Calcium-dependent release of NO from intracellular S-nitrosothiols
The paper describes a novel cellular mechanism for rapid calcium‐dependent nitric oxide (NO) release. This release occurs due to NO liberation from S ‐nitrosothiols. We have analysed the changes of NO concentration in acutely isolated pancreatic acinar cells. Supramaximal acetylcholine (ACh) stimula...
Gespeichert in:
| Veröffentlicht in: | The EMBO journal 2006-07, Vol.25 (13), p.3024-3032 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext bestellen |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 3032 |
|---|---|
| container_issue | 13 |
| container_start_page | 3024 |
| container_title | The EMBO journal |
| container_volume | 25 |
| creator | Chvanov, Michael Gerasimenko, Oleg V Petersen, Ole H Tepikin, Alexei V |
| description | The paper describes a novel cellular mechanism for rapid calcium‐dependent nitric oxide (NO) release. This release occurs due to NO liberation from
S
‐nitrosothiols. We have analysed the changes of NO concentration in acutely isolated pancreatic acinar cells. Supramaximal acetylcholine (ACh) stimulation induced a Ca
2+
‐dependent increase in the fluorescence in the majority of cells loaded with the NO probe DAF‐FM via a patch pipette. The ACh‐induced NO signals were insensitive to inhibitors of calmodulin and protein kinase C but were inhibited by calpain antagonists. The initial part of the NO signals induced by 10 μM ACh showed little sensitivity to inhibition of NO synthase (NOS); however, cell pretreatment with NO donors (increasing cellular
S
‐nitrosothiol contents) substantially enhanced the initial component of NO responses. Pancreatic acinar cells were able to generate fast calcium‐dependent NO responses when stimulated with physiological or supramaximal doses of secretagogues. Importantly, the source of this NO is the already available
S
‐nitrosothiol store rather than
de novo
synthesis by NOS. A similar mechanism of NO release was found in dorsal root ganglia neurons. |
| doi_str_mv | 10.1038/sj.emboj.7601207 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_C6C</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1500983</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>19494327</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5827-9a9648f4b52dc11b88aadda0e58c8416782e0dd41c13d924d83436972b2f31fb3</originalsourceid><addsrcrecordid>eNqFkc1v1DAUxC0EokvhzglFHLhl8Vcc-4JEV22hKttKFHG0nPildUjixU5o-9_jJau2IKGebMm_Gc97g9BrgpcEM_k-tkvoK98uS4EJxeUTtCBc4Dxdi6dogakgOSdS7aEXMbYY40KW5DnaI0ImPcULdLAyXe2mPrewgcHCMGYBOjARMt9k67OsCb7P3DAGU0PXTZ0J2dd8cGPw0Y9XznfxJXrWmC7Cq925j74dHV6sPuWnZ8efVx9P87qQtMyVUYLLhlcFtTUhlZTGWGswFLKWnIhSUsDWclITZhXlVjLOhCppRRtGmortow-z72aqerA1bEN1ehNcb8Kt9sbpv18Gd6Uv_S9NCoyVZMng3c4g-J8TxFH3Lm6nMgP4KWohRfqQ4kdBorjijJYJfPsP2PopDGkLiSmoEFTRBOEZqtPOYoDmLjLBelujjq3-U6Pe1Zgkbx6Oei_Y9ZYANQPXroPbRw314ZeDk3tzMmtjkg2XEB6E_n-gfNa4OMLN3X8m_NCiZGWhv6-Ptbg4Pz9ZHa01Zr8Bh0nL6Q</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>195266292</pqid></control><display><type>article</type><title>Calcium-dependent release of NO from intracellular S-nitrosothiols</title><source>Springer Nature OA Free Journals</source><creator>Chvanov, Michael ; Gerasimenko, Oleg V ; Petersen, Ole H ; Tepikin, Alexei V</creator><creatorcontrib>Chvanov, Michael ; Gerasimenko, Oleg V ; Petersen, Ole H ; Tepikin, Alexei V</creatorcontrib><description>The paper describes a novel cellular mechanism for rapid calcium‐dependent nitric oxide (NO) release. This release occurs due to NO liberation from
S
‐nitrosothiols. We have analysed the changes of NO concentration in acutely isolated pancreatic acinar cells. Supramaximal acetylcholine (ACh) stimulation induced a Ca
2+
‐dependent increase in the fluorescence in the majority of cells loaded with the NO probe DAF‐FM via a patch pipette. The ACh‐induced NO signals were insensitive to inhibitors of calmodulin and protein kinase C but were inhibited by calpain antagonists. The initial part of the NO signals induced by 10 μM ACh showed little sensitivity to inhibition of NO synthase (NOS); however, cell pretreatment with NO donors (increasing cellular
