Requirement of the Inositol Trisphosphate Receptor for Activation of Store-Operated Ca2+Channels
The coupling mechanism between endoplasmic reticulum (ER) calcium ion (Ca2+) stores and plasma membrane (PM) store-operated channels (SOCs) is crucial to Ca2+signaling but has eluded detection. SOCs may be functionally related to the TRP family of receptor-operated channels. Direct comparison of end...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 2000-03, Vol.287 (5458), p.1647-1651 |
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| container_title | Science (American Association for the Advancement of Science) |
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| creator | Ma, Hong-Tao Patterson, Randen L. van Rossum, Damian B. Birnbaumer, Lutz Mikoshiba, Katsuhiko Gill, Donald L. |
| description | The coupling mechanism between endoplasmic reticulum (ER) calcium ion (Ca2+) stores and plasma membrane (PM) store-operated channels (SOCs) is crucial to Ca2+signaling but has eluded detection. SOCs may be functionally related to the TRP family of receptor-operated channels. Direct comparison of endogenous SOCs with stably expressed TRP3 channels in human embryonic kidney (HEK293) cells revealed that TRP3 channels differ in being store independent. However, condensed cortical F-actin prevented activation of both SOC and TRP3 channels, which suggests that ER-PM interactions underlie coupling of both channels. A cell-permeant inhibitor of inositol trisphosphate receptor (InsP3R) function, 2-aminoethoxydiphenyl borate, prevented both receptor-induced TRP3 activation and store-induced SOC activation. It is concluded that InsP3Rsmediate both SOC and TRP channel opening and that the InsP3Ris essential for maintaining coupling between store emptying and physiological activation of SOCs. |
| doi_str_mv | 10.1126/science.287.5458.1647 |
| format | Article |
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SOCs may be functionally related to the TRP family of receptor-operated channels. Direct comparison of endogenous SOCs with stably expressed TRP3 channels in human embryonic kidney (HEK293) cells revealed that TRP3 channels differ in being store independent. However, condensed cortical F-actin prevented activation of both SOC and TRP3 channels, which suggests that ER-PM interactions underlie coupling of both channels. A cell-permeant inhibitor of inositol trisphosphate receptor (InsP3R) function, 2-aminoethoxydiphenyl borate, prevented both receptor-induced TRP3 activation and store-induced SOC activation. It is concluded that InsP3Rsmediate both SOC and TRP channel opening and that the InsP3Ris essential for maintaining coupling between store emptying and physiological activation of SOCs.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.287.5458.1647</identifier><identifier>PMID: 10698739</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Society for the Advancement of Science</publisher><subject>Actins ; Actins - metabolism ; Agonists ; Biological and medical sciences ; Borates ; Boron Compounds - pharmacology ; Calcium - metabolism ; Calcium Channels - chemistry ; Calcium Channels - metabolism ; Calcium Signaling ; Carbachol - pharmacology ; Cell Line ; Cell lines ; Cell Membrane - metabolism ; Cell membranes. Ionic channels. Membrane pores ; Cell structures and functions ; Delta cells ; Diglycerides - metabolism ; Diglycerides - pharmacology ; Endoplasmic Reticulum - metabolism ; Enzyme Inhibitors - pharmacology ; Fundamental and applied biological sciences. Psychology ; HEK293 cells ; Humans ; Inositol 1,4,5-Trisphosphate Receptors ; Inositols ; Ionomycin - pharmacology ; Macrocyclic Compounds ; Molecular and cellular biology ; Neurons ; Oxazoles - pharmacology ; Phosphoprotein Phosphatases - antagonists & inhibitors ; Receptors ; Receptors, Cytoplasmic and Nuclear - chemistry ; Receptors, Cytoplasmic and Nuclear - metabolism ; Strontium - metabolism ; Thapsigargin - pharmacology ; Transfection ; TRPC Cation Channels ; Type C Phospholipases - metabolism</subject><ispartof>Science (American Association for the Advancement of Science), 2000-03, Vol.287 (5458), p.1647-1651</ispartof><rights>Copyright 2000 American Association for the Advancement of Science</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3074652$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3074652$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,780,784,803,27924,27925,58017,58250</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1318135$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10698739$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Hong-Tao</creatorcontrib><creatorcontrib>Patterson, Randen L.