Literatura académica sobre el tema "Polycomb machinery"
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Artículos de revistas sobre el tema "Polycomb machinery"
Chen, Xin, Mark Hiller, Yasemin Sancak y Margaret T. Fuller. "Tissue-Specific TAFs Counteract Polycomb to Turn on Terminal Differentiation". Science 310, n.º 5749 (3 de noviembre de 2005): 869–72. http://dx.doi.org/10.1126/science.1118101.
Texto completoCruz-Becerra, Grisel, Mandy Juárez, Viviana Valadez-Graham y Mario Zurita. "Analysis of Drosophila p8 and p52 mutants reveals distinct roles for the maintenance of TFIIH stability and male germ cell differentiation". Open Biology 6, n.º 10 (octubre de 2016): 160222. http://dx.doi.org/10.1098/rsob.160222.
Texto completoKuehner y Yao. "The Dynamic Partnership of Polycomb and Trithorax in Brain Development and Diseases". Epigenomes 3, n.º 3 (21 de agosto de 2019): 17. http://dx.doi.org/10.3390/epigenomes3030017.
Texto completoFlora, Pooja, Gil Dalal, Idan Cohen y Elena Ezhkova. "Polycomb Repressive Complex(es) and Their Role in Adult Stem Cells". Genes 12, n.º 10 (24 de septiembre de 2021): 1485. http://dx.doi.org/10.3390/genes12101485.
Texto completoChiacchiera, Fulvio y Diego Pasini. "Control of adult intestinal identity by the Polycomb repressive machinery". Cell Cycle 16, n.º 3 (28 de noviembre de 2016): 243–44. http://dx.doi.org/10.1080/15384101.2016.1252582.
Texto completoBreiling, Achim, Edgar Bonte, Simona Ferrari, Peter B. Becker y Renato Paro. "The Drosophila Polycomb Protein Interacts with Nucleosomal Core Particles In Vitro via Its Repression Domain". Molecular and Cellular Biology 19, n.º 12 (1 de diciembre de 1999): 8451–60. http://dx.doi.org/10.1128/mcb.19.12.8451.
Texto completoKaundal, Babita, Anup K. Srivastava, Mohammed Nadim Sardoiwala, Surajit Karmakar y Subhasree Roy Choudhury. "A NIR-responsive indocyanine green-genistein nanoformulation to control the polycomb epigenetic machinery for the efficient combinatorial photo/chemotherapy of glioblastoma". Nanoscale Advances 1, n.º 6 (2019): 2188–207. http://dx.doi.org/10.1039/c9na00212j.
Texto completoLuo, Xi, Kelly Schoch, Sharayu V. Jangam, Venkata Hemanjani Bhavana, Hillary K. Graves, Sujay Kansagra, Joan M. Jasien et al. "Rare deleterious de novo missense variants in Rnf2/Ring2 are associated with a neurodevelopmental disorder with unique clinical features". Human Molecular Genetics 30, n.º 14 (16 de abril de 2021): 1283–92. http://dx.doi.org/10.1093/hmg/ddab110.
Texto completoLeicher, Rachel, Eva J. Ge, Xingcheng Lin, Matthew J. Reynolds, Wenjun Xie, Thomas Walz, Bin Zhang, Tom W. Muir y Shixin Liu. "Single-molecule and in silico dissection of the interaction between Polycomb repressive complex 2 and chromatin". Proceedings of the National Academy of Sciences 117, n.º 48 (18 de noviembre de 2020): 30465–75. http://dx.doi.org/10.1073/pnas.2003395117.
Texto completoLee, Patrick C., Phuong Le, Keegan Korthauer, Jingwei Cheng, John Doench, James A. DeCaprio, Derin B. Keskin y Catherine J. Wu. "Identifying regulators of reversible MHC I loss in Merkel cell carcinoma through genome-scale screens". Journal of Immunology 204, n.º 1_Supplement (1 de mayo de 2020): 243.18. http://dx.doi.org/10.4049/jimmunol.204.supp.243.18.
Texto completoTesis sobre el tema "Polycomb machinery"
Lee, Ming-Kang. "PRC1, PRC2 and BAP1 : Three tightly-linked chromatin modifiers involved in transcriptional regulation". Electronic Thesis or Diss., Université Paris sciences et lettres, 2021. http://www.theses.fr/2021UPSLS055.
Texto completoIn eukaryotes, the maintenance of cell identity entails the precise control of gene expression, which results from the concerted actions of transcription factors and factors controlling chromatin structure. Polycomb repressive complex 1 and 2 (PRC1 and PRC2) are chromatin modifiers that orchestrate transcriptional repression by catalyzing H2Aub and H3K27me3, respectively. By contrast, BRCA1-associated protein 1 (BAP1) promotes transcription by removing H2Aub, acting as an antagonist of PRC1. However, the detailed mechanism of how BAP1 regulates transcription remains largely elusive. The interplay between PRC1 and PRC2 is also far from being fully understood. My PhD study aimed at investigating the underlying mechanisms for these two important questions.(1) BAP1 is recruited to a subset of active enhancers where it stabilizes BRD4 occupancy.In these studies, we showed that BAP1 promotes transcription by opposing PRC1 activity, and that BAP1 is mostly inert in its absence. Genome-wide analysis revealed that BAP1 is recruited to a subset of active enhancers. Besides, inactivation of BAP1 led to accumulation of H2Aub and impaired BRD4 recruitment. Consistently, super-resolution microscopy demonstrated reduced condensates of BRD4 and MED1 in BAP1-KO cells. This suggests that BAP1 has a crucial function for the integrity of a subset of enhancers. Importantly, by treating isogenic cells with BET inhibitors, we showed that cells mutant for BAP1 display a more pronounced proliferative response. This result suggests that further perturbation of enhancers function could be a therapeutic strategy for BAP1-null malignancies.(2) PRC2 represses transcription independently of PRC1PRC1 and PRC2 are long considered cooperating to maintain gene repression. However, analyzing transcriptomic profiles of PRC1-null, PRC2-null and PRC1/2-null cells, we demonstrated that both PRC1 and PRC2 can autonomously repress transcription. Through both unbiased and candidate-based approaches, we focus on identifying downstream effectors of PRC2-mediated silencing in the absence of PRC1. This includes investigating the roles of previously proposed H3K27me3 readers. While this study is still ongoing, it is likely that it will reveal new actor for PRC2-mediated repression