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| Hauptseite > Publikationsdatenbank > Cardiac pacemaker function of HCN4 channels in mice is confined to embryonic development and requires cyclic AMP > print |
| Hauptseite > Publikationsdatenbank > Cardiac pacemaker function of HCN4 channels in mice is confined to embryonic development and requires cyclic AMP > print |
| 001 | 61425 | ||
| 005 | 20200402210454.0 | ||
| 024 | 7 | _ | |2 pmid |a pmid:18219271 |
| 024 | 7 | _ | |2 pmc |a pmc:PMC2262033 |
| 024 | 7 | _ | |2 DOI |a 10.1038/emboj.2008.3 |
| 024 | 7 | _ | |2 WOS |a WOS:000253409300010 |
| 037 | _ | _ | |a PreJuSER-61425 |
| 041 | _ | _ | |a eng |
| 082 | _ | _ | |a 570 |
| 084 | _ | _ | |2 WoS |a Biochemistry & Molecular Biology |
| 084 | _ | _ | |2 WoS |a Cell Biology |
| 100 | 1 | _ | |a Harzheim, D. |b 0 |u FZJ |0 P:(DE-Juel1)VDB28136 |
| 245 | _ | _ | |a Cardiac pacemaker function of HCN4 channels in mice is confined to embryonic development and requires cyclic AMP |
| 260 | _ | _ | |a London [u.a.] |b Nature Publishing Group |c 2008 |
| 300 | _ | _ | |a 692 - 703 |
| 336 | 7 | _ | |a Journal Article |0 PUB:(DE-HGF)16 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a article |2 DRIVER |
| 440 | _ | 0 | |a Embo Journal |x 0261-4189 |0 1793 |v 27 |
| 500 | _ | _ | |a Record converted from VDB: 12.11.2012 |
| 520 | _ | _ | |a Important targets for cAMP signalling in the heart are hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels that underlie the depolarizing 'pacemaker' current, I(f). We studied the role of I(f) in mice, in which binding of cAMP to HCN4 channels was abolished by a single amino-acid exchange (R669Q). Homozygous HCN4(R669Q/R669Q) mice die during embryonic development. Prior to E12, homozygous and heterozygous embryos display reduced heart rates and show no or attenuated responses to catecholaminergic stimulation. Adult heterozygous mice display normal heart rates at rest and during exercise. However, following beta-adrenergic stimulation, hearts exhibit pauses and sino-atrial node block. Our results demonstrate that in the embryo, HCN4 is a true cardiac pacemaker and elevation of HCN4 channel activity by cAMP is essential for viability. In adult mice, an important function of HCN4 channels is to prevent sinus pauses during and after stress while their role as a pacemaker of the murine heart is put into question. Most importantly, our results indicate that HCN4 channels can fulfil their physiological function only when cAMP is bound. |
| 536 | _ | _ | |a Funktion und Dysfunktion des Nervensystems |c P33 |2 G:(DE-HGF) |0 G:(DE-Juel1)FUEK409 |x 0 |
| 588 | _ | _ | |a Dataset connected to Web of Science, Pubmed |
| 650 | _ | 2 | |2 MeSH |a Animals |
| 650 | _ | 2 | |2 MeSH |a Cells, Cultured |
| 650 | _ | 2 | |2 MeSH |a Cyclic AMP: physiology |
| 650 | _ | 2 | |2 MeSH |a Cyclic Nucleotide-Gated Cation Channels: genetics |
| 650 | _ | 2 | |2 MeSH |a Cyclic Nucleotide-Gated Cation Channels: physiology |
| 650 | _ | 2 | |2 MeSH |a Embryonic Development: physiology |
| 650 | _ | 2 | |2 MeSH |a Female |
| 650 | _ | 2 | |2 MeSH |a Heart: physiology |
| 650 | _ | 2 | |2 MeSH |a Heart Rate |
| 650 | _ | 2 | |2 MeSH |a Mice |
| 650 | _ | 2 | |2 MeSH |a Mice, Inbred C57BL |
| 650 | _ | 2 | |2 MeSH |a Mice, Transgenic |
| 650 | _ | 2 | |2 MeSH |a Mutation |
| 650 | _ | 2 | |2 MeSH |a Myocytes, Cardiac: physiology |
| 650 | _ | 2 | |2 MeSH |a Pregnancy |
| 650 | _ | 7 | |0 0 |2 NLM Chemicals |a Cyclic Nucleotide-Gated Cation Channels |
| 650 | _ | 7 | |0 0 |2 NLM Chemicals |a HCN3 protein, mouse |
| 650 | _ | 7 | |0 60-92-4 |2 NLM Chemicals |a Cyclic AMP |
| 650 | _ | 7 | |a J |2 WoSType |
| 653 | 2 | 0 | |2 Author |a cardiology |
| 653 | 2 | 0 | |2 Author |a cyclic nucleotides |
| 653 | 2 | 0 | |2 Author |a heart |
| 653 | 2 | 0 | |2 Author |a ion channel |
| 653 | 2 | 0 | |2 Author |a signalling |
| 700 | 1 | _ | |a Pfeiffer, K.H. |b 1 |u FZJ |0 P:(DE-Juel1)VDB74441 |
| 700 | 1 | _ | |a Fabritz, L. |b 2 |0 P:(DE-HGF)0 |
| 700 | 1 | _ | |a Kremmer, E. |b 3 |0 P:(DE-HGF)0 |
| 700 | 1 | _ | |a Buch, T. |b 4 |0 P:(DE-HGF)0 |
| 700 | 1 | _ | |a Waisman, A. |b 5 |0 P:(DE-HGF)0 |
| 700 | 1 | _ | |a Kirchhof, P. |b 6 |0 P:(DE-HGF)0 |
| 700 | 1 | _ | |a Kaupp, U. B. |b 7 |u FZJ |0 P:(DE-Juel1)VDB728 |
| 700 | 1 | _ | |a Seifert, R. |b 8 |u FZJ |0 P:(DE-Juel1)VDB1505 |
| 773 | _ | _ | |a 10.1038/emboj.2008.3 |g Vol. 27, p. 692 - 703 |p 692 - 703 |q 27<692 - 703 |0 PERI:(DE-600)1467419-1 |t The @EMBO journal online |v 27 |y 2008 |x 0261-4189 |
| 856 | 7 | _ | |2 Pubmed Central |u http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2262033 |
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| 914 | 1 | _ | |y 2008 |
| 915 | _ | _ | |0 StatID:(DE-HGF)0010 |a JCR/ISI refereed |
| 920 | 1 | _ | |k INB-1 |l Zelluläre Biophysik |d 31.12.2008 |g INB |0 I:(DE-Juel1)VDB804 |x 0 |
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| 981 | _ | _ | |a I:(DE-Juel1)IBI-1-20200312 |
| 981 | _ | _ | |a I:(DE-Juel1)ICS-4-20110106 |
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