</creatorcontrib><creatorcontrib>van Rossum, Damian B.</creatorcontrib><creatorcontrib>Birnbaumer, Lutz</creatorcontrib><creatorcontrib>Mikoshiba, Katsuhiko</creatorcontrib><creatorcontrib>Gill, Donald L.</creatorcontrib><title>Requirement of the Inositol Trisphosphate Receptor for Activation of Store-Operated Ca2+Channels</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>The coupling mechanism between endoplasmic reticulum (ER) calcium ion (Ca2+) stores and plasma membrane (PM) store-operated channels (SOCs) is crucial to Ca2+signaling but has eluded detection. SOCs may be functionally related to the TRP family of receptor-operated channels. Direct comparison of endogenous SOCs with stably expressed TRP3 channels in human embryonic kidney (HEK293) cells revealed that TRP3 channels differ in being store independent. However, condensed cortical F-actin prevented activation of both SOC and TRP3 channels, which suggests that ER-PM interactions underlie coupling of both channels. A cell-permeant inhibitor of inositol trisphosphate receptor (InsP3R) function, 2-aminoethoxydiphenyl borate, prevented both receptor-induced TRP3 activation and store-induced SOC activation. It is concluded that InsP3Rsmediate both SOC and TRP channel opening and that the InsP3Ris essential for maintaining coupling between store emptying and physiological activation of SOCs.</description><subject>Actins</subject><subject>Actins - metabolism</subject><subject>Agonists</subject><subject>Biological and medical sciences</subject><subject>Borates</subject><subject>Boron Compounds - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Calcium Channels - chemistry</subject><subject>Calcium Channels - metabolism</subject><subject>Calcium Signaling</subject><subject>Carbachol - pharmacology</subject><subject>Cell Line</subject><subject>Cell lines</subject><subject>Cell Membrane - metabolism</subject><subject>Cell membranes. Ionic channels. Membrane pores</subject><subject>Cell structures and functions</subject><subject>Delta cells</subject><subject>Diglycerides - metabolism</subject><subject>Diglycerides - pharmacology</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>HEK293 cells</subject><subject>Humans</subject><subject>Inositol 1,4,5-Trisphosphate Receptors</subject><subject>Inositols</subject><subject>Ionomycin - pharmacology</subject><subject>Macrocyclic Compounds</subject><subject>Molecular and cellular biology</subject><subject>Neurons</subject><subject>Oxazoles - pharmacology</subject><subject>Phosphoprotein Phosphatases - antagonists & inhibitors</subject><subject>Receptors</subject><subject>Receptors, Cytoplasmic and Nuclear - chemistry</subject><subject>Receptors, Cytoplasmic and Nuclear - metabolism</subject><subject>Strontium - metabolism</subject><subject>Thapsigargin - pharmacology</subject><subject>Transfection</subject><subject>TRPC Cation Channels</subject><subject>Type C Phospholipases - metabolism</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFj1tLw0AQhRdRbK3-A5U8-CaJu9ns7bEEL4VCodbnutlMyJbczG4F_70rrfpwGJjzzXAOQjcEJ4Sk_MEZC52BJJUiYRmTCeGZOEFTghWLVYrpKZpiTHkssWATdOHcDuPgKXqOJgRzJQVVU_S-ho-9HaGFzkd9FfkaokXXO-v7JtqM1g11H6Q9RGswMPh-jKqgufH2U3vbdz9Xr2EN8WqAMYBllOv0Pq9110HjLtFZpRsHV8c5Q29Pj5v8JV6unhf5fBnXqeQ-LiCjtOQlMGI4o7xQLBMZ11oXRFNVMCElF6CrAiRQJhXPJJGQFRwroVNDZ-j28HfYFy2U22G0rR6_tr9VA3B3BLQzuqlG3Rnr_jlKJKEsYNcHbOdCqT-b4pCGpfQbbmpu7A</recordid><startdate>20000303</startdate><enddate>20000303</enddate><creator>Ma, Hong-Tao</creator><creator>Patterson, Randen L.</creator><creator>van Rossum, Damian B.</creator><creator>Birnbaumer, Lutz</creator><creator>Mikoshiba, Katsuhiko</creator><creator>Gill, Donald L.</creator><general>American Society for the Advancement of Science</general><general>American Association for the Advancement of Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20000303</creationdate><title>Requirement of the Inositol Trisphosphate Receptor for Activation of Store-Operated Ca2+Channels</title><author>Ma, Hong-Tao ; Patterson, Randen L. ; van Rossum, Damian B. ; Birnbaumer, Lutz ; Mikoshiba, Katsuhiko ; Gill, Donald L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h286t-be433d6de51c6536b954746aaab1a39b578867eafbe8e358964818e4b6097a2c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Actins</topic><topic>Actins - metabolism</topic><topic>Agonists</topic><topic>Biological and medical sciences</topic><topic>Borates</topic><topic>Boron Compounds - pharmacology</topic><topic>Calcium - metabolism</topic><topic>Calcium Channels - chemistry</topic><topic>Calcium