We are analyzing https://link.springer.com/article/10.1007/s00395-010-0149-5.

Title:
Molecular characterization of thyroid hormone-inhibited atrial L-type calcium channel expression: implication for atrial fibrillation in hyperthyroidism | Basic Research in Cardiology
Description:
Atrial fibrillation (AF) is a common complication in hyperthyroidism. Earlier studies demonstrate that thyroid hormone decreases L-type calcium channel (LCC) current expression with resultant shortening of action potential duration (APD), providing a substrate for AF. The aim of this study was to investigate the potential mechanism underlying the regulatory effect of thyroid hormone on LCC. In a hyperthyroid rat model, thyroid hormone (triiodothyronine [T3]) administration down-regulated atrial LCC expression. In vitro, treatment of murine atrial myocytes (HL-1) with T3 decreased the expression of LCC and its current, resulting in abbreviation of APD. Furthermore, T3 inhibited the activation of cyclic AMP response element (CRE)-binding protein (CREB), including phosphorylation at Ser133 and its nuclear translocation. Transient transfection studies in HL-1 cells indicated that T3 reduced LCC promoter activity. Deletion and mutation analysis of the LCC promoter region along with chromatin immunoprecipitation using anti-CREB antibody showed that CRE was essential for T3-mediated LCC gene expression. Transfection of dominant-negative CREB (mutated Ser133) and mutant thyroid hormone receptor (TR, mutated Cys51) abolished the T3-dependent effects, suggesting an association between both transcriptional factors. Co-immunoprecipitation documented an increased binding of TR with CREB after T3 treatment. The transcriptional cross-talk 3 between TR and CREB bound to CRE mediates T3-inhibited CREB activity and LCC expression. Thyroid hormone-induced TR binding of CREB inhibits CREB activity and LCC current expression, which may contribute to AF. These findings provide an important mechanistic insight into hyperthyroidism-induced AF.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Science
Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We see no obvious way the site makes money.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

article, google, scholar, pubmed, cas, thyroid, atrial, chen, fibrillation, hormone, expression, res, lin, chang, creb, lcc, receptor, remodeling, basic, access, cell, cardiol, research, calcium, yeh, channels, dois, nattel, privacy, cookies, content, molecular, ltype, hyperthyroidism, action, potential, gung, author, information, publish, search, channel, current, mechanism, underlying, activity, open, factor, rev, circ,

Topics {✒️}

akt/gsk-3β/mtor signaling pathway ion channels kwang-huei lin l-type calcium channel l-type calcium current cell signal 16 month download article/chapter camp-response element modulator long-standing atrial fibrillation author information authors platelet-derived growth factor binding protein atrial-ventricular remodeling differences transient transfection studies author correspondence anti-creb antibody showed article basic research cameiro-ramos ms chang gung university human atrial fibrillation paroxysmal atrial fibrillation atrial fibrillation 50 years nuclear receptor trα1 nuclear receptor monomers thyroid hormone t3 yung-hsin yeh thyroid hormone action thyroid hormone receptors potential mechanism underlying cardiovascular system action potential duration wei-jan chen related subjects fu-shin road full article pdf promotes vsmc differentiation human cardiac isoform 1007/s00395-009-0045 privacy choices/manage cookies anaplastic thyroid carcinoma check access instant access atrial electrical remodeling murine atrial myocytes atrial fibrillation chang ms t3-dependent effects t3 inhibited thyroid hormone lcc promoter region

