Relevant bibliographies by topics / ADN Ligase

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Academic literature on the topic 'ADN Ligase'

Author: Grafiati
Published: 4 May 2024

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Journal articles on the topic "ADN Ligase"

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Lee, Jaeseok, Youngjun Lee, Young Mee Jung, Ju Hyun Park, Hyuk Sang Yoo, and Jongmin Park. "Discovery of E3 Ligase Ligands for Target Protein Degradation." Molecules 27, no. 19 (October 2, 2022): 6515. http://dx.doi.org/10.3390/molecules27196515.

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Target protein degradation has emerged as a promising strategy for the discovery of novel therapeutics during the last decade. Proteolysis-targeting chimera (PROTAC) harnesses a cellular ubiquitin-dependent proteolysis system for the efficient degradation of a protein of interest. PROTAC consists of a target protein ligand and an E3 ligase ligand so that it enables the target protein degradation owing to the induced proximity with ubiquitin ligases. Although a great number of PROTACs has been developed so far using previously reported ligands of proteins for their degradation, E3 ligase ligands have been mostly limited to either CRBN or VHL ligands. Those PROTACs showed their limitation due to the cell type specific expression of E3 ligases and recently reported resistance toward PROTACs with CRBN ligands or VHL ligands. To overcome these hurdles, the discovery of various E3 ligase ligands has been spotlighted to improve the current PROTAC technology. This review focuses on currently reported E3 ligase ligands and their application in the development of PROTACs.
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Tomkinson, Alan E., Tasmin Naila, and Seema Khattri Bhandari. "Altered DNA ligase activity in human disease." Mutagenesis 35, no. 1 (October 20, 2019): 51–60. http://dx.doi.org/10.1093/mutage/gez026.

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Abstract The joining of interruptions in the phosphodiester backbone of DNA is critical to maintain genome stability. These breaks, which are generated as part of normal DNA transactions, such as DNA replication, V(D)J recombination and meiotic recombination as well as directly by DNA damage or due to DNA damage removal, are ultimately sealed by one of three human DNA ligases. DNA ligases I, III and IV each function in the nucleus whereas DNA ligase III is the sole enzyme in mitochondria. While the identification of specific protein partners and the phenotypes caused either by genetic or chemical inactivation have provided insights into the cellular functions of the DNA ligases and evidence for significant functional overlap in nuclear DNA replication and repair, different results have been obtained with mouse and human cells, indicating species-specific differences in the relative contributions of the DNA ligases. Inherited mutations in the human LIG1 and LIG4 genes that result in the generation of polypeptides with partial activity have been identified as the causative factors in rare DNA ligase deficiency syndromes that share a common clinical symptom, immunodeficiency. In the case of DNA ligase IV, the immunodeficiency is due to a defect in V(D)J recombination whereas the cause of the immunodeficiency due to DNA ligase I deficiency is not known. Overexpression of each of the DNA ligases has been observed in cancers. For DNA ligase I, this reflects increased proliferation. Elevated levels of DNA ligase III indicate an increased dependence on an alternative non-homologous end-joining pathway for the repair of DNA double-strand breaks whereas elevated level of DNA ligase IV confer radioresistance due to increased repair of DNA double-strand breaks by the major non-homologous end-joining pathway. Efforts to determine the potential of DNA ligase inhibitors as cancer therapeutics are on-going in preclinical cancer models.
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Cao, Weiguo. "DNA ligases and ligase-based technologies." Clinical and Applied Immunology Reviews 2, no. 1 (November 2001): 33–43. http://dx.doi.org/10.1016/s1529-1049(01)00039-3.

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Fang, Deyu, An Chen, and Sang-Myeong Lee. "Inhibition of activation-induced T cell death by AIP2-mediated ubiquitination of EGR2 (35.20)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 35.20. http://dx.doi.org/10.4049/jimmunol.182.supp.35.20.

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Abstract E3 ubiquitin ligases, which target specific molecules for proteolytic destruction, have emerged as key regulators of immune functions. Several E3 ubiquitin ligases, including c-Cbl, Cbl-b, GRAIL, Itch, and Nedd4, have been shown to negatively regulate T-cell activation. Here we report that the HECT-type E3 ligase, AIP2, positively regulates T-cell activation. Ectopic expression of AIP2 in mouse primary T cells enhances their proliferation and IL-2 production by suppressing apoptosis of T cells. AIP2 interacts with and promotes ubiquitin-mediated degradation of EGR2, a zinc finger transcription factor that has been found to regulate Fas ligand (FasL) expression during activation-induced T cell death. Suppression of AIP2 expression by small RNA interference upregulates EGR2 and FasL expression and enhances the apoptosis of T cells. Therefore, AIP2 regulates activation-induced T cell death by suppressing EGR2-mediated FasL expression via the ubiquitin pathway.
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Kennan, Alan J., V. Haridas, Kay Severin, David H. Lee, and M. Reza Ghadiri. "Ade NovoDesigned Peptide Ligase: A Mechanistic Investigation." Journal of the American Chemical Society 123, no. 9 (March 2001): 1797–803. http://dx.doi.org/10.1021/ja991266c.

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Fanucci, Francesco. "Quaternary shorelines and continental shelf of the Ligurian coast." Zeitschrift für Geomorphologie 31, no. 4 (December 17, 1987): 463–72. http://dx.doi.org/10.1127/zfg/31/1987/463.

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Gu, Jiafeng, Haihui Lu, Brigette Tippin, Noriko Shimazaki, Myron F. Goodman, and Michael R. Lieber. "XRCC4:DNA ligase IV can ligate incompatible DNA ends and can ligate across gaps." EMBO Journal 26, no. 14 (July 25, 2007): 3506–7. http://dx.doi.org/10.1038/sj.emboj.7601729.

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Thayale Purayil, Fayas, Naganeeswaran Sudalaimuthuasari, Ling Li, Ruwan Aljneibi, Aysha Mohammed Khamis Al Shamsi, Nelson David, Martin Kottackal, et al. "Transcriptome Profiling and Functional Validation of RING-Type E3 Ligases in Halophyte Sesuvium verrucosum under Salinity Stress." International Journal of Molecular Sciences 23, no. 5 (March 4, 2022): 2821. http://dx.doi.org/10.3390/ijms23052821.

