J
Juliane Stieber
Researcher at University of Erlangen-Nuremberg
Publications - 29
Citations - 3255
Juliane Stieber is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Sinoatrial node & HCN channel. The author has an hindex of 19, co-authored 29 publications receiving 3013 citations. Previous affiliations of Juliane Stieber include Technische Universität München.
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Journal ArticleDOI
Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2
Andreas Ludwig,Thomas Budde,Juliane Stieber,Sven Moosmang,Christian Wahl,Knut Holthoff,Anke Langebartels,Carsten T. Wotjak,Thomas Munsch,Xiangang Zong,Susanne Feil,Robert Feil,Marike Lancel,Kenneth R. Chien,Arthur Konnerth,Hans-Christian Pape,Martin Biel,Franz Hofmann +17 more
TL;DR: The physiological role of the HCN2 subunit is defined as a major determinant of membrane resting potential that is required for regular cardiac and neuronal rhythmicity.
Journal ArticleDOI
Ultraflexible vesicles, Transfersomes, have an extremely low pore penetration resistance and transport therapeutic amounts of insulin across the intact mammalian skin.
TL;DR: The carrier-mediated transcutaneous insulin delivery is unlikely to involve shunts, lesions or other types of skin damage, and is inferred to be transported into the body between the intact skin cells with a bio-efficiency of at least 50% of the s.c. dose action.
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The hyperpolarization-activated channel HCN4 is required for the generation of pacemaker action potentials in the embryonic heart
Juliane Stieber,Stefan Herrmann,Susanne Feil,Jana Löster,Robert Feil,Martin Biel,Franz Hofmann,Andreas Ludwig +7 more
TL;DR: It is shown that HCN4 is essential for the proper function of the developing cardiac conduction system and the proper generation of pacemaker potentials in the emerging sinoatrial node.
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Cellular expression and functional characterization of four hyperpolarization-activated pacemaker channels in cardiac and neuronal tissues
TL;DR: The results suggest that the heterogeneity of native I(h) currents is generated, at least in part, by the tissue-specific expression of HCN channel genes.
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HCN4 provides a 'depolarization reserve' and is not required for heart rate acceleration in mice.
TL;DR: It is shown that deletion of HCN4 in adult mice eliminates most of sinoatrial If and results in a cardiac arrhythmia characterized by recurrent sinus pauses, however, the mutants show no impairment in heart rate acceleration during sympathetic stimulation.