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Your search keyword '"Thijssen, Karen L."' showing total 19 results
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19 results on '"Thijssen, Karen L."'

2. Transcription-coupled DNA–protein crosslink repair by CSB and CRL4CSA-mediated degradation

Author

van Sluis, Marjolein, Yu, Qing, van der Woude, Melanie, Gonzalo-Hansen, Camila, Dealy, Shannon C., Janssens, Roel C., Somsen, Hedda B., Ramadhin, Anisha R., Dekkers, Dick H. W., Wienecke, Hannah Lena, Demmers, Joris J. P. G., Raams, Anja, Davó-Martínez, Carlota, Llerena Schiffmacher, Diana A., van Toorn, Marvin, Häckes, David, Thijssen, Karen L., Zhou, Di, Lammers, Judith G., Pines, Alex, Vermeulen, Wim, Pothof, Joris, Demmers, Jeroen A. A., van den Berg, Debbie L. C., Lans, Hannes, and Marteijn, Jurgen A.

Published
2024
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11. On the role of RNA amplification in dsRNA-triggered gene silencing

Author

Sijen, Titia, Fleenor, Jamie, Simmer, Femke, Thijssen, Karen L., Parrish, Susan, Timmons, Lisa, Plasterk, Ronald H. A., and Fire, Andrew

Subjects
Cell research -- Analysis, Messenger RNA -- Genetic aspects, Caenorhabditis elegans -- Physiological aspects, Genetic translation -- Physiological aspects, Brain research -- Analysis, Carrier proteins -- Physiological aspects, Biological sciences
Abstract

Research has been conducted on the trigger RNA amplification. The effect of this amplification on the RNA interference in Caenorhabditis elegans has been investigated and the results indicate that the amplification mechanism augments the RNA interference-based surveillance potency.

Published
2001

12. Retraction

Author

Sijen, Titia, primary, Steiner, Florian A., additional, Thijssen, Karen L., additional, and Plasterk, Ronald H. A., additional

Published
2020
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19. C. elegans model identifies genetic modifiers of alpha-synuclein inclusion formation during aging.

Author

van Ham TJ, Thijssen KL, Breitling R, Hofstra RM, Plasterk RH, and Nollen EA

Subjects
Animals, Animals, Genetically Modified, Bacterial Proteins genetics, Bacterial Proteins metabolism, Base Sequence, Brain metabolism, DNA Primers genetics, Fluorescence Recovery After Photobleaching, G-Protein-Coupled Receptor Kinases antagonists & inhibitors, G-Protein-Coupled Receptor Kinases genetics, G-Protein-Coupled Receptor Kinases metabolism, Gene Deletion, Genes, Helminth, Humans, Luminescent Proteins genetics, Luminescent Proteins metabolism, Models, Genetic, Parkinson Disease etiology, Parkinson Disease genetics, Parkinson Disease metabolism, RNA Interference, Recombinant Fusion Proteins genetics, Recombinant Fusion Proteins metabolism, alpha-Synuclein antagonists & inhibitors, Aging genetics, Aging metabolism, Caenorhabditis elegans genetics, Caenorhabditis elegans metabolism, Inclusion Bodies metabolism, alpha-Synuclein genetics, alpha-Synuclein metabolism
Abstract

Inclusions in the brain containing alpha-synuclein are the pathological hallmark of Parkinson's disease, but how these inclusions are formed and how this links to disease is poorly understood. We have developed a C. elegans model that makes it possible to monitor, in living animals, the formation of alpha-synuclein inclusions. In worms of old age, inclusions contain aggregated alpha- synuclein, resembling a critical pathological feature. We used genome-wide RNA interference to identify processes involved in inclusion formation, and identified 80 genes that, when knocked down, resulted in a premature increase in the number of inclusions. Quality control and vesicle-trafficking genes expressed in the ER/Golgi complex and vesicular compartments were overrepresented, indicating a specific role for these processes in alpha-synuclein inclusion formation. Suppressors include aging-associated genes, such as sir-2.1/SIRT1 and lagr-1/LASS2. Altogether, our data suggest a link between alpha-synuclein inclusion formation and cellular aging, likely through an endomembrane-related mechanism. The processes and genes identified here present a framework for further study of the disease mechanism and provide candidate susceptibility genes and drug targets for Parkinson's disease and other alpha-synuclein related disorders., Competing Interests: The authors have declared that no competing interests exist.

Published
2008
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