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Cornel Badorff
Researcher at Goethe University Frankfurt
Publications - 25
Citations - 3859
Cornel Badorff is an academic researcher from Goethe University Frankfurt. The author has contributed to research in topics: Cardiomyopathy & Dystrophin. The author has an hindex of 22, co-authored 25 publications receiving 3753 citations. Previous affiliations of Cornel Badorff include University of California, San Diego.
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Journal ArticleDOI
Assessment of the tissue distribution of transplanted human endothelial progenitor cells by radioactive labeling.
Alexandra Aicher,Winfried Brenner,Maaz Zuhayra,Cornel Badorff,Schirin Massoudi,Birgit Assmus,Thomas Eckey,Eberhard Henze,Andreas M. Zeiher,Stefanie Dimmeler +9 more
TL;DR: Although only a small proportion of radiolabeled EPCs are detected in nonischemic myocardium, myocardial infarction increases homing of transplanted E PCs in vivo profoundly, which might eventually provide an useful tool for monitoring the fate of transplants progenitor cells and for clinical cell therapy.
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Transdifferentiation of Blood-Derived Human Adult Endothelial Progenitor Cells Into Functionally Active Cardiomyocytes
Cornel Badorff,Ralf P. Brandes,Rüdiger Popp,Stefan Rupp,Carmen Urbich,Alexandra Aicher,Ingrid Fleming,Rudi Busse,Andreas M. Zeiher,Stefanie Dimmeler +9 more
TL;DR: EPCs from healthy volunteers and CAD patients can transdifferentiate in vitro into functionally active cardiomyocytes when cocultivated with rat cardiomers, and the therapeutic use of autologous EPCs may aid cardiomeocyte regeneration in patients with ischemic heart disease.
Journal ArticleDOI
Enteroviral protease 2A cleaves dystrophin: Evidence of cytoskeletal disruption in an acquired cardiomyopathy
Cornel Badorff,Gil-Hwan Lee,Barry J. Lamphear,Maryann E. Martone,Kevin P. Campbell,Robert E. Rhoads,Kirk U. Knowlton +6 more
TL;DR: It is demonstrated here that purified Coxsackievirus protease 2A cleaves dystrophin in vitro as predicted by computer analysis, suggesting a molecular mechanism through which enteroviral infection contributes to the pathogenesis of acquired forms of dilated cardiomyopathy.
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Akt-dependent phosphorylation of p21(Cip1) regulates PCNA binding and proliferation of endothelial cells.
Lothar Rössig,Amir S. Jadidi,Carmen Urbich,Cornel Badorff,Andreas M. Zeiher,Stefanie Dimmeler +5 more
TL;DR: It is demonstrated that Akt phosphorylates the cell cycle inhibitory protein p21Cip1 at Thr 145 in vitro and in intact cells as shown by in vitro kinase assays, site-directed mutagenesis, and phospho-peptide analysis.
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Glycogen Synthase Kinase-3 Couples AKT-dependent Signaling to the Regulation of p21Cip1 Degradation
TL;DR: Data indicate that GSK-3 triggers p21Cip1 degradation, and stimulation of AKT increases p21 cip1 via inhibitory phosphorylation of G SK-3, which indicates that a kinase downstream ofAKT regulates p21 Cip1 protein levels.