Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes
Identifieur interne : 000D89 ( Istex/Corpus ); précédent : 000D88; suivant : 000D90Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes
Auteurs : I. Parker ; Y. YaoSource :
- Cell Calcium [ 0143-4160 ] ; 1993.
Abstract
Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. Instead, Cl− channels may show an adaptive or incremental response to Ca2+, which is likely to be important for the encoding and transmission of information by Ca2+ spikes.
Url:
DOI: 10.1016/0143-4160(94)90067-1
Links to Exploration step
ISTEX:0D331AF8321E2728FB775DC21643C4B3164E485CLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes</title>
<author><name sortKey="Parker, I" sort="Parker, I" uniqKey="Parker I" first="I." last="Parker">I. Parker</name>
<affiliation><mods:affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</mods:affiliation>
</affiliation>
</author>
<author><name sortKey="Yao, Y" sort="Yao, Y" uniqKey="Yao Y" first="Y." last="Yao">Y. Yao</name>
<affiliation><mods:affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</mods:affiliation>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:0D331AF8321E2728FB775DC21643C4B3164E485C</idno>
<date when="1994" year="1994">1994</date>
<idno type="doi">10.1016/0143-4160(94)90067-1</idno>
<idno type="url">https://api.istex.fr/document/0D331AF8321E2728FB775DC21643C4B3164E485C/fulltext/pdf</idno>
<idno type="wicri:Area/Istex/Corpus">000D89</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a">Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes</title>
<author><name sortKey="Parker, I" sort="Parker, I" uniqKey="Parker I" first="I." last="Parker">I. Parker</name>
<affiliation><mods:affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</mods:affiliation>
</affiliation>
</author>
<author><name sortKey="Yao, Y" sort="Yao, Y" uniqKey="Yao Y" first="Y." last="Yao">Y. Yao</name>
<affiliation><mods:affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</mods:affiliation>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Cell Calcium</title>
<title level="j" type="abbrev">YCECA</title>
<idno type="ISSN">0143-4160</idno>
<imprint><publisher>ELSEVIER</publisher>
<date type="published" when="1993">1993</date>
<biblScope unit="volume">15</biblScope>
<biblScope unit="issue">4</biblScope>
<biblScope unit="page" from="276">276</biblScope>
<biblScope unit="page" to="288">288</biblScope>
</imprint>
<idno type="ISSN">0143-4160</idno>
</series>
<idno type="istex">0D331AF8321E2728FB775DC21643C4B3164E485C</idno>
<idno type="DOI">10.1016/0143-4160(94)90067-1</idno>
<idno type="PII">0143-4160(94)90067-1</idno>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0143-4160</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass></textClass>
<langUsage><language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. Instead, Cl− channels may show an adaptive or incremental response to Ca2+, which is likely to be important for the encoding and transmission of information by Ca2+ spikes.</div>
</front>
</TEI>
<istex><corpusName>elsevier</corpusName>
<author><json:item><name>I. Parker</name>
<affiliations><json:string>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</json:string>
</affiliations>
</json:item>
<json:item><name>Y. Yao</name>
<affiliations><json:string>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</json:string>
</affiliations>
</json:item>
</author>
<language><json:string>eng</json:string>
</language>
<abstract>Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. Instead, Cl− channels may show an adaptive or incremental response to Ca2+, which is likely to be important for the encoding and transmission of information by Ca2+ spikes.</abstract>
<qualityIndicators><score>8.092</score>
<pdfVersion>1.4</pdfVersion>
<pdfPageSize>537 x 713 pts</pdfPageSize>
<refBibsNative>true</refBibsNative>
<keywordCount>0</keywordCount>
<abstractCharCount>1496</abstractCharCount>
<pdfWordCount>6399</pdfWordCount>
<pdfCharCount>40699</pdfCharCount>
<pdfPageCount>13</pdfPageCount>
<abstractWordCount>216</abstractWordCount>
</qualityIndicators>
<title>Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes</title>
<pii><json:string>0143-4160(94)90067-1</json:string>
</pii>
<genre><json:string>research-article</json:string>
</genre>
<serie><volume>215</volume>
<pages><last>497</last>
<first>491</first>
</pages>
<genre></genre>
<language><json:string>unknown</json:string>
</language>
<title>Proc. R. Soc. Lond., B</title>
</serie>
<host><volume>15</volume>
<pii><json:string>S0143-4160(00)X0123-6</json:string>
</pii>
<pages><last>288</last>
<first>276</first>
</pages>
<issn><json:string>0143-4160</json:string>
</issn>
<issue>4</issue>
<genre><json:string>Journal</json:string>
</genre>
<language><json:string>unknown</json:string>
</language>
<title>Cell Calcium</title>
<publicationDate>1994</publicationDate>
</host>
<categories><wos><json:string>CELL BIOLOGY</json:string>