S
‐nitrosothiol contents) substantially enhanced the initial component of NO responses. Pancreatic acinar cells were able to generate fast calcium‐dependent NO responses when stimulated with physiological or supramaximal doses of secretagogues. Importantly, the source of this NO is the already available
S
‐nitrosothiol store rather than
de novo
synthesis by NOS. A similar mechanism of NO release was found in dorsal root ganglia neurons.</description><identifier>ISSN: 0261-4189</identifier><identifier>EISSN: 1460-2075</identifier><identifier>DOI: 10.1038/sj.emboj.7601207</identifier><identifier>PMID: 16810320</identifier><identifier>CODEN: EMJODG</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Acetylcholine - pharmacology ; Acrylates - pharmacology ; Animals ; Biochemistry ; Calcium ; Calcium - physiology ; Calmodulin - antagonists & inhibitors ; Calmodulin - metabolism ; Calpain - antagonists & inhibitors ; Calpain - metabolism ; Cells, Cultured ; EMBO37 ; Fluoresceins ; Fluorescence ; Fluorescent Dyes ; glutathione ; Glutathione - metabolism ; Intracellular Space - metabolism ; Male ; Mice ; Neurons - cytology ; Neurons - physiology ; Nitric oxide ; Nitric Oxide - biosynthesis ; Nitric Oxide Donors - pharmacology ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - metabolism ; NOS ; Pancreas ; Pancreas - cytology ; Physiology ; Protein Kinase C - antagonists & inhibitors ; Protein Kinase C - metabolism ; S-nitrosothiols ; S-Nitrosothiols - metabolism ; Signal transduction</subject><ispartof>The EMBO journal, 2006-07, Vol.25 (13), p.3024-3032</ispartof><rights>European Molecular Biology Organization 2006</rights><rights>Copyright © 2006 European Molecular Biology Organization</rights><rights>Copyright Nature Publishing Group Jul 12, 2006</rights><rights>Copyright © 2006, European Molecular Biology Organization 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5827-9a9648f4b52dc11b88aadda0e58c8416782e0dd41c13d924d83436972b2f31fb3</citedby><cites>FETCH-LOGICAL-c5827-9a9648f4b52dc11b88aadda0e58c8416782e0dd41c13d924d83436972b2f31fb3</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/PMC1500983/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1500983/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,41096,42165,45550,45551,46384,46808,51551,53766,53768</link.rule.ids><linktorsrc>$$Uhttps://doi.org/10.1038/sj.emboj.7601207$$EView_record_in_Springer_Nature$$FView_record_in_$$GSpringer_Nature</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16810320$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chvanov, Michael</creatorcontrib><creatorcontrib>Gerasimenko, Oleg V</creatorcontrib><creatorcontrib>Petersen, Ole H</creatorcontrib><creatorcontrib>Tepikin, Alexei V</creatorcontrib><title>Calcium-dependent release of NO from intracellular S-nitrosothiols</title><title>The EMBO journal</title><addtitle>EMBO J</addtitle><addtitle>EMBO J</addtitle><description>The paper describes a novel cellular mechanism for rapid calcium‐dependent nitric oxide (NO) release. This release occurs due to NO liberation from
S
‐nitrosothiols. We have analysed the changes of NO concentration in acutely isolated pancreatic acinar cells. Supramaximal acetylcholine (ACh) stimulation induced a Ca
2+
‐dependent increase in the fluorescence in the majority of cells loaded with the NO probe DAF‐FM via a patch pipette. The ACh‐induced NO signals were insensitive to inhibitors of calmodulin and protein kinase C but were inhibited by calpain antagonists. The initial part of the NO signals induced by 10 μM ACh showed little sensitivity to inhibition of NO synthase (NOS); however, cell pretreatment with NO donors (increasing cellular
S
‐nitrosothiol contents) substantially enhanced the initial component of NO responses. Pancreatic acinar cells were able to generate fast calcium‐dependent NO responses when stimulated with physiological or supramaximal doses of secretagogues. Importantly, the source of this NO is the already available