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Owing to their sessile nature, plants have developed a tapestry of molecular and physiological mechanisms to overcome diverse environmental challenges, including abiotic stresses. Adaptive radiation in certain lineages, such as Aizoaceae, enable their success in colonizing arid regions and is driven by evolutionary selection. Sesuvium verrucosum (commonly known as Western sea-purslane) is a highly salt-tolerant succulent halophyte belonging to the Aizoaceae family; thus, it provides us with the model-platform for studying plant adaptation to salt stress. Various transcriptional and translational mechanisms are employed by plants to cope with salt stress. One of the systems, namely, ubiquitin-mediated post-translational modification, plays a vital role in plant tolerance to abiotic stress and other biological process. E3 ligase plays a central role in target recognition and protein specificity in ubiquitin-mediated protein degradation. Here, we characterize E3 ligases in Sesuvium verrucosum from transcriptome analysis of roots in response to salinity stress. Our de novo transcriptome assembly results in 131,454 transcripts, and the completeness of transcriptome was confirmed by BUSCO analysis (99.3% of predicted plant-specific ortholog genes). Positive selection analysis shows 101 gene families under selection; these families are enriched for abiotic stress (e.g., osmotic and salt) responses and proteasomal ubiquitin-dependent protein catabolic processes. In total, 433 E3 ligase transcripts were identified in S. verrucosum; among these transcripts, single RING-type classes were more abundant compared to multi-subunit RING-type E3 ligases. Additionally, we compared the number of single RING-finger E3 ligases with ten different plant species, which confirmed the abundance of single RING-type E3 ligases in different plant species. In addition, differential expression analysis showed significant changes in 13 single RING-type E3 ligases (p-value < 0.05) under salinity stress. Furthermore, the functions of the selected E3 ligases genes (12 genes) were confirmed by yeast assay. Among them, nine genes conferred salt tolerance in transgenic yeast. This functional assay supports the possible involvement of these E3 ligase in salinity stress. Our results lay a foundation for translational research in glycophytes to develop stress tolerant crops.
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Gong, Yao, and Yue Chen. "UbE3-APA: a bioinformatic strategy to elucidate ubiquitin E3 ligase activities in quantitative proteomics study." Bioinformatics 38, no. 8 (February 9, 2022): 2211–18. http://dx.doi.org/10.1093/bioinformatics/btac069.

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Abstract Motivation Ubiquitination is widely involved in protein homeostasis and cell signaling. Ubiquitin E3 ligases are critical regulators of ubiquitination that recognize and recruit specific ubiquitination targets for the final rate-limiting step of ubiquitin transfer reactions. Understanding the ubiquitin E3 ligase activities will provide knowledge in the upstream regulator of the ubiquitination pathway and reveal potential mechanisms in biological processes and disease progression. Recent advances in mass spectrometry-based proteomics have enabled deep profiling of ubiquitylome in a quantitative manner. Yet, functional analysis of ubiquitylome dynamics and pathway activity remains challenging. Results Here, we developed a UbE3-APA, a computational algorithm and stand-alone python-based software for Ub E3 ligase Activity Profiling Analysis. Combining an integrated annotation database with statistical analysis, UbE3-APA identifies significantly activated or suppressed E3 ligases based on quantitative ubiquitylome proteomics datasets. Benchmarking the software with published quantitative ubiquitylome analysis confirms the genetic manipulation of SPOP enzyme activity through overexpression and mutation. Application of the algorithm in the re-analysis of a large cohort of ubiquitination proteomics study revealed the activation of PARKIN and the co-activation of other E3 ligases in mitochondria depolarization-induced mitophagy process. We further demonstrated the application of the algorithm in the DIA (data-independent acquisition)-based quantitative ubiquitylome analysis. Availability and implementation Source code and binaries are freely available for download at URL: https://github.com/Chenlab-UMN/Ub-E3-ligase-Activity-Profiling-Analysis, implemented in python and supported on Linux and MS Windows. Supplementary information Supplementary data are available at Bioinformatics online.
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Alomari, Arqam, Robert Gowland, Callum Southwood, Jak Barrow, Zoe Bentley, Jashel Calvin-Nelson, Alice Kaminski, et al. "Identification of Novel Inhibitors of Escherichia coli DNA Ligase (LigA)." Molecules 26, no. 9 (April 25, 2021): 2508. http://dx.doi.org/10.3390/molecules26092508.

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Present in all organisms, DNA ligases catalyse the formation of a phosphodiester bond between a 3′ hydroxyl and a 5′ phosphate, a reaction that is essential for maintaining genome integrity during replication and repair. Eubacterial DNA ligases use NAD+ as a cofactor and possess low sequence and structural homology relative to eukaryotic DNA ligases which use ATP as a cofactor. These key differences enable specific targeting of bacterial DNA ligases as an antibacterial strategy. In this study, four small molecule accessible sites within functionally important regions of Escherichia coli ligase (EC-LigA) were identified using in silico methods. Molecular docking was then used to screen for small molecules predicted to bind to these sites. Eight candidate inhibitors were then screened for inhibitory activity in an in vitro ligase assay. Five of these (geneticin, chlorhexidine, glutathione (reduced), imidazolidinyl urea and 2-(aminomethyl)imidazole) showed dose-dependent inhibition of EC-LigA with half maximal inhibitory concentrations (IC50) in the micromolar to millimolar range (11–2600 µM). Two (geneticin and chlorhexidine) were predicted to bind to a region of EC-LigA that has not been directly investigated previously, raising the possibility that there may be amino acids within this region that are important for EC-LigA activity or that the function of essential residues proximal to this region are impacted by inhibitor interactions with this region. We anticipate that the identified small molecule binding sites and inhibitors could be pursued as part of an antibacterial strategy targeting bacterial DNA ligases.
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Dissertations / Theses on the topic "ADN Ligase"

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Touzé, Elodie Giegé Richard. "Cristallogenèse et études structurales appliquées aux aminoacyl-ARNt synthétases." Strasbourg : Université Louis Pasteur, 2008. http://eprints-scd-ulp.u-strasbg.fr:8080/911/01/TOUZE_Elodie_2007.pdf.

