Relevant bibliographies by topics / XRCC4/ADN ligase IV/Cernunnos-XLF

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'XRCC4/ADN ligase IV/Cernunnos-XLF'

Author: Grafiati
Published: 7 September 2022
Last updated: 18 September 2022

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Journal articles on the topic "XRCC4/ADN ligase IV/Cernunnos-XLF"

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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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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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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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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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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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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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Roch, Benoit, Vincent Abramowski, Olivier Etienne, et al. "A XRCC4 mutant mouse, a model for human X4 syndrome, reveals interplays with Xlf, PAXX, and ATM in lymphoid development." eLife 10 (September 14, 2021). http://dx.doi.org/10.7554/elife.69353.

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We developed a Xrcc4M61R separation of function mouse line to overcome the embryonic lethality of Xrcc4 deficient mice. XRCC4M61R protein does not interact with Xlf, thus obliterating XRCC4-Xlf filament formation while preserving the ability to stabilize DNA Ligase IV. X4M61R mice, which are DNA repair deficient, phenocopy the Nhej1-/- (known as Xlf -/-) setting with a minor impact on the development of the adaptive immune system. The core NHEJ DNA repair factor XRCC4 is therefore not mandatory for V(D)J recombination aside from its role in stabilizing DNA ligase IV. In contrast, Xrcc4M61R mic
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Tang, Jialin, Zhongxia Li, Qiong Wu, Muhammad Irfan, Weili Li, and Xiangyu Liu. "Role of Paralogue of XRCC4 and XLF in DNA Damage Repair and Cancer Development." Frontiers in Immunology 13 (March 2, 2022). http://dx.doi.org/10.3389/fimmu.2022.852453.

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Non-homologous end joining (cNHEJ) is a major pathway to repair double-strand breaks (DSBs) in DNA. Several core cNHEJ are involved in the progress of the repair such as KU70 and 80, DNA-dependent protein kinase catalytic subunit (DNA-PKcs), Artemis, X-ray repair cross-complementing protein 4 (XRCC4), DNA ligase IV, and XRCC4-like factor (XLF). Recent studies have added a number of new proteins during cNHEJ. One of the newly identified proteins is Paralogue of XRCC4 and XLF (PAXX), which acts as a scaffold that is required to stabilize the KU70/80 heterodimer at DSBs sites and promotes the ass
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Dissertations / Theses on the topic "XRCC4/ADN ligase IV/Cernunnos-XLF"

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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.

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En cancérologie, la radiothérapie est une des armes essentielles pour éradiquer les cellules tumorales. Les cassures des deux brins de l'ADN dites "double-brin" qu'elle induit sont particulièrement toxiques et constituent la principale cause de mort cellulaire. La NHEJ (Jonction d'Extrémités Non-Homologues) est la voie métabolique majeure de réparation de ces cassures double-brin de l'ADN et par ce mécanisme, les cellules humaines adoptent une résistance à la radiothérapie. Ce mécanisme de réparation constitue donc une cible de choix pour un traitement anticancéreux combiné en vue d'augmenter
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De, Melo Abinadabe Jackson. "Molecular basis for the structural role of human DNA ligase IV." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4040.

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Les défauts dans la réparation des cassures double-brin de l'ADN (DSBs) peuvent avoir d'importantes conséquences pouvant entrainer une instabilité génomique et conduire à la mort cellulaire ou au développement de cancers. Dans la plupart des cellules mammifères, le mécanisme de Jonction des Extrémités Non Homologues (NHEJ) est le principal mécanisme de réparation des DSBs. L'ADN Ligase IV (LigIV) est une protéine unique dans sa capacité à promouvoir la NHEJ classique. Elle s'associe avec deux autres protéines structuralement similaires, XRCC4 et XLF (ou Cernunnos). LigIV interagit directement
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Amram, Jérémy. "Etude structurale et fonctionnelle des complexes multi-protéiques de la voie de réparation NHEJ chez l’homme." Thesis, Paris 11, 2015. http://www.theses.fr/2015PA114822/document.

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La voie de réparation NHEJ (Non-Homologous End-Joining) est une voie majeure de réparation des cassures double-brin chez l’homme. Les protéines de cette voie interagissent et forment des complexes dynamiques dont les mécanismes moléculaires sont encore largement méconnus. Nous avons dans un premier temps mis au point des protocoles de production à l’échelle de plusieurs milligrammes des protéines cœur de la voie NHEJ en cellules d’insecte à l’aide du système MultiBac. Nous avons ainsi purifié les complexes Ku70/Ku80 et Ligase4/XRCC4 et les protéines Cernunnos et Artemis à homogénéité. Des essa
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