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Hans M. Eppenberger

Researcher at École Polytechnique Fédérale de Lausanne

Publications -  157
Citations -  11779

Hans M. Eppenberger is an academic researcher from École Polytechnique Fédérale de Lausanne. The author has contributed to research in topics: Creatine kinase & Myofibril. The author has an hindex of 55, co-authored 157 publications receiving 11517 citations. Previous affiliations of Hans M. Eppenberger include ETH Zurich & Novartis.

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Journal ArticleDOI

Intracellular compartmentation, structure and function of creatine kinase isoenzymes in tissues with high and fluctuating energy demands: the 'phosphocreatine circuit' for cellular energy homeostasis.

Theo Wallimann, +4 more
- 01 Jan 1992 - 
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Major nucleolar proteins shuttle between nucleus and cytoplasm

R.A. Borer, +3 more
- 10 Feb 1989 - 
TL;DR: These unexpected results suggest a role for these major nucleolar proteins in the nucleocytoplasmic transport of ribosomal components and suggest that transient exposure of shuttling proteins to the cy toplasm may provide a mechanism for cytop lasmic regulation of nuclear activities.
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Rapid and reversible translocation of the catalytic subunit of cAMP-dependent protein kinase type II from the Golgi complex to the nucleus.

Erich A. Nigg, +3 more
- 01 Nov 1985 - 
TL;DR: The results suggest that nuclear translocation of activated protein kinase subunits may represent an important link between hormonal stimuli and physiological responses in unstimulated interphase bovine epithelial cells.
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Modulation of anthracycline-induced myofibrillar disarray in rat ventricular myocytes by neuregulin-1beta and anti-erbB2: potential mechanism for trastuzumab-induced cardiotoxicity.

Douglas B. Sawyer, +4 more
- 02 Apr 2002 - 
TL;DR: The increased susceptibility of myofilaments to doxorubicin in the presence of antibody to erbB2 may explain the contractile dysfunction seen in patients receiving concurrent trastuzumab and anthracyclines.
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Anthracyclines induce calpain-dependent titin proteolysis and necrosis in cardiomyocytes.

Chee Chew Lim, +8 more
- 27 Feb 2004 - 
TL;DR: Calpain activation is an early event after doxorubicin treatment in cardiomyocytes and appears to target the degradation of titin, which may predispose cardiomers to diastolic dysfunction, myofilament instability, and cell death by necrosis.