</wos>
</categories>
<publicationDate>1993</publicationDate>
<copyrightDate>1994</copyrightDate>
<doi><json:string>10.1016/0143-4160(94)90067-1</json:string>
</doi>
<id>0D331AF8321E2728FB775DC21643C4B3164E485C</id>
<fulltext><json:item><original>true</original>
<mimetype>application/pdf</mimetype>
<extension>pdf</extension>
<uri>https://api.istex.fr/document/0D331AF8321E2728FB775DC21643C4B3164E485C/fulltext/pdf</uri>
</json:item>
<json:item><original>true</original>
<mimetype>text/plain</mimetype>
<extension>txt</extension>
<uri>https://api.istex.fr/document/0D331AF8321E2728FB775DC21643C4B3164E485C/fulltext/txt</uri>
</json:item>
<json:item><original>false</original>
<mimetype>application/zip</mimetype>
<extension>zip</extension>
<uri>https://api.istex.fr/document/0D331AF8321E2728FB775DC21643C4B3164E485C/fulltext/zip</uri>
</json:item>
<istex:fulltextTEI uri="https://api.istex.fr/document/0D331AF8321E2728FB775DC21643C4B3164E485C/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes</title>
</titleStmt>
<publicationStmt><authority>ISTEX</authority>
<publisher>ELSEVIER</publisher>
<availability><p>ELSEVIER</p>
</availability>
<date>1994</date>
</publicationStmt>
<sourceDesc><biblStruct type="inbook"><analytic><title level="a">Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes</title>
<author><persName><forename type="first">I.</forename>
<surname>Parker</surname>
</persName>
<note type="biography">Please send reprint requests to: Dr Ian Parker, Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of California, Irvine, CA 92717, USA.</note>
<affiliation>Please send reprint requests to: Dr Ian Parker, Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of California, Irvine, CA 92717, USA.</affiliation>
<affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</affiliation>
</author>
<author><persName><forename type="first">Y.</forename>
<surname>Yao</surname>
</persName>
<affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</affiliation>
</author>
</analytic>
<monogr><title level="j">Cell Calcium</title>
<title level="j" type="abbrev">YCECA</title>
<idno type="pISSN">0143-4160</idno>
<idno type="PII">S0143-4160(00)X0123-6</idno>
<imprint><publisher>ELSEVIER</publisher>
<date type="published" when="1993"></date>
<biblScope unit="volume">15</biblScope>
<biblScope unit="issue">4</biblScope>
<biblScope unit="page" from="276">276</biblScope>
<biblScope unit="page" to="288">288</biblScope>
</imprint>
</monogr>
<idno type="istex">0D331AF8321E2728FB775DC21643C4B3164E485C</idno>
<idno type="DOI">10.1016/0143-4160(94)90067-1</idno>
<idno type="PII">0143-4160(94)90067-1</idno>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><creation><date>1994</date>
</creation>
<langUsage><language ident="en">en</language>
</langUsage>
<abstract xml:lang="en"><p>Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. Instead, Cl− channels may show an adaptive or incremental response to Ca2+, which is likely to be important for the encoding and transmission of information by Ca2+ spikes.</p>
</abstract>
</profileDesc>
<revisionDesc><change when="1993-10-07">Registration</change>
<change when="1993">Published</change>
</revisionDesc>
</teiHeader>
</istex:fulltextTEI>
</fulltext>
<metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration>
<istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType>
<istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>YCECA</jid>
<aid>94900671</aid>
<ce:pii>0143-4160(94)90067-1</ce:pii>
<ce:doi>10.1016/0143-4160(94)90067-1</ce:doi>
<ce:copyright type="unknown" year="1994"></ce:copyright>
</item-info>
<head><ce:title>Relation between intracellular Ca<ce:sup>2+</ce:sup>
signals and Ca<ce:sup>2+</ce:sup>
-activated Cl<ce:sup>−</ce:sup>
current in <ce:italic>Xenopus</ce:italic>
oocytes</ce:title>
<ce:author-group><ce:author><ce:given-name>I.</ce:given-name>
<ce:surname>Parker</ce:surname>
<ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>Y.</ce:given-name>
<ce:surname>Yao</ce:surname>
</ce:author>
<ce:affiliation><ce:textfn>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</ce:textfn>
</ce:affiliation>
<ce:correspondence id="COR1"><ce:label>∗</ce:label>
<ce:text>Please send reprint requests to: Dr Ian Parker, Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of California, Irvine, CA 92717, USA.</ce:text>
</ce:correspondence>
</ce:author-group>
<ce:date-received day="27" month="7" year="1993"></ce:date-received>
<ce:date-accepted day="7" month="10" year="1993"></ce:date-accepted>
<ce:abstract><ce:section-title>Abstract</ce:section-title>
<ce:abstract-sec><ce:simple-para>Activation of inositol 1,4,5-trisphosphate (InsP<ce:inf>3</ce:inf>
) signalling in <ce:italic>Xenopus</ce:italic>
oocytes causes intracellular Ca<ce:sup>2+</ce:sup>
mobilization and thereby activates a Ca<ce:sup>2+</ce:sup>
-dependent Cl<ce:sup>−</ce:sup>
membrane conductance. Measurements of cytosolic Ca<ce:sup>2+</ce:sup>
