Littérature scientifique sur le sujet « Isogenic cellular models »
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Articles de revues sur le sujet "Isogenic cellular models"
Paredes-Redondo, A., et Y. Y. Lin. « Developing novel human isogenic cellular models for Duchenne muscular dystrophy ». Neuromuscular Disorders 27 (mars 2017) : S6. http://dx.doi.org/10.1016/s0960-8966(17)30234-1.
Texte intégralZhang, Yuting, Emily Wilt et Xin Lu. « Human Isogenic Cell Line Models for Neutrophils and Myeloid-Derived Suppressor Cells ». International Journal of Molecular Sciences 21, no 20 (18 octobre 2020) : 7709. http://dx.doi.org/10.3390/ijms21207709.
Texte intégralBenarroch, Louise, Julia Madsen-Østerbye, Mohamed Abdelhalim, Kamel Mamchaoui, Jessica Ohana, Anne Bigot, Vincent Mouly, Gisèle Bonne, Anne T. Bertrand et Philippe Collas. « Cellular and Genomic Features of Muscle Differentiation from Isogenic Fibroblasts and Myoblasts ». Cells 12, no 15 (3 août 2023) : 1995. http://dx.doi.org/10.3390/cells12151995.
Texte intégralPavan, Eleonora, Maximiliano Ormazabal, Paolo Peruzzo, Emilio Vaena, Paula Rozenfeld et Andrea Dardis. « CRISPR/Cas9 Editing for Gaucher Disease Modelling ». International Journal of Molecular Sciences 21, no 9 (5 mai 2020) : 3268. http://dx.doi.org/10.3390/ijms21093268.
Texte intégralKarwacka, Marianna, et Marta Olejniczak. « Advances in Modeling Polyglutamine Diseases Using Genome Editing Tools ». Cells 11, no 3 (2 février 2022) : 517. http://dx.doi.org/10.3390/cells11030517.
Texte intégralKlementieva, Natalia, Daria Goliusova, Julia Krupinova, Vladislav Yanvarev, Alexandra Panova, Natalia Mokrysheva et Sergey L. Kiselev. « A Novel Isogenic Human Cell-Based System for MEN1 Syndrome Generated by CRISPR/Cas9 Genome Editing ». International Journal of Molecular Sciences 22, no 21 (8 novembre 2021) : 12054. http://dx.doi.org/10.3390/ijms222112054.
Texte intégralBoussaad, Ibrahim, Emily K. Dolezal, Fabiana Perna, Stephen D. Nimer et Eirini P. Papapetrou. « IPS Cells From Del(7q)-MDS Patients Display Impaired Proliferation and Hematopoietic Commitment ». Blood 120, no 21 (16 novembre 2012) : 174. http://dx.doi.org/10.1182/blood.v120.21.174.174.
Texte intégralMuto, Valentina, Federica Benigni, Valentina Magliocca, Rossella Borghi, Elisabetta Flex, Valentina Pallottini, Alessandro Rosa, Claudia Compagnucci et Marco Tartaglia. « CRISPR/Cas9 and piggyBac Transposon-Based Conversion of a Pathogenic Biallelic TBCD Variant in a Patient-Derived iPSC Line Allows Correction of PEBAT-Related Endophenotypes ». International Journal of Molecular Sciences 24, no 9 (28 avril 2023) : 7988. http://dx.doi.org/10.3390/ijms24097988.
Texte intégralLi, Fenfang, Igor Cima, Jess Honganh Vo, Min-Han Tan et Claus Dieter Ohl. « Single Cell Hydrodynamic Stretching and Microsieve Filtration Reveal Genetic, Phenotypic and Treatment-Related Links to Cellular Deformability ». Micromachines 11, no 5 (9 mai 2020) : 486. http://dx.doi.org/10.3390/mi11050486.
Texte intégralPatel, Ronak, Shyanne Page et Abraham Jacob Al-Ahmad. « Isogenic blood-brain barrier models based on patient-derived stem cells display inter-individual differences in cell maturation and functionality ». Journal of Neurochemistry 142, no 1 (14 mai 2017) : 74–88. http://dx.doi.org/10.1111/jnc.14040.
Texte intégralThèses sur le sujet "Isogenic cellular models"
Rakotomalala-Andrianasolo, Andria. « Développement et caractérisation de modèles cellulaires pour l'étude du rôle de l'oncohistone H3.3 K27M dans le phénotype agressif et la réponse aux thérapies des gliomes pédiatriques diffus de la ligne médiane ». Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS015.
Texte intégralH3K27-altered DMG treatment is one of the most significant challenges in pediatric neuro-oncology,with no improvement in patient survival over the past 50 years. In 2012, it was shown that DMGs harbor a specific histone 3 mutation (oncohistone) called H3.3 K27M with a very high prevalence (70-80% of cases). Although theH3.3 K27M impact on the epigenetic landscape has been well described, studies are needed to understand betterits role in DMG cells’ aggressiveness and response to therapies.To study the H3.3 K27M mutation impact on DMG cell phenotypes precisely, we developed andcharacterized pediatric high-grade glioma isogenic cellular models induced and knock-out for the oncohistone.Using these models, we aimed to decipher the oncohistone impact on DMG cell biology and response to anticancertherapies, including radiation therapy, the only current standard of care for DMGs. Characterization of our H3.3 K27M-induced pediatric supratentorial glioma cell lines reveals that the oncohistone affects the response to ionizing radiations and specific targeted therapies in a cellular context-dependentway. Based on these results, we settled to characterize oncohistone biological impacts in a more relevant cellular context of DMG. In that sense, we established H3.3 K27M knock-out cellular models and characterized them regarding their parental DMG H3.3 K27M mutated cell lines. Through omic (transcriptomic and proteomic)and cell metabolism characterizations of these models, we notably showed the H3.3 K27M mutation impact on DMG cells’ lipid metabolism. In 3D spheroid models, this H3.3 K27M-induced lipid metabolism rewiring appeared conditioned by microenvironment factors still under investigation.On the other hand, a functional pharmacological screen identified H3.3 K27M-driven dependencies tospecific DNA repair pathways. In addition, ongoing radiobiological characterization of our models indicates anH3.3 K27M-associated radiosensitivity correlating with a decrease in DNA repair efficiency following ionizingradiations. Beyond this DNA repair impact, our pharmacological screen also revealed an H3.3 K27M-relatedsensitivity to cardiac glycoside drugs. This result makes sense with our transcriptomic data showing enrichmentin genes involved in cardiomyopathies and ion homeostasis among differentially expressed genes with theoncohistone. In this context, we began unraveling the molecular and biological processes underlying thisH3.3 K27M-driven effect.Finally, we used our isogenic cellular models to show that the H3.3 K27M oncohistone drives lipidmetabolism modifications. These metabolic changes could prime H3K27-altered DMG cells to specific regulatedcell death pathways (e.g., ferroptosis) and affect the response to certain therapies. Moreover, the H3.3 K27Mseems to drive specific sensitivities, notably to radiation therapy and cardiac glycoside drugs. Understanding the underlying molecular mechanisms governing these H3.3 K27M-associated Achille heels could highlight newinsights into the oncohistone role in DMG cells and provide rationales for developing new therapeutic strategies