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Journal articles on the topic 'Cernunnos'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

Malivert, Laurent, Isabelle Callebaut, Paola Rivera-Munoz, et al. "The C-Terminal Domain of Cernunnos/XLF Is Dispensable for DNA Repair In Vivo." Molecular and Cellular Biology 29, no. 5 (2008): 1116–22. http://dx.doi.org/10.1128/mcb.01521-08.

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ABSTRACT The core nonhomologous end-joining DNA repair pathway is composed of seven factors: Ku70, Ku80, DNA-PKcs, Artemis, XRCC4 (X4), DNA ligase IV (L4), and Cernunnos/XLF (Cernunnos). Although Cernunnos and X4 are structurally related and participate in the same complex together with L4, they have distinct functions during DNA repair. L4 relies on X4 but not on Cernunnos for its stability, and L4 is required for optimal interaction of Cernunnos with X4. We demonstrate here, using in vitro-generated Cernunnos mutants and a series of functional assays in vivo, that the C-terminal region of Ce

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2

Du, Likun, Roujun Peng, Andrea Björkman, et al. "Cernunnos influences human immunoglobulin class switch recombination and may be associated with B cell lymphomagenesis." Journal of Experimental Medicine 209, no. 2 (2012): 291–305. http://dx.doi.org/10.1084/jem.20110325.

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Cernunnos is involved in the nonhomologous end-joining (NHEJ) process during DNA double-strand break (DSB) repair. Here, we studied immunoglobulin (Ig) class switch recombination (CSR), a physiological process which relies on proper repair of the DSBs, in B cells from Cernunnos-deficient patients. The pattern of in vivo generated CSR junctions is altered in these cells, with unusually long microhomologies and a lack of direct end-joining. The CSR junctions from Cernunnos-deficient patients largely resemble those from patients lacking DNA ligase IV, Artemis, or ATM, suggesting that these factor

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3

Çipe, 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.

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Artemis, DNA ligase IV, DNA protein kinase catalytic subunit, and Cernunnos/XLF genes in nonhomologous end joining pathways of DNA repair mechanisms have been identified as responsible for radiosensitive SCID. Here, we present a 3-year-old girl patient with severe growth retardation, bird-like face, recurrent perianal abscess, pancytopenia, and polydactyly. Firstly, she was thought as Fanconi anemia and spontaneous DNA breaks were seen on chromosomal analysis. After that DEB test was found to be normal and Fanconi anemia was excluded. Because of that she had low IgG and IgA levels, normal IgM

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4

Meyer-Bahlburg, Almut, Frank Dressler, and Ulrich Baumann. "Chronic arthritis in a boy with Cernunnos immunodeficiency." Clinical Immunology 154, no. 1 (2014): 47–48. http://dx.doi.org/10.1016/j.clim.2014.06.003.

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5

Vertet, Hugues. "Observations sur le dieu «Cernunnos» de l'autel de Paris." Bulletin de la Société Nationale des Antiquaires de France 1985, no. 1 (1987): 163–77. http://dx.doi.org/10.3406/bsnaf.1987.9155.

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6

Faraci, Maura, Edoardo Lanino, Concetta Micalizzi, et al. "Unrelated hematopoietic stem cell transplantation for Cernunnos-XLF deficiency." Pediatric Transplantation 13, no. 6 (2009): 785–89. http://dx.doi.org/10.1111/j.1399-3046.2008.01028.x.

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7

Dahm, Kirsten. "Role and regulation of human XRCC4-like factor/cernunnos." Journal of Cellular Biochemistry 104, no. 5 (2008): 1534–40. http://dx.doi.org/10.1002/jcb.21726.

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8

SØRENSEN, MARTIN V., HYUN SOO RHO, WON-GI MIN, DONGSUNG KIM, and CHEON YOUNG CHANG. "An exploration of Echinoderes (Kinorhyncha: Cyclorhagida) in Korean and neighboring waters, with the description of four new species and a redescription of E. tchefouensis Lou, 1934." Zootaxa 3368, no. 1 (2012): 161. http://dx.doi.org/10.11646/zootaxa.3368.1.8.

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A large collection of kinorhynch specimens from coastal and subtidal localities around the Korean Peninsula and in the East China Sea was examined, and the material included several species of undescribed or poorly known species of Echinoderes Claparède, 1863. The present paper is part of a series dealing with echinoderid species from this material, and inludes descriptions of four new species of Echinoderes, E. aspinosus sp. nov., E. cernunnos sp. nov., E. microaperturus sp. nov. and E. obtuspinosus sp. nov., and redescriprion of the poorly known Echinoderes tchefouensis Lou, 1934.