Channels - metabolism</topic><topic>Calcium Signaling</topic><topic>Carbachol - pharmacology</topic><topic>Cell Line</topic><topic>Cell lines</topic><topic>Cell Membrane - metabolism</topic><topic>Cell membranes. Ionic channels. Membrane pores</topic><topic>Cell structures and functions</topic><topic>Delta cells</topic><topic>Diglycerides - metabolism</topic><topic>Diglycerides - pharmacology</topic><topic>Endoplasmic Reticulum - metabolism</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>HEK293 cells</topic><topic>Humans</topic><topic>Inositol 1,4,5-Trisphosphate Receptors</topic><topic>Inositols</topic><topic>Ionomycin - pharmacology</topic><topic>Macrocyclic Compounds</topic><topic>Molecular and cellular biology</topic><topic>Neurons</topic><topic>Oxazoles - pharmacology</topic><topic>Phosphoprotein Phosphatases - antagonists & inhibitors</topic><topic>Receptors</topic><topic>Receptors, Cytoplasmic and Nuclear - chemistry</topic><topic>Receptors, Cytoplasmic and Nuclear - metabolism</topic><topic>Strontium - metabolism</topic><topic>Thapsigargin - pharmacology</topic><topic>Transfection</topic><topic>TRPC Cation Channels</topic><topic>Type C Phospholipases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Hong-Tao</creatorcontrib><creatorcontrib>Patterson, Randen L.</creatorcontrib><creatorcontrib>van Rossum, Damian B.</creatorcontrib><creatorcontrib>Birnbaumer, Lutz</creatorcontrib><creatorcontrib>Mikoshiba, Katsuhiko</creatorcontrib><creatorcontrib>Gill, Donald L.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Science (American Association for the Advancement of Science)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Hong-Tao</au><au>Patterson, Randen L.</au><au>van Rossum, Damian B.</au><au>Birnbaumer, Lutz</au><au>Mikoshiba, Katsuhiko</au><au>Gill, Donald L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Requirement of the Inositol Trisphosphate Receptor for Activation of Store-Operated Ca2+Channels</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>2000-03-03</date><risdate>2000</risdate><volume>287</volume><issue>5458</issue><spage>1647</spage><epage>1651</epage><pages>1647-1651</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><coden>SCIEAS</coden><abstract>The coupling mechanism between endoplasmic reticulum (ER) calcium ion (Ca2+) stores and plasma membrane (PM) store-operated channels (SOCs) is crucial to Ca2+signaling but has eluded detection. SOCs may be functionally related to the TRP family of receptor-operated channels. Direct comparison of endogenous SOCs with stably expressed TRP3 channels in human embryonic kidney (HEK293) cells revealed that TRP3 channels differ in being store independent. However, condensed cortical F-actin prevented activation of both SOC and TRP3 channels, which suggests that ER-PM interactions underlie coupling of both channels. A cell-permeant inhibitor of inositol trisphosphate receptor (InsP3R) function, 2-aminoethoxydiphenyl borate, prevented both receptor-induced TRP3 activation and store-induced SOC activation. It is concluded that InsP3Rsmediate both SOC and TRP channel opening and that the InsP3Ris essential for maintaining coupling between store emptying and physiological activation of SOCs.</abstract><cop>Washington, DC</cop><pub>American Society for the Advancement of Science</pub><pmid>10698739</pmid><doi>10.1126/science.287.5458.1647</doi><tpages>5</tpages></addata></record> |
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| subjects | Actins Actins - metabolism Agonists Biological and medical sciences Borates Boron Compounds - pharmacology Calcium - metabolism Calcium Channels - chemistry Calcium Channels - metabolism Calcium Signaling Carbachol - pharmacology Cell Line Cell lines Cell Membrane - metabolism Cell membranes. Ionic channels. Membrane pores Cell structures and functions Delta cells Diglycerides - metabolism Diglycerides - pharmacology Endoplasmic Reticulum - metabolism Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology HEK293 cells Humans Inositol 1,4,5-Trisphosphate Receptors Inositols Ionomycin - pharmacology Macrocyclic Compounds Molecular and cellular biology Neurons Oxazoles - pharmacology Phosphoprotein Phosphatases - antagonists & inhibitors Receptors Receptors, Cytoplasmic and Nuclear - chemistry Receptors, Cytoplasmic and Nuclear - metabolism Strontium - metabolism Thapsigargin - pharmacology Transfection TRPC Cation Channels Type C Phospholipases - metabolism |
| title | Requirement of the Inositol Trisphosphate Receptor for Activation of Store-Operated Ca2+Channels |
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