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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 la sensibilité des cellules cancéreuses aux rayons ionisants (radiosensibilisation). Au cours du mécanisme NHEJ, la ligature finale des extrémités d'ADN est assurée par le complexe protéique tripartite: XRCC4/ADN Ligase IV/Cernunnos-XLF. Les interfaces protéiques concernées représentent toutes des cibles potentielles dans une stratégie rationnelle d'isolement de molécules inhibitrices, guidée par les structures tridimensionnelles de chaque protéine. A travers des expériences de criblage virtuel et de validation à la fois biophysique et biochimique, nous avons isolé les premières molécules capable de prévenir in vitro les interactions protéine-protéine pour les complexes XRCC4/Lig4 et XRCC4/Cer-XLF, respectivement. Ces composés sont des points de départ pour l'élaboration d'inhibiteurs potentiels de plus haute affinité grâce à l'apport de la biologie structurale, en vue d'un effet radiosensibilisant cellulaire
Radiotherapy 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
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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 avec XRCC4 pour former un complexe stable, tandis que l'interaction entre XLF et ce complexe est médiée par XRCC4. XLF stimule fortement l'activité de ligation du complexe LigIV/XRCC4 par un mécanisme encore indéterminé. Récemment, un rôle structurel non catalytique a été attribué à LigIV (Cottarel et al., 2013). Dans le travail de thèse présenté ici, nous avons reconstitué l'étape de ligation de la NHEJ en utilisant des protéines recombinantes produites dans des bactéries afin d’une part, d'explorer les bases moléculaires du rôle structural de LigIV, d’autre part de comprendre le mécanisme par lequel XLF stimule le complexe de ligation, et enfin de mieux comprendre comment ces trois protéines coopèrent au cours de la NHEJ. Nos analyses biochimiques suggèrent que XLF via son interaction avec XRCC4 lié à LigIV, pourrait induire un changement conformationnel dans la LigIV. Ce réarrangement de la ligase exposerait son interface de liaison à l'ADN ce qui lui permettrait alors de ponter deux molécules indépendantes d'ADN, une capacité indépendante de l'activité catalytique de LigIV
Failure to repair DNA double-strand breaks (DSBs) may have deleterious consequences inducing genomic instability and even cell death. In most mammalian cells, Non-Homologous End Joining (NHEJ) is a prominent DSB repair pathway. DNA ligase IV (LigIV) is unique in its ability to promote classical NHEJ. It associates with two structurally related proteins called XRCC4 and XLF (aka Cernunnos). LigIV directly interacts with XRCC4 forming a stable complex while the XLF interaction with this complex is mediated by XRCC4. XLF strongly stimulates the ligation activity of the LigIV/XRCC4 complex by an unknown mechanism. Recently, a structural noncatalytic role of LigIV has been uncovered (Cottarel et al., 2013). Here, we have reconstituted the end joining ligation step using recombinant proteins produced in bacteria to explore not only the molecular basis for the structural role of LigIV, but also to understand the mechanism by which XLF stimulates the ligation complex, and how these three proteins work together during NHEJ. Our biochemical analysis suggests that XLF, through interactions with LigIV/XRCC4 complex, could induce a conformational change in LigIV. Rearrangement of the LigIV would expose its DNA binding interface that is able to bridge two independent DNA molecules. This bridging ability is fully independent of LigIV’s catalytic activity. We have mutated this interface in order to attempt to disrupt the newly identified DNA bridging ability. In vitro analysis of this LigIV mutant will be presented as well as a preliminary in vivo analysis
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Wu, Pei-Yu. "Le complexe de ligation dans la réaction de réparation des cassures de l'ADN par recombination non homologué." Toulouse 3, 2008. http://www.theses.fr/2008TOU30064.

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Les cassures double-brin (CDB) de l'ADN sont produites lors d'événements physiologiques ou physiopathologiques comme la recombinaison V(D)J, le blocage de fourches de replication, ou bien induites par des agents physiques ou chimiques à activité clastogène. Les CDB représentent une lésion hautement toxique et sont réparées par recombinaison homologue ou par recombinaison non-homologue (NHEJ). Chez les mammifères, la voie NHEJ représente le processus majoritaire de réparation responsable de la survie cellulaire après endommagement de l'ADN. Suite à la production de CDB, par exemple par des rayonnements ionisants (RI), l'he��térodimère Ku70/80 se lie aux extrémités de la cassure et recrute la sous-unité catalytique DNA-PKcs. Ce Complexe-1 ou DNA-PK (i. E Ku70/Ku80/DNA-PKcs) forme une synapse qui maintient rapprochées les extrémités de la cassure, acquiert une activité sérine-thréonine kinase qui par auto-phosphorylation de la DNA-PKcs induit un changement de conformation favorisant le recrutement du 2ème complexe impliqué dans la ligation des extrémités. Ce Complexe-2 est un hétérotrimère composé de XRCC4, Ligase IV et Cernnunos-XLF. Ce travail a eu pour objectif de mieux comprendre les interactions internes et externes des partenaires du Complexe-2. Nous avons établi le domaine minimal d'interaction fonctionnelle de la Ligase IV (XIR-BRCT2) avec XRCC4 et montré que son expression cellulaire induit une sensibilisation au RI et autres agents clastogènes. Le mécanisme de sensibilisation repose sur un déplacement de la Ligase IV du Complexe-2 suivie de sa dégradation aboutissant à une perte de recrutement stable du complexe sur la chromatine endommagée. .
DNA double-strand breaks (DSBs) are the most lethal threats among all the DNA damages in cells. They can arise not only endogenously from normal physiological processes such as V(D)J recombination or toxic lesions like DNA replication forks collapses, but also exogenously from DNA damaging agents like ionizing radiation (IR) or radiomimetic compounds. In mammals, DSBs are mainly repaired by homologous recombination (HR) during S and G2 phases of the cell cycle when sister chromatids are available, and, more predominantly, in all the phases of cell cycle by the non-homologous end-joining (NHEJ) pathway without any requirement for homology guidance. The NHEJ machinery is also involved in V(D)J recombination to rearrange B-cell immunoglobulin and T-cell receptor genes. Deficiency in NHEJ consequently results in hypersensitivity to IR, immunodeficiency, as well as chromosomal instability. After DSBs induction, Ku70/Ku80 heterodimer binds to free DNA ends, allowing the subsequent recruitment and activation of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs). The resulting DNA-PK holoenzyme (i. E. Ku/DNA-PKcs or Complex-1) tethers two DNA termini and form the synaptic complex that may further activates DNA-PKcs by several (auto)phosphorylation events. Upon activation, Complex-1 undergoes conformational changes to accommodate the ligation complex (Complex-2) and accessory factors that make DNA ends compatible with ligation, when necessary. Complex-2 comprises XRCC4, DNA LigIV (LigIV) and the more recently identified factor Cernunnos-XLF (Cer-XLF). The three partners interact with each other and Complex-2 also binds Complex-1 and accessory factors, thus accounting for its highly efficient end-joining activity. In this work we aimed at characterizing the intimate interaction network between Complex-2 factors. .
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Nassar, Joelle. "Caractérisation de la fonction de OBI1, une E3 ubiquitine ligase, dans la réplication de l'ADN." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTT039.