S
‐nitrosothiol store rather than
de novo
synthesis by NOS. A similar mechanism of NO release was found in dorsal root ganglia neurons.</description><subject>Acetylcholine - pharmacology</subject><subject>Acrylates - pharmacology</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Calcium</subject><subject>Calcium - physiology</subject><subject>Calmodulin - antagonists & inhibitors</subject><subject>Calmodulin - metabolism</subject><subject>Calpain - antagonists & inhibitors</subject><subject>Calpain - metabolism</subject><subject>Cells, Cultured</subject><subject>EMBO37</subject><subject>Fluoresceins</subject><subject>Fluorescence</subject><subject>Fluorescent Dyes</subject><subject>glutathione</subject><subject>Glutathione - metabolism</subject><subject>Intracellular Space - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Neurons - cytology</subject><subject>Neurons - physiology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Donors - pharmacology</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>NOS</subject><subject>Pancreas</subject><subject>Pancreas - cytology</subject><subject>Physiology</subject><subject>Protein Kinase C - antagonists & inhibitors</subject><subject>Protein Kinase C - metabolism</subject><subject>S-nitrosothiols</subject><subject>S-Nitrosothiols - metabolism</subject><subject>Signal transduction</subject><issn>0261-4189</issn><issn>1460-2075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkc1v1DAUxC0EokvhzglFHLhl8Vcc-4JEV22hKttKFHG0nPildUjixU5o-9_jJau2IKGebMm_Gc97g9BrgpcEM_k-tkvoK98uS4EJxeUTtCBc4Dxdi6dogakgOSdS7aEXMbYY40KW5DnaI0ImPcULdLAyXe2mPrewgcHCMGYBOjARMt9k67OsCb7P3DAGU0PXTZ0J2dd8cGPw0Y9XznfxJXrWmC7Cq925j74dHV6sPuWnZ8efVx9P87qQtMyVUYLLhlcFtTUhlZTGWGswFLKWnIhSUsDWclITZhXlVjLOhCppRRtGmortow-z72aqerA1bEN1ehNcb8Kt9sbpv18Gd6Uv_S9NCoyVZMng3c4g-J8TxFH3Lm6nMgP4KWohRfqQ4kdBorjijJYJfPsP2PopDGkLiSmoEFTRBOEZqtPOYoDmLjLBelujjq3-U6Pe1Zgkbx6Oei_Y9ZYANQPXroPbRw314ZeDk3tzMmtjkg2XEB6E_n-gfNa4OMLN3X8m_NCiZGWhv6-Ptbg4Pz9ZHa01Zr8Bh0nL6Q</recordid><startdate>20060712</startdate><enddate>20060712</enddate><creator>Chvanov, Michael</creator><creator>Gerasimenko, Oleg V</creator><creator>Petersen, Ole H</creator><creator>Tepikin, Alexei V</creator><general>John Wiley & Sons, Ltd</general><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><scope>BSCLL</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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PCBAR</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20060712</creationdate><title>Calcium-dependent release of NO from intracellular S-nitrosothiols</title><author>Chvanov, Michael ; Gerasimenko, Oleg V ; Petersen, Ole H ; Tepikin, Alexei V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5827-9a9648f4b52dc11b88aadda0e58c8416782e0dd41c13d924d83436972b2f31fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Acrylates - pharmacology</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Calcium</topic><topic>Calcium - physiology</topic><topic>Calmodulin - antagonists & inhibitors</topic><topic>Calmodulin - metabolism</topic><topic>Calpain - antagonists & inhibitors</topic><topic>Calpain - metabolism</topic><topic>Cells, Cultured</topic><topic>EMBO37</topic><topic>Fluoresceins</topic><topic>Fluorescence</topic><topic>Fluorescent Dyes</topic><topic>glutathione</topic><topic>Glutathione - metabolism</topic><topic>Intracellular Space - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Neurons - cytology</topic><topic>Neurons - physiology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Donors - pharmacology</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>NOS</topic><topic>Pancreas</topic><topic>Pancreas - cytology</topic><topic>Physiology</topic><topic>Protein Kinase C - antagonists & inhibitors</topic><topic>Protein Kinase C - metabolism</topic><topic>S-nitrosothiols</topic><topic>S-Nitrosothiols - metabolism</topic><topic>Signal transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chvanov, Michael</creatorcontrib><creatorcontrib>Gerasimenko, Oleg