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9

Tsai, 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 (2007): 7851–56. http://dx.doi.org/10.1073/pnas.0702620104.

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10

Riballo, 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 (2008): 482–92. http://dx.doi.org/10.1093/nar/gkn957.

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11

Yano, Ken-ichi, Keiko Morotomi-Yano, and Hidenori Akiyama. "Cernunnos/XLF: A new player in DNA double-strand break repair." International Journal of Biochemistry & Cell Biology 41, no. 6 (2009): 1237–40. http://dx.doi.org/10.1016/j.biocel.2008.10.005.

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12

Avagyan, Serine, Michael Churchill, Kenta Yamamoto, et al. "Hematopoietic stem cell dysfunction underlies the progressive lymphocytopenia in XLF/Cernunnos deficiency." Blood 124, no. 10 (2014): 1622–25. http://dx.doi.org/10.1182/blood-2014-05-574863.

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Key Points XLF-deficient mice recapitulate the lymphocytopenia of XLF-deficient patients. Premature aging of hematopoietic stem cells underlies the severe and progressive lymphocytopenia in XLF-deficient mice.

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13

Schwartz, Michal, Yifat S. Oren, Assaf C. Bester, et al. "Impaired Replication Stress Response in Cells from Immunodeficiency Patients Carrying Cernunnos/XLF Mutations." PLoS ONE 4, no. 2 (2009): e4516. http://dx.doi.org/10.1371/journal.pone.0004516.

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14

Çağdaş, Deniz, Tuba Turul Özgür, Gülten Türkkanı Asal, et al. "Two SCID cases with Cernunnos-XLF deficiency successfully treated by hematopoietic stem cell transplantation." Pediatric Transplantation 16, no. 5 (2011): E167—E171. http://dx.doi.org/10.1111/j.1399-3046.2011.01491.x.

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15

Malivert, Laurent, Virginie Ropars, Marcela Nunez, et al. "Delineation of the Xrcc4-interacting Region in the Globular Head Domain of Cernunnos/XLF." Journal of Biological Chemistry 285, no. 34 (2010): 26475–83. http://dx.doi.org/10.1074/jbc.m110.138156.

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16

Zha, S., F. W. Alt, H. L. Cheng, J. W. Brush, and G. Li. "Defective DNA repair and increased genomic instability in Cernunnos-XLF-deficient murine ES cells." Proceedings of the National Academy of Sciences 104, no. 11 (2007): 4518–23. http://dx.doi.org/10.1073/pnas.0611734104.

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17

Li, Gang, Frederick W. Alt, Hwei-Ling Cheng, et al. "Lymphocyte-Specific Compensation for XLF/Cernunnos End-Joining Functions in V(D)J Recombination." Molecular Cell 31, no. 5 (2008): 631–40. http://dx.doi.org/10.1016/j.molcel.2008.07.017.

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18

Hentges, Pierre, Peter Ahnesorg, Robert S. Pitcher, et al. "Evolutionary and Functional Conservation of the DNA Non-homologous End-joining Protein, XLF/Cernunnos." Journal of Biological Chemistry 281, no. 49 (2006): 37517–26. http://dx.doi.org/10.1074/jbc.m608727200.

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19

Revy, Patrick, and Jean-Pierre de Villartay. "Cernunnos, un nouveau facteur de la réparation de l’ADN essentiel pour le système immunitaire." médecine/sciences 22, no. 6-7 (2006): 569–70. http://dx.doi.org/10.1051/medsci/20062267569.

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20

Buck, Dietke, Laurent Malivert, Régina de Chasseval, et al. "Cernunnos, a Novel Nonhomologous End-Joining Factor, Is Mutated in Human Immunodeficiency with Microcephaly." Cell 124, no. 2 (2006): 287–99. http://dx.doi.org/10.1016/j.cell.2005.12.030.

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21

Li, Yi, Dimitri Y. Chirgadze, Victor M. Bolanos-Garcia, et al. "Crystal structure of human XLF/Cernunnos reveals unexpected differences from XRCC4 with implications for NHEJ." EMBO Journal 27, no. 1 (2007): 290–300. http://dx.doi.org/10.1038/sj.emboj.7601942.

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22

Wu, Peï-Yu, Philippe Frit, Laurent Malivert, et al. "Interplay between Cernunnos-XLF and Nonhomologous End-joining Proteins at DNA Ends in the Cell." Journal of Biological Chemistry 282, no. 44 (2007): 31937–43. http://dx.doi.org/10.1074/jbc.m704554200.

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23

Menon, Vijay, and Lawrence F. Povirk. "XLF/Cernunnos: An important but puzzling participant in the nonhomologous end joining DNA repair pathway." DNA Repair 58 (October 2017): 29–37. http://dx.doi.org/10.1016/j.dnarep.2017.08.003.