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La division cellulaire est l’un des processus cellulaires les plus complexes. Pour que cette division se déroule correctement, la cellule doit répliquer de manière fiable l’intégralité de son génome. Durant ce processus, la réplication de l’ADN est initiée a des sites prédéfinis du génome, appelés « origines de réplication ». Vu qu’un dysfonctionnement de l'activité des origines est lié à plusieurs pathologies humaines, leur activation doit être hautement régulée. Plusieurs protéines ont été trouvées aux origines de la réplication, mais aucune n’explique comment ces origines sont reconnues et sélectionnées pour l’activation. Notre groupe de recherche vise à comprendre comment les origines de réplication sont régulées dans les cellules de métazoaires. Dans ce but, une approche protéomique a été réalisée pour définir l'interactome des origines de réplication humaine, dans l’objectif d'identifier de nouveaux facteurs qui pourraient être impliqués dans la régulation des origines. À l'aide de cette approche, une nouvelle ubiquitine ligase, nommée OBI1 (ORC-ubiquitine-ligase-1), a été identifiée avant mon arrivée au laboratoire. OBI1 se lie au complexe de reconnaissance des origines (complexe ORC) et mon projet vise à mieux caractériser le rôle de cette nouvelle protéine dans la réplication de l'ADN. Notre stratégie expérimentale est basée sur deux modèles différents: un modèle in vivo de cellules humaines en culture et un système de réplication de l'ADN in vitro dérivé d'œufs de Xénope.Nos analyses sur des cellules humaines ont d’abord révélé qu’OBI1 était crucial pour la prolifération cellulaire. Cette observation a été ensuite attribuée à son rôle dans la réplication de l’ADN et plus précisément dans l’activation des origines de réplication. En effet, la déplétion d’OBI1 a montré une diminution de recrutement à la chromatine de facteurs impliqués dans l’activation des origines. De plus, une analyse fonctionnelle a montré qu'OBI1 multiubiquitine ORC3 et ORC5, deux sous-unités du complexe ORC. Cette ubiquitination a été ensuite liée au rôle d’OBI1 dans l’activation des origines de réplication, après que la surexpression des mutants ORC3 / 5 non-ubiquitinables ait donné des résultats similaires à ceux observés lors de la déplétion d’OBI1. Dans l’ensemble, nos résultats ont démontré qu’OBI1 est une protéine essentielle à l’activation des origines et nous ont permis de mettre en place une hypothèse suggérant qu’en ubiquitinant ORC3/5, OBI1 pourrait jouer un rôle dans la sélection des origines destinées à l’activation, parmi toutes les origines définies antérieurement. Après cette étude, maintenant publiée, nous avons voulu aborder le rôle de la multiubiquitination des ORC dans l’activation des origines. Nos expériences préliminaires suggèrent un rôle de l'histone acétyl-transférase (HAT) GCN5 / KAT2A.Dans la deuxième partie de mon projet, nous avons utilisé le système in vitro, basé sur des extraits d'œufs de xénope, pour étudier le rôle de l'OBI1 et de l'ubiquitination dans l'activation des origines de réplication. Nos analyses ont confirmé la conservation d’OBI1 chez Xenopus Laevis et son recrutement a la chromatine lors de la réplication. Nous avons montré que l'ubiquitination se produit sur la chromatine lors de l'activation de l'origine. De plus, en utilisant des inhibiteurs de E1, nous avons constaté que l’ubiquitination est importante pour l’activation des origines. De façon intéressante, la déplétion de OBI1 dans ce système embryonnaire a suggéré un rôle diffèrent d’OBI1 dans l’activation des origines dans le système embryonnaire comparé aux conditions plus somatiques.Finalement, la découverte de ce nouveau facteur d'initiation a fourni des informations essentielles sur le rôle de l'ubiquitination et d’OBI1 dans l'activation et la sélection des origines de réplication. Une telle sélection pourrait également participer à la régulation du « timing » de la réplication de l'ADN
Cell division is one of the most complex processes a cell undergoes. For this to happen properly, the genetic material stored in a cell must be faithfully copied or replicated. During this process, DNA replication is initiated at pre-defined sites in the genome, called "origins of replication". The activation of these origins is highly regulated, as a dysfunction in origin activity is linked to several human pathologies. Several proteins have been found at replication origins, but none of them explain how to be activated origins are recognized and selected. Our research group aims to understand how DNA replication origins are regulated in metazoan cells, to this aim, a proteomic approach was performed to define the interactome of human replication origins. Our goal was to identify new factors that could be involved in replication origin regulation. Using this methodology, a novel E3 ubiquitin ligase, named OBI1 (for ORC-ubiquitin-ligase-1), was identified prior to my arrival in the laboratory. OBI1 binds the origin recognition complex (ORC complex) and my project aimed at further characterizing the role of this new protein in DNA replication. Our experimental strategy used two different model systems: an in-vivo model based on human cells in culture, and an in-vitro DNA replication system derived from Xenopus eggs.Our analyses in human cells revealed that OBI1 was a crucial gene involved in cellular proliferation, this observation was later attributed to OBI1’s role in DNA replication and more specifically, to replication origin activation. Indeed, OBI1 knockdown resulted in a deficient origin firing and a decrease in the chromatin recruitment of factors involved in origin firing. A further functional analysis showed that OBI1 multiubiquitylates two subunits of the ORC complex, ORC3 and ORC5. This ubiquitylation was directly linked to OBI1’s role in origin firing, after the over-expression of non-ubiquitylable ORC3/5 mutants yielded similar results to OBI1’s knock down. Altogether, our results demonstrated that OBI1 encoded for a protein essential for origin activation, and allowed us to propose its main role: by multiubiquitylating a subset of the ORC complex, OBI1 could select the replication origins to be activated amongst all the potential replication origins set in G1 phase of the cell cycle. After this set of experiments, now published, we wanted to address the mechanistic impact of the multiubiquitylation of ORC on origin activation. Our preliminary experiments suggest a role of the histone acetyl-transferase (HAT) GCN5/KAT2A in the “OBI1 pathway”In the second part of my project, we used the in vitro DNA replication system, based on Xenopus laevis egg extracts, to study the role of OBI1 and ubiquitylation in origin activation. Our in-vitro analyses confirmed the conservation of OBI1 in Xenopus Laevis and its recruitment to the chromatin during DNA replication. We showed that de novo ubiquitylation takes place on chromatin during origin activation. Moreover, using E1 inhibitors, we found that active ubiquitylation is important for efficient origin firing. Interestingly, our loss of function experiments suggested that OBI1’s impact on origin activation could defer in early development when compared to somatic-like conditions.Taken together, the discovery of this new replication initiation factor provided key information on the role of ubiquitylation in general and OBI1 in particular on origin activation and selection. Such selection could participate as well in the regulation of the timing of DNA replication
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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 essais de cristallisation, des études par SAXS et des analyses par microscopie électronique ont été réalisés sur différents complexes formés par ces protéines cœur du NHEJ. Nous avons également caractérisé par chromatographie d’exclusion de taille et calorimétrie, les interactions effectuées entre les protéines de la voie NHEJ. L’ensemble de ces travaux a permis d’établir des bases biochimiques solides en vue des études structurales et fonctionnelles de la voie NHEJ chez l’homme
Human DNA repair pathway NHEJ (Non-Homologous End-Joining) is a major pathway of double-strand breaks repair. The proteins involved in this pathway interact and form dynamic complexes whose molecular mechanisms are largely unknown. Firstly, we established protocols to be able to purify milligrams of those NHEJ pathway core proteins using MultiBac insect cells system. We then purified Ku70/Ku80 and Ligase4/XRCC4 complexes, Artemis and Cernunnos to homogeneity. Crystallogenesis assays, SAXS experiments and Transmission Electronic Microscopy experiments have been performed on several complexes formed by these core NHEJ proteins. We also characterized the interactions between these proteins by Size Exclusion Chromatography and Isothermal Calorimetry. These experiments have led to biochemical results sufficient to establish a solid basis to initiate the structural and functional study of the Human NHEJ Pathway
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Aoufouchi, Said. "Adn ligases chez les eucaryotes superieurs." Rennes 1, 1992. http://www.theses.fr/1992REN10016.

