Inhaltsverzeichnis
Auswahl der wissenschaftlichen Literatur zum Thema „Neuroretinal organoids“
Geben Sie eine Quelle nach APA, MLA, Chicago, Harvard und anderen Zitierweisen an
Machen Sie sich mit den Listen der aktuellen Artikel, Bücher, Dissertationen, Berichten und anderer wissenschaftlichen Quellen zum Thema "Neuroretinal organoids" bekannt.
Neben jedem Werk im Literaturverzeichnis ist die Option "Zur Bibliographie hinzufügen" verfügbar. Nutzen Sie sie, wird Ihre bibliographische Angabe des gewählten Werkes nach der nötigen Zitierweise (APA, MLA, Harvard, Chicago, Vancouver usw.) automatisch gestaltet.
Sie können auch den vollen Text der wissenschaftlichen Publikation im PDF-Format herunterladen und eine Online-Annotation der Arbeit lesen, wenn die relevanten Parameter in den Metadaten verfügbar sind.
Zeitschriftenartikel zum Thema "Neuroretinal organoids"
Atac, David, Kevin Maggi, Silke Feil, Jordi Maggi, Elisa Cuevas, Jane C. Sowden, Samuel Koller und Wolfgang Berger. „Identification and Characterization of ATOH7-Regulated Target Genes and Pathways in Human Neuroretinal Development“. Cells 13, Nr. 13 (03.07.2024): 1142. http://dx.doi.org/10.3390/cells13131142.
Der volle Inhalt der QuelleTakata, Nozomu, Deepti Abbey, Luciano Fiore, Sandra Acosta, Ruopeng Feng, Hyea Jin Gil, Alfonso Lavado et al. „An Eye Organoid Approach Identifies Six3 Suppression of R-spondin 2 as a Critical Step in Mouse Neuroretina Differentiation“. Cell Reports 21, Nr. 6 (November 2017): 1534–49. http://dx.doi.org/10.1016/j.celrep.2017.10.041.
Der volle Inhalt der QuelleAfting, Cassian, Tobias Walther, Oliver M. Drozdowski, Christina Schlagheck, Ulrich S. Schwarz, Joachim Wittbrodt und Kerstin Göpfrich. „DNA microbeads for spatio-temporally controlled morphogen release within organoids“. Nature Nanotechnology, 09.09.2024. http://dx.doi.org/10.1038/s41565-024-01779-y.
Der volle Inhalt der QuelleLiu, Wei, Rupendra Shrestha, Albert Lowe, Xusheng Zhang und Ludovic Spaeth. „Self-formation of concentric zones of telencephalic and ocular tissues and directional retinal ganglion cell axons“. eLife 12 (04.09.2023). http://dx.doi.org/10.7554/elife.87306.3.
Der volle Inhalt der QuelleIsla-Magrané, Helena, Maddalen Zufiaurre-Seijo, José García-Arumí und Anna Duarri. „All-trans retinoic acid modulates pigmentation, neuroretinal maturation, and corneal transparency in human multiocular organoids“. Stem Cell Research & Therapy 13, Nr. 1 (28.07.2022). http://dx.doi.org/10.1186/s13287-022-03053-1.
Der volle Inhalt der QuelleDissertationen zum Thema "Neuroretinal organoids"
Frank, Elie. „Modélisation du Syndrome d'Alström à partir de cellules souches pluripotentes humaines pour l'identification de cibles moléculaires d'intérêt thérapeutique“. Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASQ041.
Der volle Inhalt der QuelleAlström syndrome (AS) is a monogenic recessive multi-systemic disease characterized by hearing and vision loss, obesity, type 2 diabetes, cardiomyopathy and progressive liver and kidney failure. Symptoms affecting vision develop in the first few weeks after birth and gradually lead to total loss of sight. At present, there is no cure for this disease, and only solutions that reduce the effects of the symptoms can be proposed.The aim of this thesis is to develop a cellular model of AS with a view to understanding the molecular mechanisms driving the disease and identifying therapeutic targets.We obtained different clones with pathological or de novo mutations using genome-editing systems associated with CRISPR/Cas9. We characterized these model clones by seeking to identify specific phenotypic markers within the hiPSCs. The mutations generated did not change the properties of these cells.In a second step, still with the aim of identifying a pathological phenotype, we differentiated the model iPSC lines into RPE cells.Again, no specific phenotypic marker was identified. Finally, we differentiated our model hiPSC lines into neuroretinal organoids to study retinal cells development within these structures with a particular focus on photoreceptors. We were able to observe the absence or reduced expression of opsins characteristic of cones and rods in organoids derived from ALMS1-mutant hiPSCs. In addition, these organoids showed increased cell death compared with organoids derived from healthy hiPSC lines. This suggests that photoreceptors degenerate during differentiation within organoids. The mechanisms by which mutations in ALMS1 lead to this degeneration remain unclear.The cellular models of AS presented in this thesis therefore reproduce a pathological phenotype and will be invaluable tools for understanding the mechanisms responsible for the visual symptoms of the disease, and pave the way for screening strategies aimed at identifying new therapeutic targets