorcontrib>Nehrke, Keith</creatorcontrib><title>Mitochondrial ATP-sensitive potassium channel activity and hypoxic preconditioning are independent of an inwardly rectifying potassium channel subunit in C. elegans</title><title>FEBS letters</title><description>Hypoxic preconditioning (HP) is an evolutionarily-conserved mechanism that protects an organism against stress. The mitochondrial ATP-sensitive K
+
channel (mK
ATP
) plays an essential role in the protective signaling, but remains molecularly undefined. Several lines of evidence suggest that mK
ATP
may arise from an inward rectifying K
+
channel (Kir). The genetic model organism
C. elegans
exhibits HP and displays mK
ATP
activity. Here, we investigate the tissue expression profile of the three
C. elegans
Kir genes and demonstrate that mutant strains where the irk genes have been deleted either individually or in combination can be protected by HP and exhibit robust mK
ATP
channel activity in purified mitochondria. These data suggest that the mK
ATP
in
C. elegans
does not arise from a Kir derived channel.</description><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNqljU1OwzAQhS0EouXnCEhzgQTb6Y-7QUIViA0Si-4jJ5kkUzl2ZDuF3IeDYiQ2iCWbGc1737zH2J3gueBic3_MW6yCwZhLLmTORc6lOGNLobZFVqw26pwtORerbL3dFQt2FcKRp1uJ3SVbSCmVEDu1ZJ-vFF3dO9t40gYeD29ZQBso0glhdFGHQNMAda-tRQO6TgbFGbRtoJ9H90E1jB7rFJB-nCXbgfYIZBscMQ0bwbUJT8q79o2ZIdGR2vmb_FsQpmqyFBMN-xzQYKdtuGEXrTYBb3_2NXt4fjrsX7JxqgZs6lTitSlHT4P2c-k0lb8dS33ZuVNZSKXWXBb_DvgCTr-BTg</recordid><startdate>20120121</startdate><enddate>20120121</enddate><creator>Wojtovich, Andrew P.</creator><creator>DiStefano, Peter</creator><creator>Sherman, Teresa</creator><creator>Brookes, Paul S.</creator><creator>Nehrke, Keith</creator><scope>5PM</scope></search><sort><creationdate>20120121</creationdate><title>Mitochondrial ATP-sensitive potassium channel activity and hypoxic preconditioning are independent of an inwardly rectifying potassium channel subunit in C. elegans</title><author>Wojtovich, Andrew P. ; DiStefano, Peter ; Sherman, Teresa ; Brookes, Paul S. ; Nehrke, Keith</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmedcentral_primary_oai_pubmedcentral_nih_gov_32885023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wojtovich, Andrew P.</creatorcontrib><creatorcontrib>DiStefano, Peter</creatorcontrib><creatorcontrib>Sherman, Teresa</creatorcontrib><creatorcontrib>Brookes, Paul S.</creatorcontrib><creatorcontrib>Nehrke, Keith</creatorcontrib><collection>PubMed Central (Full Participant titles)</collection><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wojtovich, Andrew P.</au><au>DiStefano, Peter</au><au>Sherman, Teresa</au><au>Brookes, Paul S.</au><au>Nehrke, Keith</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial ATP-sensitive potassium channel activity and hypoxic preconditioning are independent of an inwardly rectifying potassium channel subunit in C. elegans</atitle><jtitle>FEBS letters</jtitle><date>2012-01-21</date><risdate>2012</risdate><volume>586</volume><issue>4</issue><spage>428</spage><epage>434</epage><pages>428-434</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>Hypoxic preconditioning (HP) is an evolutionarily-conserved mechanism that protects an organism against stress. The mitochondrial ATP-sensitive K
+
channel (mK
ATP
) plays an essential role in the protective signaling, but remains molecularly undefined. Several lines of evidence suggest that mK
ATP
may arise from an inward rectifying K
+
channel (Kir). The genetic model organism
C. elegans
exhibits HP and displays mK
ATP
activity. Here, we investigate the tissue expression profile of the three
C. elegans
Kir genes and demonstrate that mutant strains where the irk genes have been deleted either individually or in combination can be protected by HP and exhibit robust mK
ATP
channel activity in purified mitochondria. These data suggest that the mK
ATP
in
C. elegans
does not arise from a Kir derived channel.</abstract><pmid>22281198</pmid><doi>10.1016/j.febslet.2012.01.021</doi></addata></record> |
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| identifier | ISSN: 0014-5793 |
| ispartof | FEBS letters, 2012-01, Vol.586 (4), p.428-434 |
| issn | 0014-5793 1873-3468 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3288502 |
| source | Wiley Online Library Journals Frontfile Complete; Elsevier ScienceDirect Journals; Wiley Online Library Free Content; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| title | Mitochondrial ATP-sensitive potassium channel activity and hypoxic preconditioning are independent of an inwardly rectifying potassium channel subunit in C. elegans |
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