J
Julia Goldau
Researcher at University of Cologne
Publications - 3
Citations - 775
Julia Goldau is an academic researcher from University of Cologne. The author has contributed to research in topics: Interleukin 6 & Phosphorylation. The author has an hindex of 3, co-authored 3 publications receiving 638 citations. Previous affiliations of Julia Goldau include Max Planck Society.
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Signaling by IL-6 promotes alternative activation of macrophages to limit endotoxemia and obesity-associated resistance to insulin
Jan Mauer,Bhagirath Chaurasia,Julia Goldau,Merly C. Vogt,Johan Ruud,Khoa D. Nguyen,Sebastian Theurich,A. Christine Hausen,Joel Schmitz,Hella S. Brönneke,Emma Estevez,Tamara L Allen,Andrea Mesaros,Linda Partridge,Mark A. Febbraio,Ajay Chawla,F. Thomas Wunderlich,Jens C. Brüning +17 more
TL;DR: The results identify signaling via IL-6 as an important determinant of the alternative activation of macrophages and assign an unexpected homeostatic role to IL- 6 in limiting inflammation.
Journal ArticleDOI
Myeloid-Cell-Derived VEGF Maintains Brain Glucose Uptake and Limits Cognitive Impairment in Obesity
Alexander Jais,Alexander Jais,Maite Solas,Maite Solas,Heiko Backes,Bhagirath Chaurasia,André Kleinridders,Sebastian Theurich,Sebastian Theurich,Jan Mauer,Jan Mauer,Sophie M. Steculorum,Sophie M. Steculorum,Brigitte Hampel,Brigitte Hampel,Julia Goldau,Julia Goldau,Jens Alber,Jens Alber,Carola Förster,Sabine A. Eming,Markus Schwaninger,Napoleone Ferrara,Gerard Karsenty,Jens C. Brüning +24 more
TL;DR: The experiments reveal that transient, HFD-elicited reduction of brain glucose uptake initiates a compensatory increase of VEGF production and assign obesity-associated macrophage activation a homeostatic role to restore cerebral glucose metabolism, preserve cognitive function, and limit neurodegeneration in obesity.
Journal ArticleDOI
Phosphoinositide-Dependent Kinase 1 Provides Negative Feedback Inhibition to Toll-Like Receptor-Mediated NF-κB Activation in Macrophages
TL;DR: It is shown that mice with conditional disruption of PDK-1 specifically in myeloid lineage cells show enhanced susceptibility to lipopolysaccharide (LPS)-induced septic shock accompanied by exaggerated liver failure, and experiments reveal a novel PDk-1-dependent negative feedback inhibition of TLR-induced NF-κB activation in macrophages in vivo.