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Wolfgang Weninger

Researcher at Medical University of Vienna

Publications -  362
Citations -  25279

Wolfgang Weninger is an academic researcher from Medical University of Vienna. The author has contributed to research in topics: Cytotoxic T cell & Immune system. The author has an hindex of 72, co-authored 325 publications receiving 21882 citations. Previous affiliations of Wolfgang Weninger include University of Pennsylvania & Royal Prince Alfred Hospital.

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Cell Cycle Phase-Specific Drug Resistance as an Escape Mechanism of Melanoma Cells

TL;DR: G1-arrested melanoma cells, irrespective of the underlying cause mediating G1 arrest, are resistant to apoptosis induced by the proteasome inhibitor bortezomib or the alkylating agent temozolomide, and are more sensitive to mitogen-activated protein kinase pathway inhibitor-induced cell death.
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Two distinct activation states of plasmacytoid dendritic cells induced by influenza virus and CpG 1826 oligonucleotide.

TL;DR: In this paper, a transgenic mouse model that facilitates the isolation of highly pure plasmacytoid dendritic cells (pDC) populations was used to investigate the effect of pathogen recognition on pDC activation and function.
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Embedding embryos for high-resolution episcopic microscopy (HREM)

TL;DR: This protocol describes the procedure for embedding E11.5 mouse embryos for HREM imaging and recommends whole-mount staining for gene expression patterns using the 4-nitro blue tetrazolium chloride (NBT)/5-bromo-4-chloro-3-indolyl phosphate (BCIP) or LacZ detection system before embedding of samples.
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Imaging- and Flow Cytometry-based Analysis of Cell Position and the Cell Cycle in 3D Melanoma Spheroids.

TL;DR: The use of the fluorescence ubiquitination cell cycle indicator (FUCCI) system along with cytometry and image analysis using commercial software to characterize the cell cycle status of cells with respect to their position inside melanoma spheroids is described.
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HDAC inhibitors restore BRAF-inhibitor sensitivity by altering PI3K and survival signalling in a subset of melanoma.

TL;DR: Together treatment with the BRAFi encorafenib and HDACi panobinostat in 2D and 3D culture systems synergistically induced caspase‐dependent apoptotic cell death and results suggest that a combination of HDAC and MAPK inhibitors may play a role in treatment of melanoma where the resistance mechanisms are due to activation of MAPK‐independent pathways.