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24

Ochi, Takashi, Bancinyane Lynn Sibanda, Qian Wu, Dimitri Y. Chirgadze, Victor M. Bolanos-Garcia, and Tom L. Blundell. "Structural Biology of DNA Repair: Spatial Organisation of the Multicomponent Complexes of Nonhomologous End Joining." Journal of Nucleic Acids 2010 (2010): 1–19. http://dx.doi.org/10.4061/2010/621695.

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Nonhomologous end joining (NHEJ) plays a major role in double-strand break DNA repair, which involves a series of steps mediated by multiprotein complexes. A ring-shaped Ku70/Ku80 heterodimer forms first at broken DNA ends, DNA-dependent protein kinase catalytic subunit (DNA-PKcs) binds to mediate synapsis and nucleases process DNA overhangs. DNA ligase IV (LigIV) is recruited as a complex with XRCC4 for ligation, with XLF/Cernunnos, playing a role in enhancing activity of LigIV. We describe how a combination of methods—X-ray crystallography, electron microscopy and small angle X-ray scatterin

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25

Carrillo, Jaime, Oriol Calvete, Laura Pintado-Berninches, et al. "Mutations in XLF/NHEJ1/Cernunnos gene results in downregulation of telomerase genes expression and telomere shortening." Human Molecular Genetics 26, no. 10 (2017): 1900–1914. http://dx.doi.org/10.1093/hmg/ddx098.

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26

Vera, G., P. Rivera-Munoz, V. Abramowski, et al. "Cernunnos Deficiency Reduces Thymocyte Life Span and Alters the T Cell Repertoire in Mice and Humans." Molecular and Cellular Biology 33, no. 4 (2012): 701–11. http://dx.doi.org/10.1128/mcb.01057-12.

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27

Ropars, V., P. Drevet, P. Legrand, et al. "Structural characterization of filaments formed by human Xrcc4-Cernunnos/XLF complex involved in nonhomologous DNA end-joining." Proceedings of the National Academy of Sciences 108, no. 31 (2011): 12663–68. http://dx.doi.org/10.1073/pnas.1100758108.

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28

Cottarel, Jessica, Philippe Frit, Oriane Bombarde, et al. "A noncatalytic function of the ligation complex during nonhomologous end joining." Journal of Cell Biology 200, no. 2 (2013): 173–86. http://dx.doi.org/10.1083/jcb.201203128.

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Nonhomologous end joining is the primary deoxyribonucleic acid (DNA) double-strand break repair pathway in multicellular eukaryotes. To initiate repair, Ku binds DNA ends and recruits the DNA-dependent protein kinase (DNA-PK) catalytic subunit (DNA-PKcs) forming the holoenzyme. Early end synapsis is associated with kinase autophosphorylation. The XRCC4 (X4)–DNA Ligase IV (LIG4) complex (X4LIG4) executes the final ligation promoted by Cernunnos (Cer)–X4-like factor (XLF). In this paper, using a cell-free system that recapitulates end synapsis and DNA-PKcs autophosphorylation, we found a defect

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29

Revy, Patrick, Laurent Malivert, and Jean-Pierre de Villartay. "Cernunnos-XLF, a recently identified non-homologous end-joining factor required for the development of the immune system." Current Opinion in Allergy and Clinical Immunology 6, no. 6 (2006): 416–20. http://dx.doi.org/10.1097/01.all.0000246623.72365.43.

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30

Mahaney, Brandi L., Katheryn Meek, and Susan P. Lees-Miller. "Repair of ionizing radiation-induced DNA double-strand breaks by non-homologous end-joining." Biochemical Journal 417, no. 3 (2009): 639–50. http://dx.doi.org/10.1042/bj20080413.

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DNA DSBs (double-strand breaks) are considered the most cytotoxic type of DNA lesion. They can be introduced by external sources such as IR (ionizing radiation), by chemotherapeutic drugs such as topoisomerase poisons and by normal biological processes such as V(D)J recombination. If left unrepaired, DSBs can cause cell death. If misrepaired, DSBs may lead to chromosomal translocations and genomic instability. One of the major pathways for the repair of IR-induced DSBs in mammalian cells is NHEJ (non-homologous end-joining). The main proteins required for NHEJ in mammalian cells are the Ku het

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31

YU, Y., B. MAHANEY, K. YANO, et al. "DNA-PK and ATM phosphorylation sites in XLF/Cernunnos are not required for repair of DNA double strand breaks." DNA Repair 7, no. 10 (2008): 1680–92. http://dx.doi.org/10.1016/j.dnarep.2008.06.015.

