2025 |
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| 47. | Reisbitzer, Annika; Hollitzer, Cecilia; Geraci, Adriana; Schaefer, Jessye; Burghaus, Maximilian; Bruns, Jonas; Urban, Joachim; Kurz, Thomas; Krauß, Sybille Inhibition of class IIa HDACs reduces mutant HTT aggregation by affecting RNA stability Artikel Frontiers in Molecular Neuroscience , 2025. @article{Reisbitzer2025, title = {Inhibition of class IIa HDACs reduces mutant HTT aggregation by affecting RNA stability}, author = {Annika Reisbitzer and Cecilia Hollitzer and Adriana Geraci and Jessye Schaefer and Maximilian Burghaus and Jonas Bruns and Joachim Urban and Thomas Kurz and Sybille Krauß}, editor = {Frontiers in Molecular Neuroscience }, doi = {10.3389/fnmol.2025.1579194}, year = {2025}, date = {2025-06-18}, journal = {Frontiers in Molecular Neuroscience }, abstract = {Huntington’s disease (HD) is a fatal inherited neurological disorder for which there are no curative treatments available. Patients suffer from progressive impairment in cognitive and motor functions. Transcriptional dysregulation is a major molecular disease mechanism of HD. Transcription is regulated by a variety of epigenetic marks, including acetylation of histone proteins. This acetylation is controlled by opposing activities of histone acetyltransferases and histone deacetylases (HDACs). Based on recent observations that inhibition of HDACs can ameliorate disease phenotypes in different model systems ranging from cell culture to yeast, Drosophila and mouse models, the development of HDAC inhibitors as therapeutics for HD is promising. Recently, class IIa HDAC enzymes (4, 5, 7, 9) and specifically HDAC 4, have been identified as potential targets for the treatment of HD.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Huntington’s disease (HD) is a fatal inherited neurological disorder for which there are no curative treatments available. Patients suffer from progressive impairment in cognitive and motor functions. Transcriptional dysregulation is a major molecular disease mechanism of HD. Transcription is regulated by a variety of epigenetic marks, including acetylation of histone proteins. This acetylation is controlled by opposing activities of histone acetyltransferases and histone deacetylases (HDACs). Based on recent observations that inhibition of HDACs can ameliorate disease phenotypes in different model systems ranging from cell culture to yeast, Drosophila and mouse models, the development of HDAC inhibitors as therapeutics for HD is promising. Recently, class IIa HDAC enzymes (4, 5, 7, 9) and specifically HDAC 4, have been identified as potential targets for the treatment of HD. |
| 46. | Shahsanaei, Majid; Atapour, Masoud; Shamanian, Morteza; Farahbakhsh, Nastaran; Raghu, Swathi N V; Kowald, Torsten; Krauß, Sybille; Hejazi, Seyedsina; Mohajernia, Shiva; Killian, Manuela S Journal of Magnesium and Alloys, S. in press, 2025. @article{Shahsanaei2025, title = {Effect of nanostructured MgO directly grown on pure magnesium substrate on its in vitro corrosion and bioactivity behaviour}, author = {Majid Shahsanaei and Masoud Atapour and Morteza Shamanian and Nastaran Farahbakhsh and Swathi N.V. Raghu and Torsten Kowald and Sybille Krauß and Seyedsina Hejazi and Shiva Mohajernia and Manuela S. Killian}, editor = {Journal of Magnesium and Alloys}, doi = {10.1016/j.jma.2025.05.006}, year = {2025}, date = {2025-06-06}, journal = {Journal of Magnesium and Alloys}, pages = {in press}, abstract = {This study introduces a nanostructured MgO coating fabricated via anodization in a non-aqueous electrolyte, offering a novel approach to addressing the challenges of corrosion resistance and biofunctionality. The surface was characterized before and after immersion testing using field emission scanning electron microscopy (FESEM), energy-dispersive X-ray spectroscopy (EDX), and X-ray diffraction (XRD). Electrochemical impedance spectroscopy (EIS) and potentiodynamic polarization tests demonstrated a 2-fold reduction in the corrosion resistance compared to untreated magnesium. Biomineralization studies demonstrated the uniform formation of apatite with a Ca/P ratio of 1.35 on the nanostructured surface after 14 days in simulated body fluid (SBF), surpassing that of microstructured MgO. Hydrogen evolution decreased from 912±38 µL cm-2 for untreated Mg to 615±32 µL cm-2 for the Mg/MgO nanostructure and 545±29 µL cm-2 for the Mg/MgO/HA sample. These findings highlight the potential of nanostructured MgO coatings to advance Mg-based implants by providing enhanced corrosion protection, improved biomineralization, reduced hemolysis and increased cell viability, and reduced H2 generation.}, keywords = {}, pubstate = {published}, tppubtype = {article} } This study introduces a nanostructured MgO coating fabricated via anodization in a non-aqueous electrolyte, offering a novel approach to addressing the challenges of corrosion resistance and biofunctionality. The surface was characterized before and after immersion testing using field emission scanning electron microscopy (FESEM), energy-dispersive X-ray spectroscopy (EDX), and X-ray diffraction (XRD). Electrochemical impedance spectroscopy (EIS) and potentiodynamic polarization tests demonstrated a 2-fold reduction in the corrosion resistance compared to untreated magnesium. Biomineralization studies demonstrated the uniform formation of apatite with a Ca/P ratio of 1.35 on the nanostructured surface after 14 days in simulated body fluid (SBF), surpassing that of microstructured MgO. Hydrogen evolution decreased from 912±38 µL cm-2 for untreated Mg to 615±32 µL cm-2 for the Mg/MgO nanostructure and 545±29 µL cm-2 for the Mg/MgO/HA sample. These findings highlight the potential of nanostructured MgO coatings to advance Mg-based implants by providing enhanced corrosion protection, improved biomineralization, reduced hemolysis and increased cell viability, and reduced H2 generation. |
| 45. | Nabariya, Deepti Kailash; Knüpfer, Lisa Maria; Hartwich, Patrick; Killian, Manuela S; Centler, Florian; Krauß, Sybille Molecular and Cellular Probes , 81 , 2025. @article{Nabariya2025, title = {Transcriptomic analysis of intracellular RNA granules and small extracellular vesicles: Unmasking their overlap in a cell model of Huntington's disease}, author = {Deepti Kailash Nabariya and Lisa Maria Knüpfer and Patrick Hartwich and Manuela S. Killian and Florian Centler and Sybille Krauß}, editor = {Molecular and Cellular Probes }, doi = {10.1016/j.mcp.2025.102026}, year = {2025}, date = {2025-06-02}, journal = {Molecular and Cellular Probes }, volume = {81}, abstract = {Huntington's disease (HD) arises from the abnormal expansion of a CAG repeat in the HTT gene. The mutant CAG repeat triggers aberrant RNA-protein interactions and translates into toxic aggregate-prone polyglutamine protein. These aberrant RNA-protein ineractions also seed the formation of cytoplasmic liquid-like granules, such as stress granules. Emerging evidence demonstrates that granules formed via liquid-liquid phase separation can mature into gel-like inclusions that persist within the cell and may act as precursor to aggregates that occur in patients' tissue. Thus, deregulation of RNA granules is an important component of neurodegeneration. Interestingly, both the formation of intracellular membrane-less organelles like stress granules and the secretion of small extracellular vesicles (sEVs) increase upon stress and under disease conditions. sEVs are lipid membrane-bound particles that are secreted from all cell types and may participate in the spreading of misfolded proteins and aberrant RNA-protein complexes across the central nervous system in neurodegenerative diseases like HD. In this study, we performed a comparative transcriptomic analysis of sEVs and RNA granules in an HD model. RNA granules and sEVs were isolated from an inducible HD cell model. Both sEVs and RNA granules were isolated from induced (HD) and non-induced (control) cells and analyzed by RNA sequencing. Our comparative analysis between the transcriptomics data of HD RNA granules and sEVs showed that: (I) intracellular RNA granules and extracellular RNA vesicles share content, (II) several non-coding RNAs translocate to RNA granules, and (III) the composition of RNA granules and sEVs is affected in HD cells. Our data showing common transcripts in intracellular RNA granules and extracellular sEVs suggest that formation of RNA granules and sEV loading may be related. Moreover, we found a high abundance of lncRNAs in both control and HD samples, with several transcripts under REST regulation, highlighting their potential role in HD pathogenesis and selective incorporation into sEVs. The transcriptome cargo of RNA granules or sEVs may serve as a source for diagnostic strategies. For example, disease-specific RNA-signatures of sEVs can serve as biomarker of central nervous system diseases. Therefore, we compared our dataset to transcriptomic data from HD patient sEVs in blood. However, our data suggest that the cell-type specific signature of sEV-secreted RNAs as well as their high variability may make it difficult to detect these biomarkers in blood.