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Klaus Willecke

Researcher at University of Bonn

Publications -  343
Citations -  34057

Klaus Willecke is an academic researcher from University of Bonn. The author has contributed to research in topics: Connexin & Gap junction. The author has an hindex of 103, co-authored 342 publications receiving 32483 citations. Previous affiliations of Klaus Willecke include Roche Diagnostics & University of Geneva.

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Structural and functional diversity of connexin genes in the mouse and human genome

TL;DR: This review compares currently identified connexin genes in both the mouse and human genome and discusses the functions of gap junctions deduced from targeted mouse mutants and human genetic disorders.
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Gap junctions and the connexin protein family

TL;DR: Functional properties, like permeabilities, charge selectivity and unitary conductivity were investigated after directed expression of these connexins in cultured cell lines or paired Xenopus oocytes and targeted deletion of their coding sequence in the mouse genome allowed study of the biological relevance of Cx37, CX40, Cx43 and Cx45 with regard to cardiovascular morphology and function.
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Specific permeability and selective formation of gap junction channels in connexin-transfected HeLa cells.

TL;DR: The hypothesis that different connexin channels show different permeabilities to second messenger molecules as well as metabolites and may fulfill in this way their specific role in growth control and differentiation of cell types is supported.
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Astroglial metabolic networks sustain hippocampal synaptic transmission.

TL;DR: It is shown that the gap-junction subunit proteins connexin 43 and 30 allow intercellular trafficking of glucose and its metabolites through astroglial networks for the delivery of energetic metabolites from blood vessels to distal neurons.
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hGFAP-cre transgenic mice for manipulation of glial and neuronal function in vivo.

TL;DR: It was found that lacZ expression was primarily limited to the central nervous system, but therein was widespread in neurons and ependyma, suggesting that the hGFAP promoter is active in a multi‐potential neural stem cell.