Questions {❓}

Johannessen M, Delghandi MP, Moens U (2004) What turns CREB on?
Maia AL, Harney JW, Larsen PR (1996) Is there a negative TRE in the luciferase reporter cDNA?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Molecular characterization of thyroid hormone-inhibited atrial L-type calcium channel expression: implication for atrial fibrillation in hyperthyroidism
         description:Atrial fibrillation (AF) is a common complication in hyperthyroidism. Earlier studies demonstrate that thyroid hormone decreases L-type calcium channel (LCC) current expression with resultant shortening of action potential duration (APD), providing a substrate for AF. The aim of this study was to investigate the potential mechanism underlying the regulatory effect of thyroid hormone on LCC. In a hyperthyroid rat model, thyroid hormone (triiodothyronine [T3]) administration down-regulated atrial LCC expression. In vitro, treatment of murine atrial myocytes (HL-1) with T3 decreased the expression of LCC and its current, resulting in abbreviation of APD. Furthermore, T3 inhibited the activation of cyclic AMP response element (CRE)-binding protein (CREB), including phosphorylation at Ser133 and its nuclear translocation. Transient transfection studies in HL-1 cells indicated that T3 reduced LCC promoter activity. Deletion and mutation analysis of the LCC promoter region along with chromatin immunoprecipitation using anti-CREB antibody showed that CRE was essential for T3-mediated LCC gene expression. Transfection of dominant-negative CREB (mutated Ser133) and mutant thyroid hormone receptor (TR, mutated Cys51) abolished the T3-dependent effects, suggesting an association between both transcriptional factors. Co-immunoprecipitation documented an increased binding of TR with CREB after T3 treatment. The transcriptional cross-talk 3 between TR and CREB bound to CRE mediates T3-inhibited CREB activity and LCC expression. Thyroid hormone-induced TR binding of CREB inhibits CREB activity and LCC current expression, which may contribute to AF. These findings provide an important mechanistic insight into hyperthyroidism-induced AF.
         datePublished:2011-01-14T00:00:00Z
         dateModified:2011-01-14T00:00:00Z
         pageStart:163
         pageEnd:174
         sameAs:https://doi.org/10.1007/s00395-010-0149-5
         keywords:
            AMP-activated protein kinase signal transduction
            Atrial fibrillation
            Ion channels
            Signal transduction
            Thyroid
            Cardiology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig4_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig5_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig6_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig7_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig8_HTML.gif
         isPartOf:
            name:Basic Research in Cardiology
            issn:
               1435-1803
               0300-8428
            volumeNumber:106
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer-Verlag
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Wei-Jan Chen
               affiliation:
                     name:Chang Gung University College of Medicine
                     address:
                        name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:Yung-Hsin Yeh
               affiliation:
                     name:Chang Gung University College of Medicine
                     address:
                        name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Kwang-Huei Lin
               affiliation:
                     name:Chang Gung University
                     address:
                        name:Department of Biochemistry, Chang Gung University, Tao-Yuan, Taiwan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Gwo-Jyh Chang
               affiliation:
                     name:Chang Gung University
                     address:
                        name:Graduate Institute of Clinical Medical Sciences, Chang Gung University, Tao-Yuan, Taiwan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Chi-Tai Kuo
               affiliation:
                     name:Chang Gung University College of Medicine
                     address:
                        name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Molecular characterization of thyroid hormone-inhibited atrial L-type calcium channel expression: implication for atrial fibrillation in hyperthyroidism
      description:Atrial fibrillation (AF) is a common complication in hyperthyroidism. Earlier studies demonstrate that thyroid hormone decreases L-type calcium channel (LCC) current expression with resultant shortening of action potential duration (APD), providing a substrate for AF. The aim of this study was to investigate the potential mechanism underlying the regulatory effect of thyroid hormone on LCC. In a hyperthyroid rat model, thyroid hormone (triiodothyronine [T3]) administration down-regulated atrial LCC expression. In vitro, treatment of murine atrial myocytes (HL-1) with T3 decreased the expression of LCC and its current, resulting in abbreviation of APD. Furthermore, T3 inhibited the activation of cyclic AMP response element (CRE)-binding protein (CREB), including phosphorylation at Ser133 and its nuclear translocation. Transient transfection studies in HL-1 cells indicated that T3 reduced LCC promoter activity. Deletion and mutation analysis of the LCC promoter region along with chromatin immunoprecipitation using anti-CREB antibody showed that CRE was essential for T3-mediated LCC gene expression. Transfection of dominant-negative CREB (mutated Ser133) and mutant thyroid hormone receptor (TR, mutated Cys51) abolished the T3-dependent effects, suggesting an association between both transcriptional factors. Co-immunoprecipitation documented an increased binding of TR with CREB after T3 treatment. The transcriptional cross-talk 3 between TR and CREB bound to CRE mediates T3-inhibited CREB activity and LCC expression. Thyroid hormone-induced TR binding of CREB inhibits CREB activity and LCC current expression, which may contribute to AF. These findings provide an important mechanistic insight into hyperthyroidism-induced AF.
