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Stefan Günther  - - - 
Top co-authors See all
Manfred Jung

256 shared publications

Institute of Pharmaceutical Sciences, University of Freiburg, Albertstraße 25, 79104 Freiburg im Breisgau, Germany

Irmgard Merfort

97 shared publications

Department of Pharmaceutical Biology and Biotechnology, Albert Ludwigs University Freiburg, Stefan-Meier-Strasse 19, D-79104 Freiburg, Germany

Nils Wiedemann

51 shared publications

Institute of Biochemistry and Molecular Biology, ZBMZ, Faculty of Medicine, University of Freiburg, 79104 Freiburg, Germany; BIOSS Centre for Biological Signalling Studies, University of Freiburg, 79104 Freiburg, Germany

Bjoern Gruening

49 shared publications

University of Freiburg

S. U. Eisenhardt

46 shared publications

Universitätsklinikum Freiburg, Klinik für Plastische und Handchirurgie

Publication Record
Distribution of Articles published per year 
(2011 - 2018)
Total number of journals
published in
Publications See all
Article 2 Reads 0 Citations Bromodomain Drug Discovery – the Past, the Present, and the Future Mehrosh Pervaiz, Pankaj Mishra, Stefan Günther Published: 05 October 2018
The Chemical Record, doi: 10.1002/tcr.201800074
DOI See at publisher website
Article 0 Reads 1 Citation New insights into the structural dynamics of the kinase JNK3. Pankaj Mishra, Stefan Günther Published: 21 June 2018
Scientific Reports, doi: 10.1038/s41598-018-27867-3
DOI See at publisher website PubMed View at PubMed ABS Show/hide abstract
In this work, we study the dynamics and the energetics of the all-atom structure of a neuronal-specific serine/threonine kinase c-Jun N-terminal kinase 3 (JNK3) in three states: unphosphorylated, phosphorylated, and ATP-bound phosphorylated. A series of 2 µs atomistic simulations followed by a conformational landscape mapping and a principal component analysis supports the mechanistic understanding of the JNK3 inactivation/activation process and also indicates key structural intermediates. Our analysis reveals that the unphosphorylated JNK3 undergoes the 'open-to-closed' movement via a two-step mechanism. Furthermore, the phosphorylation and ATP-binding allow the JNK3 kinase to attain a fully active conformation. JNK3 is a widely studied target for small-drugs used to treat a variety of neurological disorders. We believe that the mechanistic understanding of the large-conformational changes upon the activation of JNK3 will aid the development of novel targeted therapeutics.
Article 0 Reads 0 Citations Gene expression profiling of human bronchial epithelial cells exposed to fine particulate matter (PM 2.5 ) from biomass ... Désirée Popadić, Katharina Heßelbach, Sigrid Richter-Brockma... Published: 01 May 2018
Toxicology and Applied Pharmacology, doi: 10.1016/j.taap.2018.03.024
DOI See at publisher website
Article 1 Read 0 Citations In vitro observations and in silico predictions of xenoestrogen mixture effects in T47D-based receptor transactivation a... Nina Schlotz, Gwang-Jin Kim, Stefan Jäger, Stefan Günther, E... Published: 01 December 2017
Toxicology in Vitro, doi: 10.1016/j.tiv.2017.08.017
DOI See at publisher website PubMed View at PubMed
PROCEEDINGS-ARTICLE 25 Reads 0 Citations Mitochondrial metabolomics reveals compartment-specific metabolic responses in yeast cells Bernd Kammerer, Daqiang Pan, Caroline Lindau, Simon Lagies, ... Published: 20 November 2017
Proceedings of The 2nd International Electronic Conference on Metabolomics, doi: 10.3390/iecm-2-04981
DOI See at publisher website ABS Show/hide abstract
Mutations in mitochondrial membrane proteins could cause physiological and metabolic alterations in mitochondria as well as in cytosol. In order to address the origin of these alterations, mitochondria and cytosol of yeast wild-type BY4741 and two mutants, sdh2Δ and atp4Δ, were isolated from whole cells. These three compartments, namely mitochondria, cytosol and whole cell, were analyzed by gas chromatography-mass spectrometry based metabolic profiling, identifying seventy-three metabolites altogether, from which sixteen or ten were not detected either in mitochondria or cytosol. Compartment-specific distribution and regulation of metabolites were observed, showing the responses to the deletions of sdh2 and atp4. Based on the metabolic signature in mitochondrial matrix and cytosol, both mutants can be discriminated from wild-type by principal component analysis. De letions of electron chain transport components, sdh2 and atp4, altered not only citrate cycle related metabolites, but also diverse metabolites including amino acids, fatty acids, purine and pyrimidine intermediates and others. By applying metabolomics to isolated mitochondria and cytosol, compartment-specific metabolic regulation can be identified, which is helpful in understanding the molecular mechanism of mitochondrial homeostasis in response to genetic mutations.
Article 0 Reads 1 Citation Disease relevant modifications of the methylome and transcriptome by particulate matter (PM2.5) from biomass combustion Katharina Heßelbach, Gwang-Jin Kim, Stephan Flemming, Thomas... Published: 27 October 2017
Epigenetics, doi: 10.1080/15592294.2017.1356555
DOI See at publisher website PubMed View at PubMed ABS Show/hide abstract
Exposure to particulate matter (PM) is recognized as a major health hazard, but molecular responses are still insufficiently described. We analyzed the epigenetic impact of ambient PM2.5 from biomass combustion on the methylome of primary human bronchial epithelial BEAS-2B cells using the Illumina HumanMethylation450 BeadChip. The transcriptome was determined by the Affymetrix HG-U133 Plus 2.0 Array. PM2.5 induced genome wide alterations of the DNA methylation pattern, including differentially methylated CpGs in the promoter region associated with CpG islands. Gene ontology analysis revealed that differentially methylated genes were significantly clustered in pathways associated with the extracellular matrix, cellular adhesion, function of GTPases, and responses to extracellular stimuli, or were involved in ion binding and shuttling. Differential methylations also affected tandem repeats. Additionally, 45 different miRNA CpG loci showed differential DNA methylation, most of them proximal to their promoter. These miRNAs are functionally relevant for lung cancer, inflammation, asthma, and other PM-associated diseases. Correlation of the methylome and transcriptome demonstrated a clear bias toward transcriptional activation by hypomethylation. Genes that exhibited both differential methylation and expression were functionally linked to cytokine and immune responses, cellular motility, angiogenesis, inflammation, wound healing, cell growth, differentiation and development, or responses to exogenous matter. Disease ontology of differentially methylated and expressed genes indicated their prominent role in lung cancer and their participation in dominant cancer related signaling pathways. Thus, in lung epithelial cells, PM2.5 alters the methylome of genes and noncoding transcripts or elements that might be relevant for PM- and lung-associated diseases.