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L'adn ligase i humaine est une proteine de 130 kda, tres sensible aux phenomenes de proteolyse et genere plusieurs produits de degradation qui conservent une activite adn ligase. Des difficultes d'ordre quantitatifs et qualitatifs, nous ont amene a changer le modele experimental pour purifier cette enzyme. Notre choix s'est porte sur l'uf de l'amphibien xenopus laevis du fait de sa grande disponibilite, et sa richesse en enzymes liees a la replication de l'adn. L'adn ligase i du xenope est une proteine 180 kda egalement sujette aux phenomenes de proteolyses qui generent majoritairement deux polypeptides de 130 et 76 kda. La purification du polypeptide 180 kda nous a permis de preparer des anticorps specifiques. L'adn ligase i du xenope est une enzyme nucleaire, presente des le premier stade de l'ovogenese et qui s'accumule progressivement jusqu'au stade v. Sa quantite demeure constante au moins jusqu'au stade bourgeon caudal. L'adn ligase ii de xenope est une proteine de poids moleculaire apparent de 80 kda. Elle n'est pas reconnue par les anticorps anti-adn ligase i. Elle est presente dans les ovocytes, les ufs vierges et apres la fecondation. Nous avons montre de facon claire que contrairement a ce qui etait decrit dans la litterature l'adn ligase i chez les deux amphibiens axolotl et pleurodele est presente avant la fecondation. Ceci est egalement vrai chez l'oursin
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Castagné, Claire. "Analyse par résonance magnétique nucléaire des interactions ADN-protéine : étude des facteurs de transcription Rev-erb [bêta] et SRY ; détermination de la structure secondaire du domaine C-terminal de la tyrosyl'RNA synthétase." Université Joseph Fourier (Grenoble), 1999. http://www.theses.fr/1999GRE10039.

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Le passage de l'adn aux proteines est une succession de reactions compliquees mais il peut etre decompose de facon simple en deux etapes principales : la transcription, qui copie fidelement l'information codee par l'adn en molecules d'arn messager, et la traduction de ces arns messagers en proteines. Pour activer la transcription d'un gene, des facteurs nommes facteurs de transcription doivent se fixer a leurs promoteurs. Nous avons etudie les interactions adn - proteine de deux d'entre eux : rev-erb et sry. D'une part, l'element de reponse aux hormones de rev-erb , le 15 mere rev-re, a ete modelise en se basant sur les contraintes obtenues par rmn. Sous sa forme libre, cette molecule d'adn adopte une conformation d'adn b quasi canonique. Les premieres etudes sur le complexe rev-erb - rev-re montrent que d'importantes deformations du duplex d'adn apparaissent. D'autre part, les complexes sry-8 mere et sry-14 mere ont ete analyses par rmn du phosphore et pour la premiere fois l'attribution complete de tous les signaux phosphore dans un complexe adn - proteine a ete realisee. Au niveau de l'etape de traduction, chaque codon de l'arn messager est reconnu par l'anticodon equivalent d'un arn de transfert charge avec l'acide amine apparente. Le chargement (ou aminoacylation) specifique d'un acide amine sur son arn de transfert apparente est catalyse par les aminoacyl-trna synthetases (aarss). La structure du domaine c-terminal de la tyrosine trna synthetase (tyrrs) de bacillus stearothermophilus est etudiee par rmn heteronucleaire et l'analyse des spectres tridimensionnelles ( 1 3c- 1 5n- 1h) nous a permis d'identifier les elements de structure secondaire qu'une etude cristallographique n'avait pas pu reveler.
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Touzé, Elodie. "Cristallogenèse et études structurales appliquées aux aminoacyl-ARNt synthétases." Phd thesis, Université Louis Pasteur - Strasbourg I, 2007. http://tel.archives-ouvertes.fr/tel-00206952.