      datePublished:2011-01-14T00:00:00Z
      dateModified:2011-01-14T00:00:00Z
      pageStart:163
      pageEnd:174
      sameAs:https://doi.org/10.1007/s00395-010-0149-5
      keywords:
         AMP-activated protein kinase signal transduction
         Atrial fibrillation
         Ion channels
         Signal transduction
         Thyroid
         Cardiology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig4_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig5_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig6_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig7_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-010-0149-5/MediaObjects/395_2010_149_Fig8_HTML.gif
      isPartOf:
         name:Basic Research in Cardiology
         issn:
            1435-1803
            0300-8428
         volumeNumber:106
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer-Verlag
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Wei-Jan Chen
            affiliation:
                  name:Chang Gung University College of Medicine
                  address:
                     name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Yung-Hsin Yeh
            affiliation:
                  name:Chang Gung University College of Medicine
                  address:
                     name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Kwang-Huei Lin
            affiliation:
                  name:Chang Gung University
                  address:
                     name:Department of Biochemistry, Chang Gung University, Tao-Yuan, Taiwan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Gwo-Jyh Chang
            affiliation:
                  name:Chang Gung University
                  address:
                     name:Graduate Institute of Clinical Medical Sciences, Chang Gung University, Tao-Yuan, Taiwan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Chi-Tai Kuo
            affiliation:
                  name:Chang Gung University College of Medicine
                  address:
                     name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Basic Research in Cardiology
      issn:
         1435-1803
         0300-8428
      volumeNumber:106
Organization:
      name:Springer-Verlag
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Chang Gung University College of Medicine
      address:
         name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
         type:PostalAddress
      name:Chang Gung University College of Medicine
      address:
         name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
         type:PostalAddress
      name:Chang Gung University
      address:
         name:Department of Biochemistry, Chang Gung University, Tao-Yuan, Taiwan
         type:PostalAddress
      name:Chang Gung University
      address:
         name:Graduate Institute of Clinical Medical Sciences, Chang Gung University, Tao-Yuan, Taiwan
         type:PostalAddress
      name:Chang Gung University College of Medicine
      address:
         name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Wei-Jan Chen
      affiliation:
            name:Chang Gung University College of Medicine
            address:
               name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Yung-Hsin Yeh
      affiliation:
            name:Chang Gung University College of Medicine
            address:
               name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
               type:PostalAddress
            type:Organization
      name:Kwang-Huei Lin
      affiliation:
            name:Chang Gung University
            address:
               name:Department of Biochemistry, Chang Gung University, Tao-Yuan, Taiwan
               type:PostalAddress
            type:Organization
      name:Gwo-Jyh Chang
      affiliation:
            name:Chang Gung University
            address:
               name:Graduate Institute of Clinical Medical Sciences, Chang Gung University, Tao-Yuan, Taiwan
               type:PostalAddress
            type:Organization
      name:Chi-Tai Kuo
      affiliation:
            name:Chang Gung University College of Medicine
            address:
               name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
               type:PostalAddress
            type:Organization
PostalAddress:
      name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
      name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
      name:Department of Biochemistry, Chang Gung University, Tao-Yuan, Taiwan
      name:Graduate Institute of Clinical Medical Sciences, Chang Gung University, Tao-Yuan, Taiwan
      name:First Cardiovascular Division, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Tao-Yuan, Taiwan
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(154)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.76s.

LINK . SPRINGER . COM {}