Immunolocalization of the mNav2.3 Na+ channel in mouse heart: upregulation in myometrium during pregnancy
T. J. Knittle, K. L. Doyle and M. M. Tamkun Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. mNav2.3 is a putative voltage-dependent sodium channel (NaC) gene expressed in both mouse heart and uterus that shares only 45% am...
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| Veröffentlicht in: | American Journal of Physiology: Cell Physiology 1996-02, Vol.270 (2), p.C688-C696 |
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| container_issue | 2 |
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| container_title | American Journal of Physiology: Cell Physiology |
| container_volume | 270 |
| creator | Knittle, T. J Doyle, K. L Tamkun, M. M |
| description | T. J. Knittle, K. L. Doyle and M. M. Tamkun
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
mNav2.3 is a putative voltage-dependent sodium channel (NaC) gene expressed
in both mouse heart and uterus that shares only 45% amino acid identity
with NaCs from gene subfamily 1. Immunofluorescence studies using
polyclonal antibodies against two distinct epitopes revealed that mNav2.3
protein in heart colocalized with nerve-specific antibody binding. Similar
mNav2.3-specific antibody staining was observed in virgin uterus. However,
mNav2.3 expression in uterine nerve disappeared during late pregnancy,
concurrent with an appearance in both the longitudinal and circular uterine
smooth muscle, which reached a maximum at term and quickly declined within
2 days postpartum. mNav2.3 expression in term uterus often colocalized on
the myocyte surface with connexin 43. The immunofluorescence results are
supported by Western analysis in which the 217-kDa NaC increased during
late pregnancy and declined 2 days postpartum. These data provide perhaps
the most dramatic example of NaC regulation. The acute and transient
upregulation in myometrium during gestation suggests the Nav2.3 channel
plays a role in uterine function at term. |
| doi_str_mv | 10.1152/ajpcell.1996.270.2.c688 |
| format | Article |
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Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
mNav2.3 is a putative voltage-dependent sodium channel (NaC) gene expressed
in both mouse heart and uterus that shares only 45% amino acid identity
with NaCs from gene subfamily 1. Immunofluorescence studies using
polyclonal antibodies against two distinct epitopes revealed that mNav2.3
protein in heart colocalized with nerve-specific antibody binding. Similar
mNav2.3-specific antibody staining was observed in virgin uterus. However,
mNav2.3 expression in uterine nerve disappeared during late pregnancy,
concurrent with an appearance in both the longitudinal and circular uterine
smooth muscle, which reached a maximum at term and quickly declined within
2 days postpartum. mNav2.3 expression in term uterus often colocalized on
the myocyte surface with connexin 43. The immunofluorescence results are
supported by Western analysis in which the 217-kDa NaC increased during
late pregnancy and declined 2 days postpartum. These data provide perhaps
the most dramatic example of NaC regulation. The acute and transient
upregulation in myometrium during gestation suggests the Nav2.3 channel
plays a role in uterine function at term.</description><identifier>ISSN: 0363-6143</identifier><identifier>ISSN: 0002-9513</identifier><identifier>EISSN: 1522-1563</identifier><identifier>DOI: 10.1152/ajpcell.1996.270.2.c688</identifier><identifier>PMID: 8779936</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Base Sequence ; Connexin 43 - metabolism ; Female ; Heart Conduction System - metabolism ; Immunologic Techniques ; Labor, Obstetric ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Molecular Probes - genetics ; Molecular Sequence Data ; Myocardium - metabolism ; Myometrium - metabolism ; Postpartum Period ; Pregnancy ; Pregnancy, Animal - metabolism ; Rabbits ; Sodium Channels - metabolism ; Uterus - metabolism</subject><ispartof>American Journal of Physiology: Cell Physiology, 1996-02, Vol.270 (2), p.C688-C696</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c261t-70fd2e9049dbd7de4cce4eb03bacda0e37c5d5bb599554abf36322dd37f7a27a3</citedby><cites>FETCH-LOGICAL-c261t-70fd2e9049dbd7de4cce4eb03bacda0e37c5d5bb599554abf36322dd37f7a27a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8779936$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Knittle, T. J</creatorcontrib><creatorcontrib>Doyle, K. L</creatorcontrib><creatorcontrib>Tamkun, M. M</creatorcontrib><title>Immunolocalization of the mNav2.3 Na+ channel in mouse heart: upregulation in myometrium during pregnancy</title><title>American Journal of Physiology: Cell Physiology</title><addtitle>Am J Physiol</addtitle><description>T. J. Knittle, K. L. Doyle and M. M. Tamkun
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
mNav2.3 is a putative voltage-dependent sodium channel (NaC) gene expressed
in both mouse heart and uterus that shares only 45% amino acid identity
with NaCs from gene subfamily 1. Immunofluorescence studies using
polyclonal antibodies against two distinct epitopes revealed that mNav2.3
protein in heart colocalized with nerve-specific antibody binding. Similar
mNav2.3-specific antibody staining was observed in virgin uterus. However,
mNav2.3 expression in uterine nerve disappeared during late pregnancy,
concurrent with an appearance in both the longitudinal and circular uterine
smooth muscle, which reached a maximum at term and quickly declined within
2 days postpartum. mNav2.3 expression in term uterus often colocalized on
the myocyte surface with connexin 43. The immunofluorescence results are
supported by Western analysis in which the 217-kDa NaC increased during