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La GlnRS de Deinococcus radiodurans se distingue des autres GlnRS par la présence d'un appendice additionnel en C-terminal (C-ter). Celui-ci adopterait le même repliement que la famille de protéines YqeY de fonction inconnue et une région de la sous-unité GatB de l'AdT. Son architecture atypique, trouvée dans 4 organismes, corresponds à la fusion de protéine de la voie directe et indirecte d'aminoacylation des ARNt. La structure cristallographique de la GlnRS-Dr n'a pas permis de résoudre la région C-ter, la maille étant suffisamment large pour l'accommoder. Des analyses en RMN du C-ter isolé ont confirmé la présence d'une région majoritairement structurée. D'autres structures ont été résolues en présence de petits substrats (glutamine, analogues d'adénylate) ainsi que la forme tronquée en C-ter. Dans 2 cas, une conformation verrouillée unique du site actif a été mise en évidence. Des analyses structurales et fonctionnelles et les propriétés de l'empilement cristallin sont exposées.
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Dorison, Hugo. "Sumo-Directed Control of the Resolvase Yen1 in Mitotic Cells Slx5-Slx8 Ubiquitin Ligase Targets Active Pools of the Yen1 Nuclease To Limit Crossover Formation SUMO-Mediated Recruitment Allows Timely Function of the Yen1 Nuclease." Thesis, université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL003.

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La réparation de cassures d’ADN double brins par recombinaison homologue nécessite la formation d’intermédiaires multibrins qui peuvent être le lieu de formation de crossovers après résolution par des nucléases. La modification de protéines par ubiquitine et SUMO est un mode de contrôle répandu parmi les protéines de la réparation de l’ADN. De plus, certaines protéines de la réparation de cassures double brins interagissent entre elles, lorsqu’elles sont sumoylées, par le biais de motifs d’interaction avec SUMO (SIMs). La nucléase Yen1 subit un contrôle rigoureux lors du cycle cellulaire dans le but de limiter la formation de crossover et ainsi de préserver l’intégrité du génome. Dans ce manuscrit, il sera mis en évidence que Yen1 est régulé de surcroit par l’ubiquitination, la sumoylation et enfin l’interaction non covalente avec le modificateur SUMO via ses SIMs désormais découverts. Yen1 est sumoylé par les SUMO ligases Siz1 et Siz2, d’autant plus en conditions de dommages à l’ADN. En plus de quoi, Yen1 est un substrat de l’ubiquitine ligase Slx5-Slx8. En absence de cette dernière, la fraction sumoylée de Yen1 persiste, ce qui mène à la localisation durable de Yen1 en accumulation ponctuelle dans le noyau. L’ubiquitination de Yen1 par Slx5-Slx8 a surtout lieu à la lysine 714. Une mutation de cette lysine augmente la formation de crossovers, et annule également les défauts de ségrégation des chromosomes qui peuvent avoir lieu en l’absence d’autres nucléases. D’autre part, l’action nucléolytique de Yen1 ne s’effectue correctement que lorsque celui-ci peut interagir de façon non covalente avec des partenaires sumoylés. Des mutations dans les SIMs de Yen1 réduisent sa capacité à découper et résoudre les intermédiaires de la recombinaison, ce qui donne lieu à une augmentation de l’instabilité génomique et de la mauvaise ségrégation des chromosomes
The repair of double-stranded DNA breaks (DSBs) by homologous recombination involves the formation of branched intermediates that can lead to crossovers following nucleolytic resolution. Ubiquitin and SUMO modification is commonplace amongst the DNA damage repair proteins. What is more, a number of DSB repair factors interact with each other when sumoylated, making use of SUMO interaction motifs (SIMs). The nuclease Yen1 is tightly controlled during the cell cycle to limit the extent of crossover formation and preserve genome integrity. In this manuscript we describe further regulation of Yen1 by ubiquitination, sumoylation and non-covalent interaction with SUMO through its newly characterized SIMs. Yen1 is sumoylated by Siz1 and Siz2 SUMO ligases, especially in conditions of DNA damage. Furthermore, Yen1 is a substrate of the Slx5-Slx8 ubiquitin ligase. Loss of Slx5-Slx8 stabilizes the sumoylated fraction of Yen1, and results in persistent localization of Yen1 in nuclear foci. Slx5-Slx8-dependent ubiquitination of Yen1 occurs mainly at K714 and mutation of this lysine increases crossover formation during DSB repair and suppresses chromosome segregation defects when other nucleases are unavailable. In addition, proper and timely nucleolytic processing from Yen1 is dependent on interactions mediated by non-covalent binding to sumoylated partners. Mutations in the motifs that allow SUMO-mediated recruitment of Yen1 leads to its mis-localization, decreasing Yen1’s ability to resolve DNA joint-molecule intermediates and resulting in increased genome instability and chromosome mis-segregation
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Books on the topic "ADN Ligase"

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Gómez, Ramón Terol. Las ligas profesionales. [Spain]: Fundación del Fútbol Profesional, 1998.

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Ligabue, Antonio. Ligabue. Cavallermaggiore [Italy]: Gribaudo, 1995.

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Bloody Liggie. St. Lucia: University of Queensland Press, 2003.

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Boulaga, F. Eboussi. Lignes de résistance. Yaoundé: Editions CLE, 1999.

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Morais, Clodomir. História das Ligas Camponesas do Brasil. Brasília, DF: Edições Instituto de Apoio Técnico aos Países de Terceiro Mundo, 1997.

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Caffier, Michel. Nancy entre les lignes. Nancy: Presses universitaires de Nancy, 1993.

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Y cómo eran las ligas de Madame Bovary? Barcelona: Ediciones Destino, 2003.

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Razauskas, Romualdas. Juoko piliulės: Anekdotai apie ligas, ligonius ir gydytojus. Vilnius: UAB Mileta, 2002.

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Fabio, Francione, ed. Il cinema di Luciano Ligabue. Alessandria: Falsopiano, 2004.

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Alechinsky, Pierre. Alechinsky: Entre les lignes. Paris: Y. Rivière, 1996.

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Book chapters on the topic "ADN Ligase"

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Chistiakov, Dimitry A. "Ligase IV Syndrome." In Advances in Experimental Medicine and Biology, 175–85. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6448-9_16.

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Schomburg, Dietmar, and Ida Schomburg. "Mn2+-dependent ADP-ribose/CDP-alcohol diphosphatase 3.6.1.53." In Class 3.4–6 Hydrolases, Lyases, Isomerases, Ligases, 303–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36260-6_22.

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Schwehr, Bradley J., David Hartnell, Massimiliano Massi, and Mark J. Hackett. "Luminescent metal complexes as emerging tools for lipid imaging." In Metal Ligand Chromophores for Bioassays, 75–114. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-19863-2_3.

