Добірка наукової літератури з теми "Chromodomain Helicase DNA binding 4 (CHD4)"
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Статті в журналах з теми "Chromodomain Helicase DNA binding 4 (CHD4)":
Kolla, Venkatadri, Koumudi Naraparaju, Tiangang Zhuang, Mayumi Higashi, Sriharsha Kolla, Gerd A. Blobel, and Garrett M. Brodeur. "The tumour suppressor CHD5 forms a NuRD-type chromatin remodelling complex." Biochemical Journal 468, no. 2 (May 22, 2015): 345–52. http://dx.doi.org/10.1042/bj20150030.
Sillibourne, James Edward, Bénédicte Delaval, Sambra Redick, Manisha Sinha, and Stephen John Doxsey. "Chromatin Remodeling Proteins Interact with Pericentrin to Regulate Centrosome Integrity." Molecular Biology of the Cell 18, no. 9 (September 2007): 3667–80. http://dx.doi.org/10.1091/mbc.e06-07-0604.
Lin, Shiaw-Yih, Jing Zhang, and David J.H. Shih. "The Tale of CHD4 in DNA Damage Response and Chemotherapeutic Response." Cancer Research and Cellular Therapeutics 3, no. 1 (July 8, 2019): 01–03. http://dx.doi.org/10.31579/2640-1053/052.
Hagman, James, Carissa Dege, Desiree Straign, Haiqun Jia, Kendra Walton, Kara Lukin, Hong Lei, Thomas Danhorn, and Ann Feeney. "Chromodomain helicase DNA-binding 4 is required for proliferation, distal VH rearrangements and developmental progression of B cell progenitors (HEM1P.221)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 50.4. http://dx.doi.org/10.4049/jimmunol.194.supp.50.4.
Chohra, Ilyas, Subhajit Giri, and Brigitte Malgrange. "Generation of a Well-Characterized Homozygous Chromodomain-Helicase-DNA-Binding Protein 4G1003D Mutant hESC Line Using CRISPR/eCas9 (ULIEGEe001-A-1)." International Journal of Molecular Sciences 24, no. 13 (June 23, 2023): 10543. http://dx.doi.org/10.3390/ijms241310543.
Larsen, Dorthe Helena, Catherine Poinsignon, Thorkell Gudjonsson, Christoffel Dinant, Mark R. Payne, Flurina J. Hari, Jannie M. Rendtlew Danielsen, et al. "The chromatin-remodeling factor CHD4 coordinates signaling and repair after DNA damage." Journal of Cell Biology 190, no. 5 (August 30, 2010): 731–40. http://dx.doi.org/10.1083/jcb.200912135.
Hosokawa, Hiroyuki, Tomoaki Tanaka, Miki Kato, Yuuki Tamaki, and Toshinori Nakayama. "Functionally distinct Gata3/Chd4 complexes coordinately establish Th2 cell identity. (P1340)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 208.13. http://dx.doi.org/10.4049/jimmunol.190.supp.208.13.
Arends, Tessa, Carissa Dege, Alexandra Bortnick, Thomas Danhorn, Jennifer R. Knapp, Haiqun Jia, Laura Harmacek, et al. "CHD4 is essential for transcriptional repression and lineage progression in B lymphopoiesis." Proceedings of the National Academy of Sciences 116, no. 22 (May 13, 2019): 10927–36. http://dx.doi.org/10.1073/pnas.1821301116.
O’Shaughnessy, Aoife, and Brian Hendrich. "CHD4 in the DNA-damage response and cell cycle progression: not so NuRDy now." Biochemical Society Transactions 41, no. 3 (May 23, 2013): 777–82. http://dx.doi.org/10.1042/bst20130027.
Smeenk, Godelieve, Wouter W. Wiegant, Hans Vrolijk, Aldo P. Solari, Albert Pastink, and Haico van Attikum. "The NuRD chromatin–remodeling complex regulates signaling and repair of DNA damage." Journal of Cell Biology 190, no. 5 (August 30, 2010): 741–49. http://dx.doi.org/10.1083/jcb.201001048.
Дисертації з теми "Chromodomain Helicase DNA binding 4 (CHD4)":
Zhong, Yichen. "Mechanistic Studies of Human Chromodomain-Helicase-DNA-Binding Protein 4." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/23473.
Fenniche, Salma. "Rôle de la NADPH OXYDASE NOX4 dans la régulation de l'expression et de l'activité de CHD4 dans les tumeurs thyroïdiennes porteuses de la mutation BRAFV600E." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL022.
Metabolic radiotherapy with radioiodine is the cornerstone of the treatment of distant metastases of differentiated thyroid cancers. This therapy depends on the expression at the basal membrane of thyrocytes of the Natrium Iodide Symporter 'NIS'. BRAFV600E mutation is present in 45 to 60% of papillary thyroid carcinomas, which represent 80% of thyroid cancers. The presence of this mutation is associated with the most aggressive thyroid tumors with low levels or absence of NIS expression. The loss of radioactive iodine uptake translates into resistance to metabolic radiotherapy, constituting a major issue for the treatment of patients with this cancer. One approach for treating patients refractory to metabolic radiotherapy is to increase iodine uptake.At the transcriptional level, our team has already shown, through a comparative analysis concerning approximately 500 PTCs from the TCGA database, that NOX4 was strongly expressed in PTCs-BRAFV600E compared to PTCs-BRAFwt. However, at the protein level, no link has been established between the BRAFV600E mutation and NOX4 in malignant and non-malignant tumors (BRAFV600E/BRAFwt). In my thesis project, we illustrate for the first time a positive correlation between the presence of BRAFV600E mutation and the overexpression of NOX4 protein in PTC tumor tissues. The overexpression of NOX4 was associated with an aggressive nature of tumors. Furthermore, we showed that 60% of infiltrating C-PTCs overexpress NOX4 independently of BRAF mutational status, suggesting that NOX4 could be considered as a potential co-marker of PTC aggressiveness. Interestingly, NOX4 protein was also overexpressed in non-malignant thyroid diseases (Basedow, goiters, and hyperplasias), with different subcellular localizations, suggesting a role for NOX4 in progression to thyroid malignancy.Furthermore, on a mechanistic level, our team has previously shown that BRAFV600E controls the expression of NOX4 under the effect of TGF-β/SMAD3 and that NOX4-derived ROS contribute to the repression of NIS. Inhibition of NOX4 promotes reactivation of the NIS. This reversibility suggests a contribution to an epigenetic mechanism. CHD4, a subunit of the NuRD remodeling complex, plays an essential role in gene repression. it was found to be strongly expressed in PTCs, in which it was associated with a poor prognosis. In this study, we showed that the TGF-β/SMAD3 pathway regulates the expression of CHD4 protein. The latter cooperates with DNMTs in repressing NIS in several thyroid tumor cells lines mutated for BRAFV600E. Furthermore, we showed that CHD4 responds to oxidative DNA damage induced by NOX4-derived ROS. Indeed, inhibition of NOX4 or its functional partner p22phox reduces the recruitment of CHD4 to chromatin. This recruitment depends on OGG1 and MSH6, two proteins involved in oxidative DNA damage repair. This study identifies CHD4 as a new therapeutic candidate in radioiodine-refractory thyroid cancers