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Huntington's disease (HD) arises from the abnormal expansion of a CAG repeat in the HTT gene. The mutant CAG repeat triggers aberrant RNA-protein interactions and translates into toxic aggregate-prone polyglutamine protein. These aberrant RNA-protein ineractions also seed the formation of cytoplasmic liquid-like granules, such as stress granules. Emerging evidence demonstrates that granules formed via liquid-liquid phase separation can mature into gel-like inclusions that persist within the cell and may act as precursor to aggregates that occur in patients' tissue. Thus, deregulation of RNA granules is an important component of neurodegeneration. Interestingly, both the formation of intracellular membrane-less organelles like stress granules and the secretion of small extracellular vesicles (sEVs) increase upon stress and under disease conditions. sEVs are lipid membrane-bound particles that are secreted from all cell types and may participate in the spreading of misfolded proteins and aberrant RNA-protein complexes across the central nervous system in neurodegenerative diseases like HD. In this study, we performed a comparative transcriptomic analysis of sEVs and RNA granules in an HD model. RNA granules and sEVs were isolated from an inducible HD cell model. Both sEVs and RNA granules were isolated from induced (HD) and non-induced (control) cells and analyzed by RNA sequencing. Our comparative analysis between the transcriptomics data of HD RNA granules and sEVs showed that: (I) intracellular RNA granules and extracellular RNA vesicles share content, (II) several non-coding RNAs translocate to RNA granules, and (III) the composition of RNA granules and sEVs is affected in HD cells. Our data showing common transcripts in intracellular RNA granules and extracellular sEVs suggest that formation of RNA granules and sEV loading may be related. Moreover, we found a high abundance of lncRNAs in both control and HD samples, with several transcripts under REST regulation, highlighting their potential role in HD pathogenesis and selective incorporation into sEVs. The transcriptome cargo of RNA granules or sEVs may serve as a source for diagnostic strategies. For example, disease-specific RNA-signatures of sEVs can serve as biomarker of central nervous system diseases. Therefore, we compared our dataset to transcriptomic data from HD patient sEVs in blood. However, our data suggest that the cell-type specific signature of sEV-secreted RNAs as well as their high variability may make it difficult to detect these biomarkers in blood. |
| 44. | Filcenkova, Larissa; Reisbitzer, Annika; Joseph, Benjamin Philipp; Weber, Verena; Carloni, Paolo; Rossetti, Giulia; Krauß, Sybille Front. Genet. , 2025. @article{Filcenkova2025, title = {Application of a novel RNA-protein interaction assay to develop inhibitors blocking RNA-binding of the HuR protein}, author = {Larissa Filcenkova and Annika Reisbitzer and Benjamin Philipp Joseph and Verena Weber and Paolo Carloni and Giulia Rossetti and Sybille Krauß}, editor = {Front. Genet. }, doi = {10.3389/fgene.2025.1549304}, year = {2025}, date = {2025-03-05}, journal = {Front. Genet. }, abstract = {RNA-protein interactions play an important regulatory role in several biological processes. For example, the RNA-binding protein HuR (human antigen R) binds to its target mRNAs and regulates their translation, stability, and subcellular localization. HuR is involved in the pathogenic processes of various diseases. Thus, small molecules blocking RNA-binding of HuR may be useful in a variety of diseases. Previously, we identified STK018404 as a small molecule targeting the HuR-RNA interaction. Based on this study we identified optimized compounds by exploiting combined structure-based and ligand-based computational approaches. To test a series of these compounds, we developed a novel readout system for the HuR-RNA interaction. Traditional methods to detect RNA-protein interaction come with some disadvantages: they require significant reagent optimization and may be difficult to optimize for weakly expressed RNA molecules. The readout often requires amplification. Thus, these methods are not well suited for quantitative analysis of RNA-protein interactions. To achieve an easy-to-perform, rapid, and robust detection of RNA-protein binding, we applied a split luciferase reporter system, to detect the interaction between HuR and its target RNA. We expressed one luciferase fragment as a fusion protein with HuR. The second luciferase fragment was Streptavidin-coated and coupled to a biotinylated RNA-oligo comprising an AU-rich HuR-binding element. The binding between HuR and its target RNA-oligo then allowed reconstitution of the functional luciferase that was detectable by luminescence. Using the split luciferase reporter system, we present here a series of optimized compounds that we developed.}, keywords = {}, pubstate = {published}, tppubtype = {article} } RNA-protein interactions play an important regulatory role in several biological processes. For example, the RNA-binding protein HuR (human antigen R) binds to its target mRNAs and regulates their translation, stability, and subcellular localization. HuR is involved in the pathogenic processes of various diseases. Thus, small molecules blocking RNA-binding of HuR may be useful in a variety of diseases. Previously, we identified STK018404 as a small molecule targeting the HuR-RNA interaction. Based on this study we identified optimized compounds by exploiting combined structure-based and ligand-based computational approaches. To test a series of these compounds, we developed a novel readout system for the HuR-RNA interaction. Traditional methods to detect RNA-protein interaction come with some disadvantages: they require significant reagent optimization and may be difficult to optimize for weakly expressed RNA molecules. The readout often requires amplification. Thus, these methods are not well suited for quantitative analysis of RNA-protein interactions. To achieve an easy-to-perform, rapid, and robust detection of RNA-protein binding, we applied a split luciferase reporter system, to detect the interaction between HuR and its target RNA. We expressed one luciferase fragment as a fusion protein with HuR. The second luciferase fragment was Streptavidin-coated and coupled to a biotinylated RNA-oligo comprising an AU-rich HuR-binding element. The binding between HuR and its target RNA-oligo then allowed reconstitution of the functional luciferase that was detectable by luminescence. Using the split luciferase reporter system, we present here a series of optimized compounds that we developed. |