V</creatorcontrib><creatorcontrib>Petersen, Ole H</creatorcontrib><creatorcontrib>Tepikin, Alexei V</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Earth, Atmospheric & Aquatic Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Earth, Atmospheric & Aquatic Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The EMBO journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Chvanov, Michael</au><au>Gerasimenko, Oleg V</au><au>Petersen, Ole H</au><au>Tepikin, Alexei V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Calcium-dependent release of NO from intracellular S-nitrosothiols</atitle><jtitle>The EMBO journal</jtitle><stitle>EMBO J</stitle><addtitle>EMBO J</addtitle><date>2006-07-12</date><risdate>2006</risdate><volume>25</volume><issue>13</issue><spage>3024</spage><epage>3032</epage><pages>3024-3032</pages><issn>0261-4189</issn><eissn>1460-2075</eissn><coden>EMJODG</coden><abstract>The paper describes a novel cellular mechanism for rapid calcium‐dependent nitric oxide (NO) release. This release occurs due to NO liberation from
S
‐nitrosothiols. We have analysed the changes of NO concentration in acutely isolated pancreatic acinar cells. Supramaximal acetylcholine (ACh) stimulation induced a Ca
2+
‐dependent increase in the fluorescence in the majority of cells loaded with the NO probe DAF‐FM via a patch pipette. The ACh‐induced NO signals were insensitive to inhibitors of calmodulin and protein kinase C but were inhibited by calpain antagonists. The initial part of the NO signals induced by 10 μM ACh showed little sensitivity to inhibition of NO synthase (NOS); however, cell pretreatment with NO donors (increasing cellular
S
‐nitrosothiol contents) substantially enhanced the initial component of NO responses. Pancreatic acinar cells were able to generate fast calcium‐dependent NO responses when stimulated with physiological or supramaximal doses of secretagogues. Importantly, the source of this NO is the already available
S
‐nitrosothiol store rather than
de novo
synthesis by NOS. A similar mechanism of NO release was found in dorsal root ganglia neurons.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>16810320</pmid><doi>10.1038/sj.emboj.7601207</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext_linktorsrc |
| identifier | ISSN: 0261-4189 |
| ispartof | The EMBO journal, 2006-07, Vol.25 (13), p.3024-3032 |
| issn | 0261-4189 1460-2075 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1500983 |
| source | Springer Nature OA Free Journals |
| subjects | Acetylcholine - pharmacology Acrylates - pharmacology Animals Biochemistry Calcium Calcium - physiology Calmodulin - antagonists & inhibitors Calmodulin - metabolism Calpain - antagonists & inhibitors Calpain - metabolism Cells, Cultured EMBO37 Fluoresceins Fluorescence Fluorescent Dyes glutathione Glutathione - metabolism Intracellular Space - metabolism Male Mice Neurons - cytology Neurons - physiology Nitric oxide Nitric Oxide - biosynthesis Nitric Oxide Donors - pharmacology Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - metabolism NOS Pancreas Pancreas - cytology Physiology Protein Kinase C - antagonists & inhibitors Protein Kinase C - metabolism S-nitrosothiols S-Nitrosothiols - metabolism Signal transduction |
| title | Calcium-dependent release of NO from intracellular S-nitrosothiols |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T20%3A25%3A09IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_C6C&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Calcium-dependent%20release%20of%20NO%20from%20intracellular%20S-nitrosothiols&rft.jtitle=The%20EMBO%20journal&rft.au=Chvanov,%20Michael&rft.date=2006-07-12&rft.volume=25&rft.issue=13&rft.spage=3024&rft.epage=3032&rft.pages=3024-3032&rft.issn=0261-4189&rft.eissn=1460-2075&rft.coden=EMJODG&rft_id=info:doi/10.1038/sj.emboj.7601207&rft_dat=%3Cproquest_C6C%3E19494327%3C/proquest_C6C%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=195266292&rft_id=info:pmid/16810320&rfr_iscdi=true |