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@ARTICLE{Harzheim:61425,
      author       = {Harzheim, D. and Pfeiffer, K.H. and Fabritz, L. and
                      Kremmer, E. and Buch, T. and Waisman, A. and Kirchhof, P.
                      and Kaupp, U. B. and Seifert, R.},
      title        = {{C}ardiac pacemaker function of {HCN}4 channels in mice is
                      confined to embryonic development and requires cyclic {AMP}},
      journal      = {The EMBO journal online},
      volume       = {27},
      issn         = {0261-4189},
      address      = {London [u.a.]},
      publisher    = {Nature Publishing Group},
      reportid     = {PreJuSER-61425},
      pages        = {692 - 703},
      year         = {2008},
      note         = {Record converted from VDB: 12.11.2012},
      abstract     = {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.},
      keywords     = {Animals / Cells, Cultured / Cyclic AMP: physiology / Cyclic
                      Nucleotide-Gated Cation Channels: genetics / Cyclic
                      Nucleotide-Gated Cation Channels: physiology / Embryonic
                      Development: physiology / Female / Heart: physiology / Heart
                      Rate / Mice / Mice, Inbred C57BL / Mice, Transgenic /
                      Mutation / Myocytes, Cardiac: physiology / Pregnancy /
                      Cyclic Nucleotide-Gated Cation Channels (NLM Chemicals) /
                      HCN3 protein, mouse (NLM Chemicals) / Cyclic AMP (NLM
                      Chemicals) / J (WoSType)},
      cin          = {INB-1},
      ddc          = {570},
      cid          = {I:(DE-Juel1)VDB804},
      pnm          = {Funktion und Dysfunktion des Nervensystems},
      pid          = {G:(DE-Juel1)FUEK409},
      shelfmark    = {Biochemistry $\&$ Molecular Biology / Cell Biology},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:18219271},
      pmc          = {pmc:PMC2262033},
      UT           = {WOS:000253409300010},
      doi          = {10.1038/emboj.2008.3},
      url          = {https://juser.fz-juelich.de/record/61425},
}