| 43. | Hoang, Gia Linh; Rock, Manuel; Tancredi, Aldo; Magauer, Thomas; Mandelli, Davide; Schulz, Jorg B; Krauss, Sybille; Rossetti, Giulia; Tollinger, Martin; Carloni, Paolo 2025. @article{Hoang2025, title = {Refining Ligand Poses in RNA/Ligand Complexes of Pharmaceutical Relevance: A Perspective by QM/MM Simulations and NMR Measurements}, author = {Gia Linh Hoang and Manuel Rock and Aldo Tancredi and Thomas Magauer and Davide Mandelli and Jorg B. Schulz and Sybille Krauss and Giulia Rossetti and Martin Tollinger and Paolo Carloni}, editor = {The Journal of Physical Chemistry Letters }, doi = {10.1021/acs.jpclett.4c03456}, year = {2025}, date = {2025-02-10}, abstract = {Predicting the binding poses of ligands targeting RNAs is challenging. Here, we propose that using first-principles quantum mechanics/molecular mechanics (QM/MM) simulations, which incorporate automatically polarization effects, can help refine the structural determinants of ligand/RNA complexes in aqueous solution. In fact, recent advances in massively parallel computer architectures (such as exascale machines), combined with the power of machine learning, are greatly expanding the domain of applicability of these types of notoriously expensive simulations. We corroborate this proposal by carrying out a QM/MM-based study on a ligand targeting CAG repeat-RNA, involved in Huntington’s disease. The calculations indeed show a clear improvement in the ligand binding properties, and they are consistent with the NMR measurements, also performed here. Thus, this type of approach may be useful for practical applications in the design of ligands targeting RNA in the near future.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Predicting the binding poses of ligands targeting RNAs is challenging. Here, we propose that using first-principles quantum mechanics/molecular mechanics (QM/MM) simulations, which incorporate automatically polarization effects, can help refine the structural determinants of ligand/RNA complexes in aqueous solution. In fact, recent advances in massively parallel computer architectures (such as exascale machines), combined with the power of machine learning, are greatly expanding the domain of applicability of these types of notoriously expensive simulations. We corroborate this proposal by carrying out a QM/MM-based study on a ligand targeting CAG repeat-RNA, involved in Huntington’s disease. The calculations indeed show a clear improvement in the ligand binding properties, and they are consistent with the NMR measurements, also performed here. Thus, this type of approach may be useful for practical applications in the design of ligands targeting RNA in the near future. |
2024 |
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| 42. | Ballarin, Giovanna; Biasiotto, Maddalena; Reisbitzer, Annika; Hegels, Marlen; Bolte, Michael; Krauß, Sybille; Berdnikova, Daria V A novel aurone RNA CAG binder inhibits the Huntingtin RNA–protein interaction Artikel RSC Medicinal Chemistry, 9, 2024 , 2024. @article{Ballarin2024, title = {A novel aurone RNA CAG binder inhibits the Huntingtin RNA–protein interaction}, author = {Giovanna Ballarin and Maddalena Biasiotto and Annika Reisbitzer and Marlen Hegels and Michael Bolte and Sybille Krauß and Daria V. Berdnikova}, editor = {RSC Medicinal Chemistry}, doi = {10.1039/d4md00403e}, year = {2024}, date = {2024-07-17}, journal = {RSC Medicinal Chemistry}, volume = {9, 2024}, abstract = {Huntington's disease (HD) is a devastating, incurable condition whose pathophysiological mechanism relies on mutant RNA CAG repeat expansions. Aberrant recruitment of RNA-binding proteins by mutant CAG hairpins contributes to the progress of neurodegeneration. In this work, we identified a novel binder based on an aurone scaffold that reduces the level of binding of HTT mRNA to the MID1 protein in vitro. The obtained results introduce aurones as a novel platform for the design of functional ligands for disease-related RNA sequences.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Huntington's disease (HD) is a devastating, incurable condition whose pathophysiological mechanism relies on mutant RNA CAG repeat expansions. Aberrant recruitment of RNA-binding proteins by mutant CAG hairpins contributes to the progress of neurodegeneration. In this work, we identified a novel binder based on an aurone scaffold that reduces the level of binding of HTT mRNA to the MID1 protein in vitro. The obtained results introduce aurones as a novel platform for the design of functional ligands for disease-related RNA sequences. |
| 41. | Reisbitzer, Annika; Krauß, Sybille The Dynamic World of RNA: Beyond Translation to Subcellular Localization and Function Artikel 2024. @article{Reisbitzer2024, title = {The Dynamic World of RNA: Beyond Translation to Subcellular Localization and Function}, author = {Annika Reisbitzer and Sybille Krauß}, editor = {Front. Genet}, doi = {10.3389/fgene.2024.1373899}, year = {2024}, date = {2024-03-12}, abstract = {RNA is a versatile and dynamic molecule that plays an important role in many aspects of cell biology and physiology. Its diverse functions reach from acting as a template for protein biosynthesis to a variety of regulatory, structural, and catalytic activities in the cell. Primary transcripts and processed RNAs are not randomly distributed in the cell but are found in specific subcellular compartments. This is particularly important in neurons, a highly polarized cell type. Several mechanisms are known to regulate RNA localization and transport, including passive diffusion, phase separation into RNA granules, and active transport. All these processes contribute to cellular RNA dynamics. Interestingly, these transport mechanisms are influenced by different regulatory elements of the RNA molecule itself, e.g., by alternative polyadenylation, or by the association with RNA-binding proteins (RBPs). Deregulation of these mechanisms is connected to pathogenic mechanisms that lead, for example, to neurodegenerative diseases.}, keywords = {}, pubstate = {published}, tppubtype = {article} } RNA is a versatile and dynamic molecule that plays an important role in many aspects of cell biology and physiology. Its diverse functions reach from acting as a template for protein biosynthesis to a variety of regulatory, structural, and catalytic activities in the cell. Primary transcripts and processed RNAs are not randomly distributed in the cell but are found in specific subcellular compartments. This is particularly important in neurons, a highly polarized cell type. Several mechanisms are known to regulate RNA localization and transport, including passive diffusion, phase separation into RNA granules, and active transport. All these processes contribute to cellular RNA dynamics. Interestingly, these transport mechanisms are influenced by different regulatory elements of the RNA molecule itself, e.g., by alternative polyadenylation, or by the association with RNA-binding proteins (RBPs). Deregulation of these mechanisms is connected to pathogenic mechanisms that lead, for example, to neurodegenerative diseases. |
2023 |
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| 40. | Joseph, Benjamin Philipp; Weber, Verena; Knüpfer, Lisa; Giorgetti, Alejandro; Alfonso-Prieto, Mercedes; Krauß*, Sybille; Carloni*, Paolo; Rossetti, Giulia Low Molecular Weight Inhibitors Targeting the RNA-Binding Protein HuR Artikel 2023. @article{Joseph2023, title = {Low Molecular Weight Inhibitors Targeting the RNA-Binding Protein HuR}, author = {Benjamin Philipp Joseph and Verena Weber and Lisa Knüpfer and Alejandro Giorgetti and Mercedes Alfonso-Prieto and Sybille Krauß* and Paolo Carloni* and Giulia Rossetti}, editor = {Int. J. Mol. Sci}, doi = {10.3390/ijms241713127}, year = {2023}, date = {2023-08-23}, abstract = {The RNA-binding protein human antigen R (HuR) regulates stability, translation, and nucleus-to-cytoplasm shuttling of its target mRNAs. This protein has been progressively recognized as a relevant therapeutic target for several pathologies, like cancer, neurodegeneration, as well as inflammation. Inhibitors of mRNA binding to HuR might thus be beneficial against a variety of diseases. Here, we present the rational identification of structurally novel HuR inhibitors. In particular, by combining chemoinformatic approaches, high-throughput virtual screening, and RNA–protein pulldown assays, we demonstrate that the 4-(2-(2,4,6-trioxotetrahydropyrimidin-5(2H)-ylidene)hydrazineyl)benzoate ligand exhibits a dose-dependent HuR inhibition effect in binding experiments. Importantly, the chemical scaffold is new with respect to the currently known HuR inhibitors, opening up a new avenue for the design of pharmaceutical agents targeting this important protein. Keywords: RNA-binding protein; human antigen R (HuR); high-throughput virtual screening; small molecule inhibitors; RNA pulldown assay}, keywords = {}, pubstate = {published}, tppubtype = {article} } The RNA-binding protein human antigen R (HuR) regulates stability, translation, and nucleus-to-cytoplasm shuttling of its target mRNAs. This protein has been progressively recognized as a relevant therapeutic target for several pathologies, like cancer, neurodegeneration, as well as inflammation. Inhibitors of mRNA binding to HuR might thus be beneficial against a variety of diseases. Here, we present the rational identification of structurally novel HuR inhibitors. In particular, by combining chemoinformatic approaches, high-throughput virtual screening, and RNA–protein pulldown assays, we demonstrate that the 4-(2-(2,4,6-trioxotetrahydropyrimidin-5(2H)-ylidene)hydrazineyl)benzoate ligand exhibits a dose-dependent HuR inhibition effect in binding experiments. Importantly, the chemical scaffold is new with respect to the currently known HuR inhibitors, opening up a new avenue for the design of pharmaceutical agents targeting this important protein. Keywords: RNA-binding protein; human antigen R (HuR); high-throughput virtual screening; small molecule inhibitors; RNA pulldown assay |