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32

Mahaney, 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 (2013): 31–41. http://dx.doi.org/10.1139/bcb-2012-0058.

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DNA double strand breaks (DSBs), induced by ionizing radiation (IR) and endogenous stress including replication failure, are the most cytotoxic form of DNA damage. In human cells, most IR-induced DSBs are repaired by the nonhomologous end joining (NHEJ) pathway. One of the most critical steps in NHEJ is ligation of DNA ends by DNA ligase IV (LIG4), which interacts with, and is stabilized by, the scaffolding protein X-ray cross-complementing gene 4 (XRCC4). XRCC4 also interacts with XRCC4-like factor (XLF, also called Cernunnos); yet, XLF has been one of the least mechanistically understood pro

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33

Musilli, 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 (2020): 2398–406. http://dx.doi.org/10.1074/jbc.ac119.010924.

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Repair of DNA double-strand breaks by the nonhomologous end joining pathway is central for proper development of the adaptive immune system. This repair pathway involves eight factors, including XRCC4-like factor (XLF)/Cernunnos and the paralog of XRCC4 and XLF, PAXX nonhomologous end joining factor (PAXX). Xlf−/− and Paxx−/− mice are viable and exhibit only a mild immunophenotype. However, mice lacking both PAXX and XLF are embryonic lethal because postmitotic neurons undergo massive apoptosis in embryos. To decipher the roles of PAXX and XLF in both variable, diversity, and joining recombina

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34

Callebaut, Isabelle, Laurent Malivert, Alain Fischer, Jean-Paul Mornon, Patrick Revy, and Jean-Pierre de Villartay. "Cernunnos Interacts with the XRCC4·DNA-ligase IV Complex and Is Homologous to the Yeast Nonhomologous End-joining Factor Nej1." Journal of Biological Chemistry 281, no. 20 (2006): 13857–60. http://dx.doi.org/10.1074/jbc.c500473200.

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35

Yazdani, Reza, Hassan Abolhassani, Javad Tafaroji, et al. "Cernunnos deficiency associated with BCG adenitis and autoimmunity: First case from the national Iranian registry and review of the literature." Clinical Immunology 183 (October 2017): 201–6. http://dx.doi.org/10.1016/j.clim.2017.07.007.

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36

Beck, 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 (2019): 60. http://dx.doi.org/10.3390/biom10010060.

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DNA double-strand breaks (DSBs) trigger the Ataxia telangiectasia mutated (ATM)-dependent DNA damage response (DDR), which consists of histone H2AX, MDC1, RNF168, 53BP1, PTIP, RIF1, Rev7, and Shieldin. Early stages of B and T lymphocyte development are dependent on recombination activating gene (RAG)-induced DSBs that form the basis for further V(D)J recombination. Non-homologous end joining (NHEJ) pathway factors recognize, process, and ligate DSBs. Based on numerous loss-of-function studies, DDR factors were thought to be dispensable for the V(D)J recombination. In particular, mice lacking M

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37

Akopiants, Konstantin, Rui-Zhe Zhou, Susovan Mohapatra та ін. "Requirement for XLF/Cernunnos in alignment-based gap filling by DNA polymerases λ and μ for nonhomologous end joining in human whole-cell extracts". Nucleic Acids Research 37, № 12 (2009): 4055–62. http://dx.doi.org/10.1093/nar/gkp283.

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38

Tilgner, Katarzyna, Irina Neganova, Chatchawan Singhapol, et al. "Brief report: A human induced pluripotent stem cell model of cernunnos deficiency reveals an important role for XLF in the survival of the primitive hematopoietic progenitors." STEM CELLS 31, no. 9 (2013): 2015–23. http://dx.doi.org/10.1002/stem.1456.

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39

Bery, Amandine, Olivier Etienne, Laura Mouton, et al. "XLF/Cernunnos Loss Impairs Mouse Brain Development by Altering Symmetric Proliferative Divisions of Neural Progenitors." SSRN Electronic Journal, 2020. http://dx.doi.org/10.2139/ssrn.3748742.

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40

Roch, Benoit, Vincent Abramowski, Julie Chaumeil, and Jean-Pierre de Villartay. "Cernunnos/Xlf Deficiency Results in Suboptimal V(D)J Recombination and Impaired Lymphoid Development in Mice." Frontiers in Immunology 10 (March 14, 2019). http://dx.doi.org/10.3389/fimmu.2019.00443.

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41

Lescale, Chloé, Vincent Abramowski, Marie Bedora-Faure, et al. "RAG2 and XLF/Cernunnos interplay reveals a novel role for the RAG complex in DNA repair." Nature Communications 7, no. 1 (2016). http://dx.doi.org/10.1038/ncomms10529.

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