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AbstractFluorescence microscopy is a key tool in the biological sciences, which finds use as a routine laboratory technique (e.g., epifluorescence microscope) or more advanced confocal, two-photon, and super-resolution applications. Through continued developments in microscopy, and other analytical methods, the importance of lipids as constituents of subcellular organelles, signalling or regulating molecules continues to emerge. The increasing recognition of the importance of lipids to fundamental cell biology (in health and disease) has prompted the development of protocols and techniques to image the distribution of lipids in cells and tissues. A diverse suite of spectroscopic and microscopy tools are continuously being developed and explored to add to the “toolbox” to study lipid biology. A relatively recent breakthrough in this field has been the development and subsequent application of metal-based luminescent complexes for imaging lipids in biological systems. These metal-based compounds appear to offer advantages with respect to their tunability of the photophysical properties, in addition to capabilities centred around selectively targeting specific lipid structures or classes of lipids. The presence of the metal centre also opens the path to alternative imaging modalities that might not be applicable to traditional organic fluorophores. This review examines the current progress and developments in metal-based luminescent complexes to study lipids, in addition to exploring potential new avenues and challenges for the field to take.
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Proske, Uwe, David L. Morgan, Tamara Hew-Butler, Kevin G. Keenan, Roger M. Enoka, Sebastian Sixt, Josef Niebauer, et al. "E3 Ubiquitin Ligases." In Encyclopedia of Exercise Medicine in Health and Disease, 269. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2315.

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Yu, Tao, Yinfeng Zhang, and Pei-feng Li. "Mitochondrial Ubiquitin Ligase in Cardiovascular Disorders." In Advances in Experimental Medicine and Biology, 327–33. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55330-6_17.

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Tauler Riera, Pedro, Maurizio Volterrani, Ferdinando Iellamo, Francesco Fallo, Andrea Ermolao, William J. Kraemer, Nicholas A. Ratamess, Avery Faigenbaum, Andrew Philp, and Keith Baar. "RANK Ligand." In Encyclopedia of Exercise Medicine in Health and Disease, 749. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2939.

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Ishino, Sonoko, and Yoshizumi Ishino. "DNA Polymerases and DNA Ligases." In Thermophilic Microbes in Environmental and Industrial Biotechnology, 429–57. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-5899-5_17.

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Fu, Lin, Chun-Ping Cui, and Lingqiang Zhang. "Regulation of Stem Cells by Cullin-RING Ligase." In Advances in Experimental Medicine and Biology, 79–98. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1025-0_6.

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Kershaw, Christopher J., and Raymond T. O’Keefe. "Splint Ligation of RNA with T4 DNA Ligase." In Recombinant and In Vitro RNA Synthesis, 257–69. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-113-4_19.

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Chang, Hsuan-Ping, and Dhaval K. Shah. "Determination of ADC Concentration by Ligand-Binding Assays." In Methods in Molecular Biology, 361–69. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9929-3_26.

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Conference papers on the topic "ADN Ligase"

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Chandra, S., and V. Kumar. "Thermodynamic Properties of LiGaS2 and LiGaSe2 using First-Principle Calculations." In 2018 5th IEEE Uttar Pradesh Section International Conference on Electrical, Electronics and Computer Engineering (UPCON). IEEE, 2018. http://dx.doi.org/10.1109/upcon.2018.8596990.

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Chandra, Satish, V. Kumar, and Yadvendra Singh. "First-principle calculations of Debye temperature of optoelectronic LiGaS2 and LiGaSe2 semiconductors under different pressures." In Optical Components and Materials XVI, edited by Michel J. Digonnet and Shibin Jiang. SPIE, 2019. http://dx.doi.org/10.1117/12.2506878.

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Barrett, Dwhyte O., Amit Maha, Yun Wang, Steven A. Soper, Dimitris E. Nikitopoulos, and Michael C. Murphy. "Design of a Microfabricated Device for the Ligase Detection Reaction (LDR)." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-62111.

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The Ligase Detection Reaction (LDR) is a mutation detection technique used to identify point mutations in deoxyribonucleic acid (DNA). A microscale Ligase Detection Reaction (LDR) device was designed and manufactured in polycarbonate. There are at least two mixing stages involved in the LDR identification process. Various micromixers were simulated in Fluent (v5.4, Lebanon, NH) and several test geometries were selected for fabrication. Passive diffusional micromixers were made with aspect ratios from 7 to 20. The mixers were made by SU-8 lithography, LIGA, laser ablation and micromilling to characterize each fabrication method. It was found that LIGA was best for making the micromixers, but was the longest process. The micromixers were fabricated and are being tested using fluorescent dyes. For a successful reaction temperatures of 0°C, 95°C and 65°C were needed. A stationary chamber method was used with thermal cycling in which the sample held while the temperature is cycled. Finite element analysis showed uniform temperatures in the rectangular 1.5 μl chambers and that air slits can effectively separate the thermal cycle zone from the 0°C cooling zone and the mixing region. A test device was laid out and micromilled with the temperature zones. A commercial thin film heater and a thermoelectric module were used with a PID controller to obtain the required process temperatures. Heating from 65°C to 95°C took 10 seconds, while cooling from 95°C to 65°C also took 10 seconds. The residence times at the required temperatures can adapt to changes in the LDR as parameters and reactant concentrations are varied.
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Lee, Tae Yoon, Dimistris E. Nikitopoulos, Daniel S. Park, Steven A. Soper, and Michael C. Murphy. "Design and Fabrication of a Ligase Detection Reaction (LDR) Microchip With an Integrated Passive Micromixer." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-42216.

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The ligase detection reaction (LDR) is a technique that can distinguish low-abundant mutant DNAs from wild-type DNAs. LDR is usually carried out on DNAs amplified using the polymerase chain reaction (PCR). In the realization of modular microfluidic systems, the DNA output of the PCR handed off to the LDR chip needs to be mixed with LDR reagents before continuing the reaction. Polymer, continuous flow ligase detection reaction (CFLDR) devices with integrated passive micromixers, were designed, fabricated and tested. The devices each consisted of: a passive mixer for mixing a PCR sample, a cocktail of primers, and ligase, an enzyme of DNA; an incubator channel (95°C) for preheating the mixture; and a thermal cycling channel for the LDR. The devices were produced by hot embossing polycarbonate (PC) substrates with brass mold inserts manufactured by micro-milling. Experiments using food dyes showed that the appropriate mixture concentrations were delivered to the preheating channel in both the pulling and pushing modes.
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Lim, Manko, Timothy A. Jackson, and Philip A. Anfinrud. "Ultrafast Near-IR Spectroscopy of Carbonmonoxymyoglobin: the Dynamics of Protein Relaxation." In International Conference on Ultrafast Phenomena. Washington, D.C.: Optica Publishing Group, 1992. http://dx.doi.org/10.1364/up.1992.thb3.