| 39. | Piccinini, A M; Krauß, S Editorial: In celebration of women in science: RNA networks and biology Artikel Front Mol Biosci, 10 , S. 1162378, 2023, ISSN: 2296-889X (Print) 2296-889x. @article{RN13764, title = {Editorial: In celebration of women in science: RNA networks and biology}, author = {A M Piccinini and S Krauß}, doi = {10.3389/fmolb.2023.1162378}, issn = {2296-889X (Print) 2296-889x}, year = {2023}, date = {2023-01-01}, journal = {Front Mol Biosci}, volume = {10}, pages = {1162378}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2022 |
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| 38. | Nabariya, D K; Heinz, A; Derksen, S; Krauß, S Front Mol Biosci, 9 , S. 1000932, 2022, ISSN: 2296-889X (Print) 2296-889x. @article{RN13762, title = {Intracellular and intercellular transport of RNA organelles in CXG repeat disorders: The strength of weak ties}, author = {D K Nabariya and A Heinz and S Derksen and S Krauß}, doi = {10.3389/fmolb.2022.1000932}, issn = {2296-889X (Print) 2296-889x}, year = {2022}, date = {2022-01-01}, journal = {Front Mol Biosci}, volume = {9}, pages = {1000932}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2021 |
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| 37. | A, Heinz; DK, Nabariya; S., Krauss Huntingtin and Its Role in Mechanisms of RNA-Mediated Toxicity Artikel Toxins (Basel), 2021. @article{Krauss2021b, title = {Huntingtin and Its Role in Mechanisms of RNA-Mediated Toxicity}, author = {Heinz A and Nabariya DK and Krauss S.}, doi = {https://doi.org/10.3390/toxins13070487}, year = {2021}, date = {2021-07-14}, journal = {Toxins (Basel)}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 36. | A., Heinz; D.K., Nabariya; S, Krauß Huntington’s Disease and Neurodegeneration Artikel Kostrzewa R.M. (eds) Handbook of Neurotoxicity. Springer, Cham. , 2021. @article{Krauss2021b, title = {Huntington’s Disease and Neurodegeneration}, author = {Heinz A. and Nabariya D.K. and Krauß S}, doi = {https://doi.org/10.1007/978-3-030-71519-9_226-1}, year = {2021}, date = {2021-06-25}, journal = {Kostrzewa R.M. (eds) Handbook of Neurotoxicity. Springer, Cham. }, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 35. | DV, Berdnikova; P, Carloni; S, Krauß; G., Rossetti Molecules, 2021. @article{Krauss2021b, title = {Role and Perspective of Molecular Simulation-Based Investigation of RNA-Ligand Interaction: From Small Molecules and Peptides to Photoswitchable RNA Binding}, author = {Berdnikova DV and Carloni P and Krauß S and Rossetti G.}, doi = {https://doi.org/10.3390/molecules26113384}, year = {2021}, date = {2021-06-03}, journal = {Molecules}, abstract = {Abstract Aberrant RNA–protein complexes are formed in a variety of diseases. Identifying the ligands that interfere with their formation is a valuable therapeutic strategy. Molecular simulation, validated against experimental data, has recently emerged as a powerful tool to predict both the pose and energetics of such ligands. Thus, the use of molecular simulation may provide insight into aberrant molecular interactions in diseases and, from a drug design perspective, may allow for the employment of less wet lab resources than traditional in vitro compound screening approaches. With regard to basic research questions, molecular simulation can support the understanding of the exact molecular interaction and binding mode. Here, we focus on examples targeting RNA–protein complexes in neurodegenerative diseases and viral infections. These examples illustrate that the strategy is rather general and could be applied to different pharmacologically relevant approaches. We close this study by outlining one of these approaches, namely the light-controllable association of small molecules with RNA, as an emerging approach in RNA-targeting therapy. }, keywords = {}, pubstate = {published}, tppubtype = {article} } Abstract Aberrant RNA–protein complexes are formed in a variety of diseases. Identifying the ligands that interfere with their formation is a valuable therapeutic strategy. Molecular simulation, validated against experimental data, has recently emerged as a powerful tool to predict both the pose and energetics of such ligands. Thus, the use of molecular simulation may provide insight into aberrant molecular interactions in diseases and, from a drug design perspective, may allow for the employment of less wet lab resources than traditional in vitro compound screening approaches. With regard to basic research questions, molecular simulation can support the understanding of the exact molecular interaction and binding mode. Here, we focus on examples targeting RNA–protein complexes in neurodegenerative diseases and viral infections. These examples illustrate that the strategy is rather general and could be applied to different pharmacologically relevant approaches. We close this study by outlining one of these approaches, namely the light-controllable association of small molecules with RNA, as an emerging approach in RNA-targeting therapy. |
| 34. | Furtado, Gabriel Vasata; Yang, Jing; Wu, Di; Papagiannopoulos, Christos I; Terpstra, Hanna M; Kuiper, Elsiena E F; Krauss, Sybille; Zhu, Wei-Guo; Kampinga, Harm H; Bergink, Steven Human Molecular Genetics, 2021, ( ). @article{Krauss2021, title = {FOXO1 controls protein synthesis and transcript abundance of mutant polyglutamine proteins, preventing protein aggregation.}, author = {Gabriel Vasata Furtado and Jing Yang and Di Wu and Christos I Papagiannopoulos and Hanna M Terpstra and E F Elsiena Kuiper and Sybille Krauss and Wei-Guo Zhu and Harm H Kampinga and Steven Bergink}, editor = { }, doi = {10.1093}, year = {2021}, date = {2021-06-01}, journal = {Human Molecular Genetics}, abstract = { Abstract FOXO1, a transcription factor downstream of the insulin/insulin like growth factor axis, has been linked to protein degradation. Elevated expression of FOXO orthologs can also prevent the aggregation of cytosine adenine guanine (CAG)-repeat disease causing polyglutamine (polyQ) proteins but whether FOXO1 targets mutant proteins for degradation is unclear. Here, we show that increased expression of FOXO1 prevents toxic polyQ aggregation in human cells while reducing FOXO1 levels has the opposite effect and accelerates it. Although FOXO1 indeed stimulates autophagy, its effect on polyQ aggregation is independent of autophagy, ubiquitin–proteasome system (UPS) mediated protein degradation and is not due to a change in mutant polyQ protein turnover. Instead, FOXO1 specifically downregulates protein synthesis rates from expanded pathogenic CAG repeat transcripts. FOXO1 orchestrates a change in the composition of proteins that occupy mutant expanded CAG transcripts, including the recruitment of IGF2BP3. This mRNA binding protein enables a FOXO1 driven decrease in pathogenic expanded CAG transcript- and protein levels, thereby reducing the initiation of amyloidogenesis. Our data thus demonstrate that FOXO1 not only preserves protein homeostasis at multiple levels, but also reduces the accumulation of aberrant RNA species that may co-contribute to the toxicity in CAG-repeat diseases.}, note = { }, keywords = {}, pubstate = {published}, tppubtype = {article} } Abstract FOXO1, a transcription factor downstream of the insulin/insulin like growth factor axis, has been linked to protein degradation. Elevated expression of FOXO orthologs can also prevent the aggregation of cytosine adenine guanine (CAG)-repeat disease causing polyglutamine (polyQ) proteins but whether FOXO1 targets mutant proteins for degradation is unclear. Here, we show that increased expression of FOXO1 prevents toxic polyQ aggregation in human cells while reducing FOXO1 levels has the opposite effect and accelerates it. Although FOXO1 indeed stimulates autophagy, its effect on polyQ aggregation is independent of autophagy, ubiquitin–proteasome system (UPS) mediated protein degradation and is not due to a change in mutant polyQ protein turnover. Instead, FOXO1 specifically downregulates protein synthesis rates from expanded pathogenic CAG repeat transcripts. FOXO1 orchestrates a change in the composition of proteins that occupy mutant expanded CAG transcripts, including the recruitment of IGF2BP3. This mRNA binding protein enables a FOXO1 driven decrease in pathogenic expanded CAG transcript- and protein levels, thereby reducing the initiation of amyloidogenesis. Our data thus demonstrate that FOXO1 not only preserves protein homeostasis at multiple levels, but also reduces the accumulation of aberrant RNA species that may co-contribute to the toxicity in CAG-repeat diseases. |