levels using fluorescent indicators, however, revealed little correspondence with Cl<ce:sup>−</ce:sup>
currents. Intracellular photorelease of InsP<ce:inf>3</ce:inf>
from a caged precursor evoked transient currents that peaked while the Ca<ce:sup>2+</ce:sup>
-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca<ce:sup>2+</ce:sup>
signal remained elevated much longer. Also, Cl<ce:sup>−</ce:sup>
currents evoked by agonist activation showed transient spikes while a wave of Ca<ce:sup>2+</ce:sup>
liberation swept across the cell, but then decreased when the Ca<ce:sup>2+</ce:sup>
signal attained a maximal level. Thus, the Cl<ce:sup>−</ce:sup>
current corresponded better to the <ce:italic>rate of rise</ce:italic>
of intracellular free Ca<ce:sup>2+</ce:sup>
, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP<ce:inf>3</ce:inf>
and caged Ca<ce:sup>2+</ce:sup>
indicated that this relationship did not arise through desensitization or inactivation of the Cl<ce:sup>−</ce:sup>
conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca<ce:sup>2+</ce:sup>
levels near the plasma membrane was responsible for the decay of Ca<ce:sup>2+</ce:sup>
-activated Cl<ce:sup>−</ce:sup>
current. Instead, Cl<ce:sup>−</ce:sup>
channels may show an adaptive or incremental response to Ca<ce:sup>2+</ce:sup>
, which is likely to be important for the encoding and transmission of information by Ca<ce:sup>2+</ce:sup>
spikes.</ce:simple-para>
</ce:abstract-sec>
</ce:abstract>
</head>
</converted-article>
</istex:document>
</istex:metadataXml>
<mods version="3.6"><titleInfo><title>Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA"><title>Relation between intracellular Ca</title>
</titleInfo>
<name type="personal"><namePart type="given">I.</namePart>
<namePart type="family">Parker</namePart>
<affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</affiliation>
<description>Please send reprint requests to: Dr Ian Parker, Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of California, Irvine, CA 92717, USA.</description>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Y.</namePart>
<namePart type="family">Yao</namePart>
<affiliation>Laboratory of Cellular and Molecular Neurobiology, Department of Psychobiology, University of Califormia at Irvine, Irvine, California, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<typeOfResource>text</typeOfResource>
<genre type="research-article" displayLabel="Full-length article"></genre>
<originInfo><publisher>ELSEVIER</publisher>
<dateIssued encoding="w3cdtf">1993</dateIssued>
<dateValid encoding="w3cdtf">1993-10-07</dateValid>
<copyrightDate encoding="w3cdtf">1994</copyrightDate>
</originInfo>
<language><languageTerm type="code" authority="iso639-2b">eng</languageTerm>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
</language>
<physicalDescription><internetMediaType>text/html</internetMediaType>
</physicalDescription>
<abstract lang="en">Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. Instead, Cl− channels may show an adaptive or incremental response to Ca2+, which is likely to be important for the encoding and transmission of information by Ca2+ spikes.</abstract>
<relatedItem type="host"><titleInfo><title>Cell Calcium</title>
</titleInfo>
<titleInfo type="abbreviated"><title>YCECA</title>
</titleInfo>
<genre type="Journal">journal</genre>
<originInfo><dateIssued encoding="w3cdtf">199404</dateIssued>
</originInfo>
<identifier type="ISSN">0143-4160</identifier>
<identifier type="PII">S0143-4160(00)X0123-6</identifier>
<part><date>199404</date>
<detail type="volume"><number>15</number>
<caption>vol.</caption>
</detail>
<detail type="issue"><number>4</number>
<caption>no.</caption>
</detail>
<extent unit="issue pages"><start>265</start>
<end>339</end>
</extent>
<extent unit="pages"><start>276</start>
<end>288</end>
</extent>
</part>
</relatedItem>
<identifier type="istex">0D331AF8321E2728FB775DC21643C4B3164E485C</identifier>
<identifier type="DOI">10.1016/0143-4160(94)90067-1</identifier>
<identifier type="PII">0143-4160(94)90067-1</identifier>
<recordInfo><recordContentSource>ELSEVIER</recordContentSource>
</recordInfo>
</mods>
</metadata>
<enrichments><istex:catWosTEI uri="https://api.istex.fr/document/0D331AF8321E2728FB775DC21643C4B3164E485C/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CELL BIOLOGY</classCode>
</textClass>
</profileDesc>
</teiHeader>
</istex:catWosTEI>
</enrichments>
</istex>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Ticri/CIDE/explor/OcrV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000D89 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000D89 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Ticri/CIDE |area= OcrV1 |flux= Istex |étape= Corpus |type= RBID |clé= ISTEX:0D331AF8321E2728FB775DC21643C4B3164E485C |texte= Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes }}
![]() | This area was generated with Dilib version V0.6.32. | ![]() |