Academic literature on the topic 'Cernunnos-XLF'
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Journal articles on the topic "Cernunnos-XLF"
Malivert, Laurent, Isabelle Callebaut, Paola Rivera-Munoz, Alain Fischer, Jean-Paul Mornon, Patrick Revy, and Jean-Pierre de Villartay. "The C-Terminal Domain of Cernunnos/XLF Is Dispensable for DNA Repair In Vivo." Molecular and Cellular Biology 29, no. 5 (December 22, 2008): 1116–22. http://dx.doi.org/10.1128/mcb.01521-08.
Full textÇipe, Funda Erol, Cigdem Aydogmus, Arzu Babayigit Hocaoglu, Merve Kilic, Gul Demet Kaya, and Elif Yilmaz Gulec. "Cernunnos/XLF Deficiency: A Syndromic Primary Immunodeficiency." Case Reports in Pediatrics 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/614238.
Full textMusilli, Stefania, Vincent Abramowski, Benoit Roch, and Jean-Pierre de Villartay. "An in vivo study of the impact of deficiency in the DNA repair proteins PAXX and XLF on development and maturation of the hemolymphoid system." Journal of Biological Chemistry 295, no. 8 (January 8, 2020): 2398–406. http://dx.doi.org/10.1074/jbc.ac119.010924.
Full textAvagyan, Serine, Michael Churchill, Kenta Yamamoto, Jennifer L. Crowe, Chen Li, Brian J. Lee, Tian Zheng, Siddhartha Mukherjee, and Shan Zha. "Hematopoietic stem cell dysfunction underlies the progressive lymphocytopenia in XLF/Cernunnos deficiency." Blood 124, no. 10 (September 4, 2014): 1622–25. http://dx.doi.org/10.1182/blood-2014-05-574863.
Full textFaraci, Maura, Edoardo Lanino, Concetta Micalizzi, Giuseppe Morreale, Daniela Di Martino, Laura Banov, Patrizia Comoli, Franco Locatelli, Annarosa Soresina, and Alessandro Plebani. "Unrelated hematopoietic stem cell transplantation for Cernunnos-XLF deficiency." Pediatric Transplantation 13, no. 6 (September 2009): 785–89. http://dx.doi.org/10.1111/j.1399-3046.2008.01028.x.
Full textMahaney, Brandi L., Michal Hammel, Katheryn Meek, John A. Tainer, and Susan P. Lees-Miller. "XRCC4 and XLF form long helical protein filaments suitable for DNA end protection and alignment to facilitate DNA double strand break repair." Biochemistry and Cell Biology 91, no. 1 (February 2013): 31–41. http://dx.doi.org/10.1139/bcb-2012-0058.
Full textBeck, Carole, Sergio Castañeda-Zegarra, Camilla Huse, Mengtan Xing, and Valentyn Oksenych. "Mediator of DNA Damage Checkpoint Protein 1 Facilitates V(D)J Recombination in Cells Lacking DNA Repair Factor XLF." Biomolecules 10, no. 1 (December 30, 2019): 60. http://dx.doi.org/10.3390/biom10010060.
Full textCottarel, Jessica, Philippe Frit, Oriane Bombarde, Bernard Salles, Aurélie Négrel, Stéphanie Bernard, Penny A. Jeggo, Michael R. Lieber, Mauro Modesti, and Patrick Calsou. "A noncatalytic function of the ligation complex during nonhomologous end joining." Journal of Cell Biology 200, no. 2 (January 21, 2013): 173–86. http://dx.doi.org/10.1083/jcb.201203128.
Full textTsai, C. J., S. A. Kim, and G. Chu. "Cernunnos/XLF promotes the ligation of mismatched and noncohesive DNA ends." Proceedings of the National Academy of Sciences 104, no. 19 (April 30, 2007): 7851–56. http://dx.doi.org/10.1073/pnas.0702620104.
Full textRiballo, Enriqueta, Lisa Woodbine, Thomas Stiff, Sarah A. Walker, Aaron A. Goodarzi, and Penny A. Jeggo. "XLF-Cernunnos promotes DNA ligase IV–XRCC4 re-adenylation following ligation." Nucleic Acids Research 37, no. 2 (December 4, 2008): 482–92. http://dx.doi.org/10.1093/nar/gkn957.
Full textDissertations / Theses on the topic "Cernunnos-XLF"
Vera, Gabriella. "Défauts de la réparation de l’ADN et développement lymphoïde : Analyse de situations pathologiques chez l’homme et la souris." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05T028/document.
Full textThroughout their development, hematopoietic cells are exposed to many DNA damages of either exogenous or endogenous origin. Living organisms evolved a variety of DNA repair mechanisms in order to face those threats, and their impairment leads to rare but severe diseases in human. Of the two mechanisms involved in the repair of DNA double-strand break (DSB) repair, one plays a major role in mammal’s Immune System (IS). The non-homologous end joining (NHEJ) pathway is essential for the correct proceeding of V(D)J recombination in lymphocyte progenitors from bone marrow and thymus. Indeed, the formation of DNA DSB is a key step of the rearrangement. In similar fashion, though to a lesser degree, NHEJ is involved in repair of AID induced breaks during immunoglobulin class switch recombination (Ig-CSR). Our team previously identified a new NHEJ factor, Cernunnos (or XLF), as being responsible for a human syndrome of severe combined immunodeficiency (SCID) associated with ionizing radiation (IR) sensitivity (RS-SCID) and microcephaly. To better understand Cernunnos role in the hematopoietic system and particularly in lymphocyte development, we engineered a knock-out (KO) mouse model for this gene. Surprisingly, lymphocyte development is almost normal in these mice, the only defect observed being a decrease of lymphocyte number. However, a refined analysis of T cell repertoire allowed us to uncover a bias in the use of V and J segments from the receptor’s α chain (TCRα). This is the signature of a survival defect in thymocytes, caused by chronic activation of the p53 dependent apoptosis pathway in response to DNA damage. Some discrete T cell populations, such as iNKTs and MAITS, would be affected. In the meantime, our team pursues the uncovering of genetic diseases and their functional description in patients showing signs of immune or hematopoietic deficiency combined to impaired DNA repair. We focused on a patient harboring clinical signs of genomic instability and hematopoietic defects with strong evidence for genetic cause. Thanks to high-throughput DNA sequencing technology and whole genome association study (WGAS), we identified several mutations, one of them striking us as pertinent
Menchon, Grégory. "Criblage virtuel et fonctionnel sur le complexe XRCC4/ADN ligase IV/Cer-XLF de ligature des cassures double-brin de l'ADN : application en radiosensibilisation tumorale." Thesis, Toulouse 3, 2015. http://www.theses.fr/2015TOU30395.
Full textRadiotherapy is a major weapon used against cancer. Radio-induced DNA double strand breaks (DSB) are the main lesions responsible for cell death. Non-homologous end-joining (NHEJ) is a predominant DSB repair mechanism which contributes to cancer cells resistance to radiotherapy. NHEJ is thus a good target for strategies which aim at increasing the radio-sensitivity of tumors. Through in silico screening and biophysical and biochemical assays, our objective was to find specific ligands for the XRCC4/Lig4 and XRCC4/Cer-XLF protein-protein interactions involved in NHEJ. Here, we isolated the first compounds able to prevent their interaction in vitro. These early stage inhibitors are promising tools for cancer therapy with the hope to develop more specific compounds for cellular assays through the 3D structure of the protein/inhibitor complexes
Book chapters on the topic "Cernunnos-XLF"
"XLF/Cernunnos." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 2116. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_18261.
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