2020 |
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| 33. | Collison, A M; Sokulsky, L A; Nightingale, S; Percival, E; LeFevre, A; Meredith, J; Krauss, S; Mattes, Fosterand P S J In vivo targeting of miR‐223 in experimental eosinophilic oesophagitis Artikel 2020. @article{Mattes2020, title = {In vivo targeting of miR‐223 in experimental eosinophilic oesophagitis}, author = {A M Collison and L A Sokulsky and S Nightingale and E Percival and A LeFevre and J Meredith and S Krauss and P S Fosterand J Mattes}, editor = {Clinical & Translational Immunology }, url = {https://doi.org/10.1002/cti2.1210}, doi = {10.1002/cti2.1210}, year = {2020}, date = {2020-11-23}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 32. | Lountzi, D; Henzel, K; Jazbec, K; Banow, D; Krauss, S; Rozman, P; Ehinger, D 2020. @article{Lountzi2020, title = {Effects of heterochronic, non-myeloablative bone marrow transplantation on age-releated behavioural changes in mice}, author = { D Lountzi and K Henzel and K Jazbec and D Banow and S Krauss and P Rozman and D Ehinger }, editor = {Mechanisms of Ageing and Develpoment }, url = {https://doi.org/10.1016/j.mad.2020.111327}, doi = {10.1016/j.mad.2020.111327}, year = {2020}, date = {2020-10-01}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2019 |
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| 31. | Krauss, S; Evert, B O The Role of MicroRNAs in Spinocerebellar Ataxia Type 3 Artikel J Mol Biol, 431 (9), S. 1729-1742, 2019, ISSN: 1089-8638 (Electronic) 0022-2836 (Linking). @article{RN33b, title = {The Role of MicroRNAs in Spinocerebellar Ataxia Type 3}, author = {S Krauss and B O Evert}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30664869}, doi = {10.1016/j.jmb.2019.01.019}, issn = {1089-8638 (Electronic) 0022-2836 (Linking)}, year = {2019}, date = {2019-01-01}, journal = {J Mol Biol}, volume = {431}, number = {9}, pages = {1729-1742}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 30. | Reichenbach, N; Delekate, A; Plescher, M; Schmitt, F; Krauss, S; Blank, N; Halle, A; Petzold, G C Inhibition of Stat3-mediated astrogliosis ameliorates pathology in an Alzheimer's disease model Artikel EMBO Mol Med, 11 (2), 2019, ISSN: 1757-4684 (Electronic) 1757-4676 (Linking). @article{RN30b, title = {Inhibition of Stat3-mediated astrogliosis ameliorates pathology in an Alzheimer's disease model}, author = {N Reichenbach and A Delekate and M Plescher and F Schmitt and S Krauss and N Blank and A Halle and G C Petzold}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30617153}, doi = {10.15252/emmm.201809665}, issn = {1757-4684 (Electronic) 1757-4676 (Linking)}, year = {2019}, date = {2019-01-01}, journal = {EMBO Mol Med}, volume = {11}, number = {2}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 29. | Schilling, J; Broemer, M; Atanassov, I; Duernberger, Y; Vorberg, I; Dieterich, C; Dagane, A; Dittmar, G; Wanker, E; van Roon-Mom, W; Winter, J; Krauss, S Deregulated Splicing Is a Major Mechanism of RNA-Induced Toxicity in Huntington's Disease Artikel J Mol Biol, 2019, ISSN: 1089-8638 (Electronic) 0022-2836 (Linking). @article{RN16b, title = {Deregulated Splicing Is a Major Mechanism of RNA-Induced Toxicity in Huntington's Disease}, author = {J Schilling and M Broemer and I Atanassov and Y Duernberger and I Vorberg and C Dieterich and A Dagane and G Dittmar and E Wanker and W van Roon-Mom and J Winter and S Krauss}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30711541}, doi = {10.1016/j.jmb.2019.01.034}, issn = {1089-8638 (Electronic) 0022-2836 (Linking)}, year = {2019}, date = {2019-01-01}, journal = {J Mol Biol}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2018 |
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| 28. | Arnoux, I; Willam, M; Griesche, N; Krummeich, J; Watari, H; Offermann, N; Weber, S; Dey, Narayan P; Chen, C; Monteiro, O; Buettner, S; Meyer, K; Bano, D; Radyushkin, K; Langston, R; Lambert, J J; Wanker, E; Methner, A; Krauss, S; Schweiger, S; Stroh, A Metformin reverses early cortical network dysfunction and behavior changes in Huntington's disease Artikel Elife, 7 , 2018, ISSN: 2050-084X (Electronic) 2050-084X (Linking). @article{RN2l, title = {Metformin reverses early cortical network dysfunction and behavior changes in Huntington's disease}, author = {I Arnoux and M Willam and N Griesche and J Krummeich and H Watari and N Offermann and S Weber and P Narayan Dey and C Chen and O Monteiro and S Buettner and K Meyer and D Bano and K Radyushkin and R Langston and J J Lambert and E Wanker and A Methner and S Krauss and S Schweiger and A Stroh}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30179155}, doi = {10.7554/eLife.38744}, issn = {2050-084X (Electronic) 2050-084X (Linking)}, year = {2018}, date = {2018-01-01}, journal = {Elife}, volume = {7}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 27. | Evert, B O; Nalavade, R; Jungverdorben, J; Matthes, F; Weber, S; Rajput, A; Bonn, S; Brustle, O; Peitz, M; Krauss, S PLoS One, 13 (8), S. e0201794, 2018, ISSN: 1932-6203 (Electronic) 1932-6203 (Linking). @article{RN3l, title = {Upregulation of miR-370 and miR-543 is associated with reduced expression of heat shock protein 40 in spinocerebellar ataxia type 3}, author = {B O Evert and R Nalavade and J Jungverdorben and F Matthes and S Weber and A Rajput and S Bonn and O Brustle and M Peitz and S Krauss}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30086154}, doi = {10.1371/journal.pone.0201794}, issn = {1932-6203 (Electronic) 1932-6203 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {PLoS One}, volume = {13}, number = {8}, pages = {e0201794}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 26. | Krauss, S; Nalavade, R; Weber, S; Carter, K; Evert, B O Microrna, 2018, ISSN: 2211-5374 (Electronic). @article{RN9b, title = {Upregulation of miR-25 and miR-181 Family Members Correlates with Reduced Expression of ATXN3 in Lymphocytes from SCA3 Patients}, author = {S Krauss and R Nalavade and S Weber and K Carter and B O Evert}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30147021}, doi = {10.2174/2211536607666180821162403}, issn = {2211-5374 (Electronic)}, year = {2018}, date = {2018-01-01}, journal = {Microrna}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 25. | Matthes, F; Hettich, M M; Schilling, J; Flores-Dominguez, D; Blank, N; Wiglenda, T; Buntru, A; Wolf, H; Weber, S; Vorberg, I; Dagane, A; Dittmar, G; Wanker, E; Ehninger, D; Krauss, S Inhibition of the MID1 protein complex: a novel approach targeting APP protein synthesis Artikel Cell Death Discovery, 4 (4), 2018. @article{RN12b, title = {Inhibition of the MID1 protein complex: a novel approach targeting APP protein synthesis}, author = {F Matthes and M M Hettich and J Schilling and D Flores-Dominguez and N Blank and T Wiglenda and A Buntru and H Wolf and S Weber and I Vorberg and A Dagane and G Dittmar and E Wanker and D Ehninger and S Krauss}, doi = {DOI 10.1038/s41420-017-0003-8}, year = {2018}, date = {2018-01-01}, journal = {Cell Death Discovery}, volume = {4}, number = {4}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 24. | Matthes, F; Massari, S; Bochicchio, A; Schorpp, K; Schilling, J; Weber, S; Offermann, N; Desantis, J; Wanker, E; Carloni, P; Hadian, K; Tabarrini, O; Rossetti, G; Krauss, S Reducing Mutant Huntingtin Protein Expression in Living Cells by a Newly Identified RNA CAG Binder Artikel ACS Chem Neurosci, 