late pregnancy and declined 2 days postpartum. These data provide perhaps
the most dramatic example of NaC regulation. The acute and transient
upregulation in myometrium during gestation suggests the Nav2.3 channel
plays a role in uterine function at term.</description><subject>Animals</subject><subject>Base Sequence</subject><subject>Connexin 43 - metabolism</subject><subject>Female</subject><subject>Heart Conduction System - metabolism</subject><subject>Immunologic Techniques</subject><subject>Labor, Obstetric</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred DBA</subject><subject>Molecular Probes - genetics</subject><subject>Molecular Sequence Data</subject><subject>Myocardium - metabolism</subject><subject>Myometrium - metabolism</subject><subject>Postpartum Period</subject><subject>Pregnancy</subject><subject>Pregnancy, Animal - metabolism</subject><subject>Rabbits</subject><subject>Sodium Channels - metabolism</subject><subject>Uterus - metabolism</subject><issn>0363-6143</issn><issn>0002-9513</issn><issn>1522-1563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkE1v1DAQhi0EKtvCT0D4xAUlOHZix9zQio9KVbnA2XLsycZV7AQ7aRV-PY52VXGaw_sxMw9C7ytSVlVDP-mH2cA4lpWUvKSClLQ0vG1foENWaVE1nL1EB8I4K3hVs9foOqUHQkhNubxCV60QUjJ-QO7W-zVM42T06P7qxU0BTz1eBsD-Xj_SkuF7_RGbQYcAI3YB-2lNgAfQcfmM1znCaR3PuV3cJg9LdKvHdo0unPBuCDqY7Q161esxwdvLvEG_v339dfxR3P38fnv8clcYyqulEKS3FCSppe2ssFAbAzV0hHXaWE2ACdPYpusaKZum1l2fX6TUWiZ6oanQ7AZ9OPfOcfqzQlqUd2lnpQPk05VoaduwmmejOBtNnFKK0Ks5Oq_jpiqidsjqAlntkFWGrKg6Zsg5-e6yYu082OfchWrWi7M-uNPw5CKoediSy5RP23Ppf33_AKibjWg</recordid><startdate>199602</startdate><enddate>199602</enddate><creator>Knittle, T. J</creator><creator>Doyle, K. L</creator><creator>Tamkun, M. M</creator><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></search><sort><creationdate>199602</creationdate><title>Immunolocalization of the mNav2.3 Na+ channel in mouse heart: upregulation in myometrium during pregnancy</title><author>Knittle, T. J ; Doyle, K. L ; Tamkun, M. M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c261t-70fd2e9049dbd7de4cce4eb03bacda0e37c5d5bb599554abf36322dd37f7a27a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Base Sequence</topic><topic>Connexin 43 - metabolism</topic><topic>Female</topic><topic>Heart Conduction System - metabolism</topic><topic>Immunologic Techniques</topic><topic>Labor, Obstetric</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred DBA</topic><topic>Molecular Probes - genetics</topic><topic>Molecular Sequence Data</topic><topic>Myocardium - metabolism</topic><topic>Myometrium - metabolism</topic><topic>Postpartum Period</topic><topic>Pregnancy</topic><topic>Pregnancy, Animal - metabolism</topic><topic>Rabbits</topic><topic>Sodium Channels - metabolism</topic><topic>Uterus - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Knittle, T. J</creatorcontrib><creatorcontrib>Doyle, K. L</creatorcontrib><creatorcontrib>Tamkun, M. M</creatorcontrib><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><jtitle>American Journal of Physiology: Cell Physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Knittle, T. J</au><au>Doyle, K. L</au><au>Tamkun, M. M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunolocalization of the mNav2.3 Na+ channel in mouse heart: upregulation in myometrium during pregnancy</atitle><jtitle>American Journal of Physiology: Cell Physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1996-02</date><risdate>1996</risdate><volume>270</volume><issue>2</issue><spage>C688</spage><epage>C696</epage><pages>C688-C696</pages><issn>0363-6143</issn><issn>0002-9513</issn><eissn>1522-1563</eissn><abstract>T. J. Knittle, K. L. Doyle and M. M. Tamkun
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
mNav2.3 is a putative voltage-dependent sodium channel (NaC) gene expressed
in both mouse heart and uterus that shares only 45% amino acid identity
with NaCs from gene subfamily 1. Immunofluorescence studies using
polyclonal antibodies against two distinct epitopes revealed that mNav2.3
protein in heart colocalized with nerve-specific antibody binding. Similar
mNav2.3-specific antibody staining was observed in virgin uterus. However,
mNav2.3 expression in uterine nerve disappeared during late pregnancy,
concurrent with an appearance in both the longitudinal and circular uterine
smooth muscle, which reached a maximum at term and quickly declined within
2 days postpartum. mNav2.3 expression in term uterus often colocalized on
the myocyte surface with connexin 43. The immunofluorescence results are
supported by Western analysis in which the 217-kDa NaC increased during
late pregnancy and declined 2 days postpartum. These data provide perhaps
the most dramatic example of NaC regulation. The acute and transient
upregulation in myometrium during gestation suggests the Nav2.3 channel
plays a role in uterine function at term.</abstract><cop>United States</cop><pmid>8779936</pmid><doi>10.1152/ajpcell.1996.270.2.c688</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0363-6143 |
| ispartof | American Journal of Physiology: Cell Physiology, 1996-02, Vol.270 (2), p.C688-C696 |
| issn | 0363-6143 0002-9513 1522-1563 |
| language | eng |
| recordid | cdi_highwire_physiology_ajpcell_270_2_C688 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Base Sequence Connexin 43 - metabolism Female Heart Conduction System - metabolism Immunologic Techniques Labor, Obstetric Male Mice Mice, Inbred C57BL Mice, Inbred DBA Molecular Probes - genetics Molecular Sequence Data Myocardium - metabolism Myometrium - metabolism Postpartum Period Pregnancy Pregnancy, Animal - metabolism Rabbits Sodium Channels - metabolism Uterus - metabolism |
| title | Immunolocalization of the mNav2.3 Na+ channel in mouse heart: upregulation in myometrium during pregnancy |
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