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Burkhard Wiesner
Researcher at Leibniz Institute for Neurobiology
Publications - 101
Citations - 5898
Burkhard Wiesner is an academic researcher from Leibniz Institute for Neurobiology. The author has contributed to research in topics: Receptor & G protein-coupled receptor. The author has an hindex of 42, co-authored 101 publications receiving 5454 citations. Previous affiliations of Burkhard Wiesner include Center of Advanced European Studies and Research & Leibniz Association.
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Journal ArticleDOI
Cellular uptake of an α-helical amphipathic model peptide with the potential to deliver polar compounds into the cell interior non-endocytically
Johannes Oehlke,Anne Scheller,Burkhard Wiesner,Eberhard Krause,Michael Beyermann,Erhard Klauschenz,Mathias Melzig,Michael Bienert +7 more
TL;DR: Evidence that multiple, probably non-endocytic mechanisms are involved in the uptake into mammalian cells of the alpha-helical amphipathic model peptide FLUOS-KLALKLALKALKAALKLA-NH2 (I) is presented.
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Formation of tight junction: determinants of homophilic interaction between classic claudins
Jörg Piontek,Lars Winkler,Hartwig Wolburg,Sebastian L. Müller,Nikolaj Zuleger,Nikolaj Zuleger,Christian Piehl,Burkhard Wiesner,Gerd Krause,Ingolf E. Blasig +9 more
TL;DR: The claudin‐claudin interaction and tight junction strand formation were investigated using systematic single mutations and an antiparallel homodimer homology model of the loop led to a novel molecular concept for tight junction formation.
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c-FLIP Mediates Resistance of Hodgkin/Reed-Sternberg Cells to Death Receptor–induced Apoptosis
Stephan Mathas,Andreas Lietz,Ioannis Anagnostopoulos,Franziska Hummel,Burkhard Wiesner,Martin Janz,Franziska Jundt,Burkhard Hirsch,Korinna Jöhrens-Leder,Hans-Peter Vornlocher,Kurt Bommert,Harald Stein,Bernd Dörken,Bernd Dörken +13 more
TL;DR: Despite expression of other NF-κB–dependent antiapoptotic proteins, the selective down-regulation of c-FLIP by small interfering RNA oligoribonucleotides was sufficient to sensitize HRS cells to CD95 and tumor necrosis factor–related apoptosis-inducing ligand–induced apoptosis.
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AKAP complex regulates Ca2+ re‐uptake into heart sarcoplasmic reticulum
Birgitte Lygren,Cathrine R. Carlson,Katja Santamaria,Valentina Lissandron,Theresa McSorley,Jessica Litzenberg,Dorothea Lorenz,Burkhard Wiesner,Walter Rosenthal,Walter Rosenthal,Manuela Zaccolo,Kjetil Taskén,Enno Klussmann,Enno Klussmann +13 more
TL;DR: This work has identified a supramolecular complex consisting of the sarcoplasmic reticulum Ca2+‐ATPase, its negative regulator phospholamban, the A‐kinase anchoring protein AKAP 18δ and PKA, and shows that AKAP18δ acts as a scaffold that coordinates PKA phosphorylation of PLN and the adrenergic effect on Ca2- re‐uptake.
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Cyclic nucleotide-gated channels on the flagellum control Ca2+ entry into sperm.
TL;DR: It is shown that the CNG channels serve as a Ca2+ entry pathway that responds more sensitively to cGMP than to cAMP, and dissimilar localization of α and β subunits may give rise to a pattern of Ca2- microdomains along the flagellum, thereby providing the structural basis for control ofFlagellar bending waves.