9 (6), S. 1399-1408, 2018, ISSN: 1948-7193 (Electronic) 1948-7193 (Linking). @article{RN29b, title = {Reducing Mutant Huntingtin Protein Expression in Living Cells by a Newly Identified RNA CAG Binder}, author = {F Matthes and S Massari and A Bochicchio and K Schorpp and J Schilling and S Weber and N Offermann and J Desantis and E Wanker and P Carloni and K Hadian and O Tabarrini and G Rossetti and S Krauss}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29506378}, doi = {10.1021/acschemneuro.8b00027}, issn = {1948-7193 (Electronic) 1948-7193 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {ACS Chem Neurosci}, volume = {9}, number = {6}, pages = {1399-1408}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 23. | Monteiro, O; Chen, C; Bingham, R; Argyrou, A; Buxton, R; Jonsson, C P; Jones, E; Bridges, A; Gatfield, K; Krauss, S; Lambert, J; Langston, R; Schweiger, S; Uings, I Neurosci Lett, 2018, ISSN: 1872-7972 (Electronic) 0304-3940 (Linking). @article{RN13b, title = {Pharmacological disruption of the MID1/a4 interaction reduces mutant Huntingtin levels in primary neuronal cultures}, author = {O Monteiro and C Chen and R Bingham and A Argyrou and R Buxton and C P Jonsson and E Jones and A Bridges and K Gatfield and S Krauss and J Lambert and R Langston and S Schweiger and I Uings}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29499308}, doi = {10.1016/j.neulet.2018.02.061}, issn = {1872-7972 (Electronic) 0304-3940 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {Neurosci Lett}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 22. | Unterbruner, K; Matthes, F; Schilling, J; Nalavade, R; Weber, S; Winter, J; Krauss, S MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression Artikel PLoS One, 13 (1), S. e0190437, 2018, ISSN: 1932-6203 (Electronic) 1932-6203 (Linking). @article{RN20b, title = {MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression}, author = {K Unterbruner and F Matthes and J Schilling and R Nalavade and S Weber and J Winter and S Krauss}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29293623}, doi = {10.1371/journal.pone.0190437}, issn = {1932-6203 (Electronic) 1932-6203 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {PLoS One}, volume = {13}, number = {1}, pages = {e0190437}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2017 |
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| 21. | Ercan, E; Eid, S; Weber, C; Kowalski, A; Bichmann, M; Behrendt, A; Matthes, F; Krauss, S; Reinhardt, P; Fulle, S; Ehrnhoefer, D E A validated antibody panel for the characterization of tau post-translational modifications Artikel Mol Neurodegener, 12 (1), S. 87, 2017, ISSN: 1750-1326 (Electronic) 1750-1326 (Linking). @article{RN27b, title = {A validated antibody panel for the characterization of tau post-translational modifications}, author = {E Ercan and S Eid and C Weber and A Kowalski and M Bichmann and A Behrendt and F Matthes and S Krauss and P Reinhardt and S Fulle and D E Ehrnhoefer}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29157277}, doi = {10.1186/s13024-017-0229-1}, issn = {1750-1326 (Electronic) 1750-1326 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {Mol Neurodegener}, volume = {12}, number = {1}, pages = {87}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 20. | Griesche, N; Pesch, V; Nalavade, R; Weber, S; König, I; Schölling, M; Möhl, C; Krauß, S tFRAP: A FRAP-Based Technique to Monitor Protein Translation in Living Cells Artikel J Anal Bioanal Tech, 8 (6), 2017, ISSN: 2155-9872. @article{RN28b, title = {tFRAP: A FRAP-Based Technique to Monitor Protein Translation in Living Cells}, author = {N Griesche and V Pesch and R Nalavade and S Weber and I König and M Schölling and C Möhl and S Krauß}, doi = {10.4172/2155-9872.1000390}, issn = {2155-9872}, year = {2017}, date = {2017-01-01}, journal = {J Anal Bioanal Tech}, volume = {8}, number = {6}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 19. | Schweiger, S; Matthes, F; Posey, K; Kickstein, E; Weber, S; Hettich, M M; Pfurtscheller, S; Ehninger, D; Schneider, R; Krauss, S Resveratrol induces dephosphorylation of Tau by interfering with the MID1-PP2A complex Artikel Sci Rep, 7 (1), S. 13753, 2017, ISSN: 2045-2322 (Electronic) 2045-2322 (Linking). @article{RN18b, title = {Resveratrol induces dephosphorylation of Tau by interfering with the MID1-PP2A complex}, author = {S Schweiger and F Matthes and K Posey and E Kickstein and S Weber and M M Hettich and S Pfurtscheller and D Ehninger and R Schneider and S Krauss}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29062069}, doi = {10.1038/s41598-017-12974-4}, issn = {2045-2322 (Electronic) 2045-2322 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {Sci Rep}, volume = {7}, number = {1}, pages = {13753}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2016 |
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| 18. | Griesche, N; Schilling, J; Weber, S; Rohm, M; Pesch, V; Matthes, F; Auburger, G; Krauss, S Regulation of mRNA translation by MID1: a common mechanism of expanded CAG repeat RNAs Artikel Front. Cell. Neurosci., 2016. @article{RN4l, title = {Regulation of mRNA translation by MID1: a common mechanism of expanded CAG repeat RNAs}, author = {N Griesche and J Schilling and S Weber and M Rohm and V Pesch and F Matthes and G Auburger and S Krauss}, doi = {doi: 10.3389/fncel.2016.00226}, year = {2016}, date = {2016-01-01}, journal = {Front. Cell. Neurosci.}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 17. | Schilling, J; Griesche, N; Krauß, S Mechanisms of RNA-Induced Toxicity in Diseases Characterised by CAG Repeat Expansions Artikel eLS. John Wiley & Sons, Ltd: Chichester., 2016. @article{RN32b, title = {Mechanisms of RNA-Induced Toxicity in Diseases Characterised by CAG Repeat Expansions}, author = {J Schilling and N Griesche and S Krauß}, doi = {DOI: 10.1002/9780470015902.a0026464}, year = {2016}, date = {2016-01-01}, journal = {eLS. John Wiley & Sons, Ltd: Chichester.}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 16. | Winter, J; Basilicata, M F; Stemmler, M P; Krauss, S The MID1 protein is a central player during development and in disease Artikel Front Biosci (Landmark Ed), 21 , S. 664-82, 2016, ISSN: 1093-4715 (Electronic) 1093-4715 (Linking). @article{RN22b, title = {The MID1 protein is a central player during development and in disease}, author = {J Winter and M F Basilicata and M P Stemmler and S Krauss}, url = {http://www.ncbi.nlm.nih.gov/pubmed/26709798}, issn = {1093-4715 (Electronic) 1093-4715 (Linking)}, year = {2016}, date = {2016-01-01}, journal = {Front Biosci (Landmark Ed)}, volume = {21}, pages = {664-82}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2015 |
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| 15. | Wagner, J; Krauss, S; Shi, S; Ryazanov, S; Steffen, J; Miklitz, C; Leonov, A; Kleinknecht, A; Goricke, B; Weishaupt, J H; Weckbecker, D; Reiner, A M; Zinth, W; Levin, J; Ehninger, D; Remy, S; Kretzschmar, H A; Griesinger, C; Giese, A; Fuhrmann, M Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies Artikel Acta Neuropathol, 130 (5), S. 619-31, 2015, ISSN: 1432-0533 (Electronic) 0001-6322 (Linking). @article{RN21b, title = {Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies}, author = {J Wagner and S Krauss and S Shi and S Ryazanov and J Steffen and C Miklitz and A Leonov and A Kleinknecht and B Goricke and J H Weishaupt and D Weckbecker and A M Reiner and W Zinth and J Levin and D Ehninger and S Remy and H A Kretzschmar and C Griesinger and A Giese and M Fuhrmann}, url = {https://www.ncbi.nlm.nih.gov/pubmed/26439832}, doi = {10.1007/s00401-015-1483-3}, issn = {1432-0533 (Electronic) 0001-6322 (Linking)}, year = {2015}, date = {2015-01-01}, journal = {Acta Neuropathol}, volume = {130}, number = {5}, pages = {619-31}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2014 |