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The conformation of a protein often influences its activity, yielding a structure-function relationship. X-ray diffraction studies have shown that the tertiary structures of ligated and deligated myoglobin (Mb) are somewhat different1. Consequently, dissociation of a ligand from Mb triggers a transition between the two tertiary conformations. The potential energy gradient causing this change is developed at the heme; the iron prefers to be in the plane of the porphyrin in ligated Mb but is displaced 0.5 Å from the plane of the porphyrin in deoxy Mb. The dynamics of this conformational transition may influence the dynamics of rebinding ligands, implying that protein dynamics are also functionally important. For example, the dynamics of ligand recombination with Mb following photolysis of MbCO or MbO2 in low-temperature glasses are similar2. In contrast, Mb expurgates CO with far greater efficiency than O2 when photolysis is carried out at biologically important temperatures3. Since protein motion is inhibited at low temperatures, protein relaxation likely accounts for the temperature-dependent difference in the quantum yield of photodissociation. The ability to discriminate against the binding and storage of CO is functionally important as endogenously produced CO would otherwise compete effectively with O2 for binding sites. A steric mechanism for discriminating against the binding of CO, involving the distal histidine, is well known. The dynamics of protein relaxation evidently provide a mechanism for discriminating against the storage of CO. We have investigated the dynamics of protein relaxation in order to probe this mechanism and thereby elucidate the relation between protein dynamics and function.
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Steimle, Timothy C., Boa-Zhong Li, and Kook Young Jung. "Molecular Beam Optical Stark and PPMODR Spectroscopy of Pt Containing Molecules." In Modern Spectroscopy of Solids, Liquids, and Gases. Washington, D.C.: Optica Publishing Group, 1995. http://dx.doi.org/10.1364/msslg.1995.ssaa4.

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Ligated platinum compounds are important in many homogeneous catalytic processes yet there is very little experimental information about the Pt-ligand bond. The most detailed information about bonding comes from the analysis of gas phase spectra recorded at a resolution sufficient to resolve the fine and hyperfine structure and shifts in spectral features caused by the application of static electric and magnetic fields. The advent of the supersonic laser ablation/reaction source (1-4) has eliminated many of the problems associated with the generation molecules containing refractory elements, such as Pt. In our laboratory we use such a molecular beam source in the optical Stark and pump/probe microwave optical double resonance (PPMODR)studies. In both techniques the detected signal is single mode cw-dye laser induced fluorescence (LIF).
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Kawaguchi, Kazutomo, Hiroyuki Takagi, Masako Takasu, Hiroaki Saito, and Hidemi Nagao. "Molecular dynamics studies of Hsp90 with ADP: Protein-ligand binding dynamics." In 4TH INTERNATIONAL SYMPOSIUM ON SLOW DYNAMICS IN COMPLEX SYSTEMS: Keep Going Tohoku. American Institute of Physics, 2013. http://dx.doi.org/10.1063/1.4794650.

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M. H. Obaid, Shatha, Taghreed H. Al-Noor, and Noor A. Hussien. "Preparation, Spectra and Biological Properties of Transition Metals ((III) and (II) Mixed - Ligand Complexes with 5-Chlorosalicylic Acid and L-Valine." In المؤتمر العلمي الدولي العاشر. شبكة المؤتمرات العربية, 2019. http://dx.doi.org/10.24897/acn.64.68.466.

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Jelínek, Michal, Vaclav Kubecek, Miroslav Cech, Sergei Smetanin, Aleksey Kurus, Sergei Lobanov, Vitaliy Vedenyapin, and Lyudmila Isaenko. "Narrowband difference-frequency generation at 4.6, 5.4, 7.5, 9.2, and 10.8 μm in LiGaS2 and LiGaSe2 pumped by 20-ps Nd:YAG laser and Raman laser seeding." In Solid State Lasers XXX: Technology and Devices, edited by W. Andrew Clarkson and Ramesh K. Shori. SPIE, 2021. http://dx.doi.org/10.1117/12.2579178.

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Barrett, Dwhyte O., Amit Maha, Yun Wang, Steven A. Soper, Dimitris E. Nikitopoulos, and Michael C. Murphy. "Design of a microfabricated device for ligase detection reaction (LDR)." In Micromachining and Microfabrication, edited by Peter Woias and Ian Papautsky. SPIE, 2004. http://dx.doi.org/10.1117/12.524681.

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Reports on the topic "ADN Ligase"

1

Royer, Lacey. Cul3 Ubiquitin Ligase and Ctb73 Protein Interactions. Portland State University Library, January 2014. http://dx.doi.org/10.15760/honors.48.

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Davidge, Brittney. The Cul3 Ubiquitin Ligase: An Essential Regulator of Diverse Cellular Processes. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.5666.

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Mitchell, Jennifer. Characterization of Functional Domains of Cul3, an E3 Ubiquitin Ligase, Using Chimeric Analysis. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1969.

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Raj, Ganesh V. Targeting Ligand Dependent and Ligand Independent Androgen Receptor Signaling in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613818.

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Raj, Ganesh V. Targeting Ligand-Dependent and Ligand-Independent Androgen Receptor Signaling in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada604653.

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SLACK, JEFFREY, M. IDENTIFICATION, PRODUCTION AND CHARACTERIZATION OF NOVEL LIGNASE PROTEINS FROM TERMITES FOR DEPOLYMERIZATION OF LIGNOCELLULOSE. Office of Scientific and Technical Information (OSTI), December 2012. http://dx.doi.org/10.2172/1056676.

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Szigethy, Geza. Rational Ligand Design for U(VI) and Pu(IV). Office of Scientific and Technical Information (OSTI), August 2009. http://dx.doi.org/10.2172/972716.

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Kelley, DAVID. Ligand-Controlled Energetics and Charge Transfer in Pure and Doped Nanocrystals. Office of Scientific and Technical Information (OSTI), February 2021. http://dx.doi.org/10.2172/1766125.

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9

Hovey, Megan. Ligand strategies for green chemistry. Catalysts for amide reduction and hydroamination. Office of Scientific and Technical Information (OSTI), January 2014. http://dx.doi.org/10.2172/1226561.

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10

Ma, Buyong, and Ruth Nussinov. Computational Study of Cytolytic Peptides: Monomeric-Oligomeric Structures and Ligand Interactions. Fort Belvoir, VA: Defense Technical Information Center, November 2005. http://dx.doi.org/10.21236/ada444931.

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