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| 14. | Kohler, A; Demir, U; Kickstein, E; Krauss, S; Aigner, J; Aranda-Orgilles, B; Karagiannidis, A I; Achmuller, C; Bu, H; Wunderlich, A; Schweiger, M R; Schaefer, G; Schweiger, S; Klocker, H; Schneider, R Mol Cancer, 13 (1), S. 146, 2014, ISSN: 1476-4598 (Electronic) 1476-4598 (Linking). @article{RN6b, title = {A hormone-dependent feedback-loop controls androgen receptor levels by limiting MID1, a novel translation enhancer and promoter of oncogenic signaling}, author = {A Kohler and U Demir and E Kickstein and S Krauss and J Aigner and B Aranda-Orgilles and A I Karagiannidis and C Achmuller and H Bu and A Wunderlich and M R Schweiger and G Schaefer and S Schweiger and H Klocker and R Schneider}, url = {http://www.ncbi.nlm.nih.gov/pubmed/24913494}, doi = {10.1186/1476-4598-13-146}, issn = {1476-4598 (Electronic) 1476-4598 (Linking)}, year = {2014}, date = {2014-01-01}, journal = {Mol Cancer}, volume = {13}, number = {1}, pages = {146}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 13. | Perez-Revuelta, B I; Hettich, M M; Ciociaro, A; Rotermund, C; Kahle, P J; Krauss, S; Monte, Di D A Cell Death Dis, 5 , S. e1209, 2014, ISSN: 2041-4889 (Electronic). @article{RN15b, title = {Metformin lowers Ser-129 phosphorylated alpha-synuclein levels via mTOR-dependent protein phosphatase 2A activation}, author = {B I Perez-Revuelta and M M Hettich and A Ciociaro and C Rotermund and P J Kahle and S Krauss and D A Di Monte}, url = {http://www.ncbi.nlm.nih.gov/pubmed/24810045}, doi = {10.1038/cddis.2014.175}, issn = {2041-4889 (Electronic)}, year = {2014}, date = {2014-01-01}, journal = {Cell Death Dis}, volume = {5}, pages = {e1209}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 12. | Schweiger, S; Dorn, S; Fuchs, M; Kohler, A; Matthes, F; Muller, E C; Wanker, E; Schneider, R; Krauss, S The E3 Ubiquitin Ligase MID1 Catalyzes Ubiquitination and Cleavage of Fu Artikel J Biol Chem, 289 (46), S. 31805-17, 2014, ISSN: 1083-351X (Electronic) 0021-9258 (Linking). @article{RN17b, title = {The E3 Ubiquitin Ligase MID1 Catalyzes Ubiquitination and Cleavage of Fu}, author = {S Schweiger and S Dorn and M Fuchs and A Kohler and F Matthes and E C Muller and E Wanker and R Schneider and S Krauss}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=25278022}, doi = {M113.541219 [pii] 10.1074/jbc.M113.541219}, issn = {1083-351X (Electronic) 0021-9258 (Linking)}, year = {2014}, date = {2014-01-01}, journal = {J Biol Chem}, volume = {289}, number = {46}, pages = {31805-17}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2013 |
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| 11. | Krauss, S; Griesche, N; Jastrzebska, E; Chen, C; Rutschow, D; Achmuller, C; Dorn, S; Boesch, S M; Lalowski, M; Wanker, E; Schneider, R; Schweiger, S Translation of HTT mRNA with expanded CAG repeats is regulated by the MID1-PP2A protein complex Artikel Nat Commun, 4 , S. 1511, 2013, ISSN: 2041-1723 (Electronic) 2041-1723 (Linking). @article{RN8b, title = {Translation of HTT mRNA with expanded CAG repeats is regulated by the MID1-PP2A protein complex}, author = {S Krauss and N Griesche and E Jastrzebska and C Chen and D Rutschow and C Achmuller and S Dorn and S M Boesch and M Lalowski and E Wanker and R Schneider and S Schweiger}, url = {http://www.ncbi.nlm.nih.gov/pubmed/23443539}, doi = {10.1038/ncomms2514}, issn = {2041-1723 (Electronic) 2041-1723 (Linking)}, year = {2013}, date = {2013-01-01}, journal = {Nat Commun}, volume = {4}, pages = {1511}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 10. | Krauss, S; Vorberg, I Prions Ex Vivo: What Cell Culture Models Tell Us about Infectious Proteins Artikel Int J Cell Biol, 2013 , S. 704546, 2013, ISSN: 1687-8876 (Print) 1687-8876 (Linking). @article{RN31b, title = {Prions Ex Vivo: What Cell Culture Models Tell Us about Infectious Proteins}, author = {S Krauss and I Vorberg}, url = {https://www.ncbi.nlm.nih.gov/pubmed/24282413}, doi = {10.1155/2013/704546}, issn = {1687-8876 (Print) 1687-8876 (Linking)}, year = {2013}, date = {2013-01-01}, journal = {Int J Cell Biol}, volume = {2013}, pages = {704546}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 9. | Nalavade, R; Griesche, N; Ryan, D P; Hildebrand, S; Krauss, S Mechanisms of RNA-induced toxicity in CAG repeat disorders Artikel Cell Death Dis, 4 , S. e752, 2013, ISSN: 2041-4889 (Electronic). @article{RN14b, title = {Mechanisms of RNA-induced toxicity in CAG repeat disorders}, author = {R Nalavade and N Griesche and D P Ryan and S Hildebrand and S Krauss}, url = {http://www.ncbi.nlm.nih.gov/pubmed/23907466}, doi = {10.1038/cddis.2013.276}, issn = {2041-4889 (Electronic)}, year = {2013}, date = {2013-01-01}, journal = {Cell Death Dis}, volume = {4}, pages = {e752}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2011 |
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| 8. | Araujo, J; Breuer, P; Dieringer, S; Krauss, S; Dorn, S; Zimmermann, K; Pfeifer, A; Klockgether, T; Wuellner, U; Evert, B O Hum Mol Genet, 20 (15), S. 2928-41, 2011, ISSN: 1460-2083 (Electronic) 0964-6906 (Linking). @article{RN1l, title = {FOXO4-dependent upregulation of superoxide dismutase-2 in response to oxidative stress is impaired in spinocerebellar ataxia type 3}, author = {J Araujo and P Breuer and S Dieringer and S Krauss and S Dorn and K Zimmermann and A Pfeifer and T Klockgether and U Wuellner and B O Evert}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21536589}, doi = {ddr197 [pii] 10.1093/hmg/ddr197}, issn = {1460-2083 (Electronic) 0964-6906 (Linking)}, year = {2011}, date = {2011-01-01}, journal = {Hum Mol Genet}, volume = {20}, number = {15}, pages = {2928-41}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 7. | Liu, E; Knutzen, C A; Krauss, S; Schweiger, S; Chiang, G G Control of mTORC1 signaling by the Opitz syndrome protein MID1 Artikel Proc Natl Acad Sci U S A, 108 (21), S. 8680-5, 2011, ISSN: 1091-6490 (Electronic) 0027-8424 (Linking). @article{RN11b, title = {Control of mTORC1 signaling by the Opitz syndrome protein MID1}, author = {E Liu and C A Knutzen and S Krauss and S Schweiger and G G Chiang}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21555591}, doi = {1100131108 [pii] 10.1073/pnas.1100131108}, issn = {1091-6490 (Electronic) 0027-8424 (Linking)}, year = {2011}, date = {2011-01-01}, journal = {Proc Natl Acad Sci U S A}, volume = {108}, number = {21}, pages = {8680-5}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2010 |
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| 6. | Kickstein, E; Krauss, S; Thornhill, P; Rutschow, D; Zeller, R; Sharkey, J; Williamson, R; Fuchs, M; Kohler, A; Glossmann, H; Schneider, R; Sutherland, C; Schweiger, S Biguanide metformin acts on tau phosphorylation via mTOR/protein phosphatase 2A (PP2A) signaling Artikel Proc Natl Acad Sci U S A, 107 (50), S. 21830-5, 2010, ISSN: 1091-6490 (Electronic) 0027-8424 (Linking). @article{RN5e, title = {Biguanide metformin acts on tau phosphorylation via mTOR/protein phosphatase 2A (PP2A) signaling}, author = {E Kickstein and S Krauss and P Thornhill and D Rutschow and R Zeller and J Sharkey and R Williamson and M Fuchs and A Kohler and H Glossmann and R Schneider and C Sutherland and S Schweiger}, url = {http://www.ncbi.nlm.nih.gov/pubmed/21098287}, doi = {10.1073/pnas.0912793107}, issn = {1091-6490 (Electronic) 0027-8424 (Linking)}, year = {2010}, date = {2010-01-01}, journal = {Proc Natl Acad Sci U S A}, volume = {107}, number = {50}, pages = {21830-5}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2009 |
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| 5. | Krauss, S; So, J; Hambrock, M; Kohler, A; Kunath, M; Scharff, C; Wessling, M; Grzeschik, K H; Schneider, R; Schweiger, S Point mutations in GLI3 lead to misregulation of its subcellular localization Artikel PLoS One, 4 (10), S. e7471, 2009. @article{RN10b, title = {Point mutations in GLI3 lead to misregulation of its subcellular localization}, author = {S Krauss and J So and M Hambrock and A Kohler and M Kunath and C Scharff and M Wessling and K H Grzeschik and R Schneider and S Schweiger}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=19829694}, year = {2009}, date = {2009-01-01}, journal = {PLoS One}, volume = {4}, number = {10}, pages = {e7471}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2008 |
|
| 4. | al Yacoub, N; Romanowska, M; Krauss, S; Schweiger, S; Foerster, J PPARdelta is a type 1 IFN target gene and inhibits apoptosis in T cells Artikel J Invest Dermatol, 128 (8), S. 1940-9, 2008, ISSN: 1523-1747 (Electronic) 0022-202X (Linking). @article{RN24b, title = {PPARdelta is a type 1 IFN target gene and inhibits apoptosis in T cells}, author = {N al Yacoub and M Romanowska and S Krauss and S Schweiger and J Foerster}, url = {https://www.ncbi.nlm.nih.gov/pubmed/18305567}, doi = {10.1038/jid.2008.32}, issn = {1523-1747 (Electronic) 0022-202X (Linking)}, year = {2008}, date = {2008-01-01}, journal = {J Invest Dermatol}, volume = {128}, number = {8}, pages = {1940-9}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
| 3. | Krauss, S; Foerster, J; Schneider, R; Schweiger, S Cancer Res, 68 (12), S. 4658-65, 2008. @article{RN7b, title = {Protein phosphatase 2A and rapamycin regulate the nuclear localization and activity of the transcription factor GLI3}, author = {S Krauss and J Foerster and R Schneider and S Schweiger}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18559511}, year = {2008}, date = {2008-01-01}, journal = {Cancer Res}, volume = {68}, number = {12}, pages = {4658-65}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2004 |
|
| 2. | Winter, J; Lehmann, T; Krauss, S; Trockenbacher, A; Kijas, Z; Foerster, J; Suckow, V; Yaspo, M L; Kulozik, A; Kalscheuer, V; Schneider, R; Schweiger, S Regulation of the MID1 protein function is fine-tuned by a complex pattern of alternative splicing Artikel Hum Genet, 114 (6), S. 541-52, 2004, ISSN: 0340-6717 (Print) 0340-6717 (Linking). @article{RN23b, title = {Regulation of the MID1 protein function is fine-tuned by a complex pattern of alternative splicing}, author = {J Winter and T Lehmann and S Krauss and A Trockenbacher and Z Kijas and J Foerster and V Suckow and M L Yaspo and A Kulozik and V Kalscheuer and R Schneider and S Schweiger}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15057556}, doi = {10.1007/s00439-004-1114-x}, issn = {0340-6717 (Print) 0340-6717 (Linking)}, year = {2004}, date = {2004-01-01}, journal = {Hum Genet}, volume = {114}, number = {6}, pages = {541-52}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2001 |
|
| 1. | Trockenbacher, A; Suckow, V; Foerster, J; Winter, J; Krauss, S; Ropers, H H; Schneider, R; Schweiger, S Nat Genet, 29 (3), S. 287-94, 2001. @article{RN19b, title = {MID1, mutated in Opitz syndrome, encodes an ubiquitin ligase that targets phosphatase 2A for degradation}, author = {A Trockenbacher and V Suckow and J Foerster and J Winter and S Krauss and H H Ropers and R Schneider and S Schweiger}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11685209}, year = {2001}, date = {2001-01-01}, journal = {Nat Genet}, volume = {29}, number = {3}, pages = {287-94}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Publikationen AG Krauß
2025 |
|
| 47. | Inhibition of class IIa HDACs reduces mutant HTT aggregation by affecting RNA stability Artikel Frontiers in Molecular Neuroscience , 2025. |
| 46. | Journal of Magnesium and Alloys, S. in press, 2025. |
| 45. | Molecular and Cellular Probes , 81 , 2025. |
| 44. | Front. Genet. , 2025. |
| 43. | 2025. |
2024 |
|
| 42. | A novel aurone RNA CAG binder inhibits the Huntingtin RNA–protein interaction Artikel RSC Medicinal Chemistry, 9, 2024 , 2024. |
| 41. | The Dynamic World of RNA: Beyond Translation to Subcellular Localization and Function Artikel 2024. |
2023 |
|
| 40. | Low Molecular Weight Inhibitors Targeting the RNA-Binding Protein HuR Artikel 2023. |
| 39. | Editorial: In celebration of women in science: RNA networks and biology Artikel Front Mol Biosci, 10 , S. 1162378, 2023, ISSN: 2296-889X (Print) 2296-889x. |
2022 |
|
| 38. | Front Mol Biosci, 9 , S. 1000932, 2022, ISSN: 2296-889X (Print) 2296-889x. |
2021 |
|
| 37. | Huntingtin and Its Role in Mechanisms of RNA-Mediated Toxicity Artikel Toxins (Basel), 2021. |
| 36. | Huntington’s Disease and Neurodegeneration Artikel Kostrzewa R.M. (eds) Handbook of Neurotoxicity. Springer, Cham. , 2021. |
| 35. | Molecules, 2021. |
| 34. | Human Molecular Genetics, 2021, ( ). |
2020 |
|
| 33. | In vivo targeting of miR‐223 in experimental eosinophilic oesophagitis Artikel 2020. |
| 32. | 2020. |
2019 |
|
| 31. | The Role of MicroRNAs in Spinocerebellar Ataxia Type 3 Artikel J Mol Biol, 431 (9), S. 1729-1742, 2019, ISSN: 1089-8638 (Electronic) 0022-2836 (Linking). |
| 30. | Inhibition of Stat3-mediated astrogliosis ameliorates pathology in an Alzheimer's disease model Artikel EMBO Mol Med, 11 (2), 2019, ISSN: 1757-4684 (Electronic) 1757-4676 (Linking). |
| 29. | Deregulated Splicing Is a Major Mechanism of RNA-Induced Toxicity in Huntington's Disease Artikel J Mol Biol, 2019, ISSN: 1089-8638 (Electronic) 0022-2836 (Linking). |
2018 |
|
| 28. | Metformin reverses early cortical network dysfunction and behavior changes in Huntington's disease Artikel Elife, 7 , 2018, ISSN: 2050-084X (Electronic) 2050-084X (Linking). |
| 27. | PLoS One, 13 (8), S. e0201794, 2018, ISSN: 1932-6203 (Electronic) 1932-6203 (Linking). |
| 26. | Microrna, 2018, ISSN: 2211-5374 (Electronic). |
| 25. | Inhibition of the MID1 protein complex: a novel approach targeting APP protein synthesis Artikel Cell Death Discovery, 4 (4), 2018. |
| 24. | Reducing Mutant Huntingtin Protein Expression in Living Cells by a Newly Identified RNA CAG Binder Artikel ACS Chem Neurosci, 9 (6), S. 1399-1408, 2018, ISSN: 1948-7193 (Electronic) 1948-7193 (Linking). |
| 23. | Neurosci Lett, 2018, ISSN: 1872-7972 (Electronic) 0304-3940 (Linking). |
| 22. | MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression Artikel PLoS One, 13 (1), S. e0190437, 2018, ISSN: 1932-6203 (Electronic) 1932-6203 (Linking). |
2017 |
|
| 21. | A validated antibody panel for the characterization of tau post-translational modifications Artikel Mol Neurodegener, 12 (1), S. 87, 2017, ISSN: 1750-1326 (Electronic) 1750-1326 (Linking). |
| 20. | tFRAP: A FRAP-Based Technique to Monitor Protein Translation in Living Cells Artikel J Anal Bioanal Tech, 8 (6), 2017, ISSN: 2155-9872. |
| 19. | Resveratrol induces dephosphorylation of Tau by interfering with the MID1-PP2A complex Artikel Sci Rep, 7 (1), S. 13753, 2017, ISSN: 2045-2322 (Electronic) 2045-2322 (Linking). |
2016 |
|
| 18. | Regulation of mRNA translation by MID1: a common mechanism of expanded CAG repeat RNAs Artikel Front. Cell. Neurosci., 2016. |
| 17. | Mechanisms of RNA-Induced Toxicity in Diseases Characterised by CAG Repeat Expansions Artikel eLS. John Wiley & Sons, Ltd: Chichester., 2016. |
| 16. | The MID1 protein is a central player during development and in disease Artikel Front Biosci (Landmark Ed), 21 , S. 664-82, 2016, ISSN: 1093-4715 (Electronic) 1093-4715 (Linking). |
2015 |
|
| 15. | Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies Artikel Acta Neuropathol, 130 (5), S. 619-31, 2015, ISSN: 1432-0533 (Electronic) 0001-6322 (Linking). |
2014 |
|
| 14. | Mol Cancer, 13 (1), S. 146, 2014, ISSN: 1476-4598 (Electronic) 1476-4598 (Linking). |
| 13. | Cell Death Dis, 5 , S. e1209, 2014, ISSN: 2041-4889 (Electronic). |
| 12. | The E3 Ubiquitin Ligase MID1 Catalyzes Ubiquitination and Cleavage of Fu Artikel J Biol Chem, 289 (46), S. 31805-17, 2014, ISSN: 1083-351X (Electronic) 0021-9258 (Linking). |
2013 |
|
| 11. | Translation of HTT mRNA with expanded CAG repeats is regulated by the MID1-PP2A protein complex Artikel Nat Commun, 4 , S. 1511, 2013, ISSN: 2041-1723 (Electronic) 2041-1723 (Linking). |
| 10. | Prions Ex Vivo: What Cell Culture Models Tell Us about Infectious Proteins Artikel Int J Cell Biol, 2013 , S. 704546, 2013, ISSN: 1687-8876 (Print) 1687-8876 (Linking). |
| 9. | Mechanisms of RNA-induced toxicity in CAG repeat disorders Artikel Cell Death Dis, 4 , S. e752, 2013, ISSN: 2041-4889 (Electronic). |
2011 |
|
| 8. | Hum Mol Genet, 20 (15), S. 2928-41, 2011, ISSN: 1460-2083 (Electronic) 0964-6906 (Linking). |
| 7. | Control of mTORC1 signaling by the Opitz syndrome protein MID1 Artikel Proc Natl Acad Sci U S A, 108 (21), S. 8680-5, 2011, ISSN: 1091-6490 (Electronic) 0027-8424 (Linking). |
2010 |
|
| 6. | Biguanide metformin acts on tau phosphorylation via mTOR/protein phosphatase 2A (PP2A) signaling Artikel Proc Natl Acad Sci U S A, 107 (50), S. 21830-5, 2010, ISSN: 1091-6490 (Electronic) 0027-8424 (Linking). |
2009 |
|
| 5. | Point mutations in GLI3 lead to misregulation of its subcellular localization Artikel PLoS One, 4 (10), S. e7471, 2009. |
2008 |
|
| 4. | PPARdelta is a type 1 IFN target gene and inhibits apoptosis in T cells Artikel J Invest Dermatol, 128 (8), S. 1940-9, 2008, ISSN: 1523-1747 (Electronic) 0022-202X (Linking). |
| 3. | Cancer Res, 68 (12), S. 4658-65, 2008. |
2004 |
|
| 2. | Regulation of the MID1 protein function is fine-tuned by a complex pattern of alternative splicing Artikel Hum Genet, 114 (6), S. 541-52, 2004, ISSN: 0340-6717 (Print) 0340-6717 (Linking). |
2001 |
|
| 1. | Nat Genet, 29 (3), S. 287-94, 2001. |