Academic literature on the topic 'BRCT domains'

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Journal articles on the topic "BRCT domains"

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Wright, Roni H. G., Edward S. Dornan, Mary M. Donaldson, and Iain M. Morgan. "TopBP1 contains a transcriptional activation domain suppressed by two adjacent BRCT domains." Biochemical Journal 400, no. 3 (2006): 573–82. http://dx.doi.org/10.1042/bj20060831.

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TopBP1 has eight BRCT [BRCA1 (breast-cancer susceptibility gene 1) C-terminus] domains and is involved in initiating DNA replication, and DNA damage checkpoint signalling and repair. Several BRCT-domain-containing proteins involved in mediating DNA repair have transcriptional regulatory domains, and as demonstrated for BRCA1 these regulatory domains are important in mediating the functions of these proteins. These transcriptional regulatory processes involve modification of chromatin, and recent evidence has clearly demonstrated that the ability to modify chromatin plays an important role in r
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Leung, Charles Chung Yun, and J. N. Mark Glover. "BRCT domains." Cell Cycle 10, no. 15 (2011): 2461–70. http://dx.doi.org/10.4161/cc.10.15.16312.

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Taylor, Richard M., Angela Thistlethwaite, and Keith W. Caldecott. "Central Role for the XRCC1 BRCT I Domain in Mammalian DNA Single-Strand Break Repair." Molecular and Cellular Biology 22, no. 8 (2002): 2556–63. http://dx.doi.org/10.1128/mcb.22.8.2556-2563.2002.

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ABSTRACT The DNA single-strand break repair (SSBR) protein XRCC1 is required for genetic stability and for embryonic viability. XRCC1 possesses two BRCA1 carboxyl-terminal (BRCT) protein interaction domains, denoted BRCT I and II. BRCT II is required for SSBR during G1 but is dispensable for this process during S/G2 and consequently for cell survival following DNA alkylation. Little is known about BRCT I, but this domain has attracted considerable interest because it is the site of a genetic polymorphism that epidemiological studies have associated with altered cancer risk. We report that the
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Williams, R. Scott, Nina Bernstein, Megan S. Lee, et al. "Structural basis for phosphorylation-dependent signaling in the DNA-damage response." Biochemistry and Cell Biology 83, no. 6 (2005): 721–27. http://dx.doi.org/10.1139/o05-153.

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The response of eukaryotic cells to DNA damage requires a multitude of protein–protein interactions that mediate the ordered repair of the damage and the arrest of the cell cycle until repair is complete. Two conserved protein modules, BRCT and forkhead-associated (FHA) domains, play key roles in the DNA-damage response as recognition elements for nuclear Ser/Thr phosphorylation induced by DNA-damage-responsive kinases. BRCT domains, first identified at the C-terminus of BRCA1, often occur as multiple tandem repeats of individual BRCT modules. Our recent structural and functional work has reve
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Mesquita, R. D., N. T. Woods, E. S. Seabra-Junior, and A. N. A. Monteiro. "Tandem BRCT Domains: DNA's Praetorian Guard." Genes & Cancer 1, no. 11 (2010): 1140–46. http://dx.doi.org/10.1177/1947601910392988.

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di Masi, Alessandra, Francesca Gullotta, Valentina Cappadonna, Loris Leboffe, and Paolo Ascenzi. "Cancer predisposing mutations in BRCT domains." IUBMB Life 63, no. 7 (2011): 503–12. http://dx.doi.org/10.1002/iub.472.

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Butcher, S. J., M. J. Coleman, and R. P. Bowater. "Investigating BRCT domains in Arabidopsis thaliana." Biochemical Society Transactions 29, no. 5 (2001): A114. http://dx.doi.org/10.1042/bst029a114c.

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Kumar, Anuradha, Woo S. Joo, Gretchen Meinke, Stephanie Moine, Elena N. Naumova, and Peter A. Bullock. "Evidence for a Structural Relationship between BRCT Domains and the Helicase Domains of the Replication Initiators Encoded by the Polyomaviridae and Papillomaviridae Families of DNA Tumor Viruses." Journal of Virology 82, no. 17 (2008): 8849–62. http://dx.doi.org/10.1128/jvi.00553-08.

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ABSTRACT Studies of DNA tumor viruses have provided important insights into fundamental cellular processes and oncogenic transformation. They have revealed, for example, that upon expression of virally encoded proteins, cellular pathways involved in DNA repair and cell cycle control are disrupted. Herein, evidence is presented that BRCT-related regions are present in the helicase domains of the viral initiators encoded by the Polyomaviridae and Papillomaviridae viral families. Of interest, BRCT domains in cellular proteins recruit factors involved in diverse pathways, including DNA repair and
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Sofueva, Sevil, Li-Lin Du, Oliver Limbo, Jessica S. Williams, and Paul Russell. "BRCT Domain Interactions with Phospho-Histone H2A Target Crb2 to Chromatin at Double-Strand Breaks and Maintain the DNA Damage Checkpoint." Molecular and Cellular Biology 30, no. 19 (2010): 4732–43. http://dx.doi.org/10.1128/mcb.00413-10.

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ABSTRACT Relocalization of checkpoint proteins to chromatin flanking DNA double-strand breaks (DSBs) is critical for cellular responses to DNA damage. Schizosaccharomyces pombe Crb2, which mediates Chk1 activation by Rad3ATR, forms ionizing radiation-induced nuclear foci (IRIF). Crb2 C-terminal BRCT domains (BRCT2) bind histone H2A phosphorylated at a C-terminal SQ motif by Tel1ATM and Rad3ATR, although the functional significance of this interaction is controversial. Here, we show that polar interactions of Crb2 serine-548 and lysine-619 with the phosphate group of phospho-H2A (γ-H2A) are cri
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Rodriguez, Maria, C. "BRCT Domains: phosphopeptide binding and signaling modules." Frontiers in Bioscience Volume, no. 13 (2008): 5905. http://dx.doi.org/10.2741/3125.

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Dissertations / Theses on the topic "BRCT domains"

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Mohammad, Duaa H. "Identification of new functions for BRCT domains." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/45806.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2008.<br>"September 2008." Leaf 125 blank.<br>Includes bibliographical references (leaves 119-124).<br>Our lab identified the tandem BRCT domains of PTIP function as a DNA damage responsive phospho binding domain that recognizes proteins phosphorylated by ATM and ATR after DNA damage. The PTIP tandem BRCT domains are responsible for phosphorylation-dependent localization of PTIP into 53BP1- and phospho-H2AX (y-H2AX)-containing nuclear foci, a marker of DNA damage. Here we report that the BRCT domains of PTIP show strong
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Hard, Ryan Lawrence. "Sequence Specificity of BUZ, PDZ, SH2, and Tandem BRCT Domains." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1377005582.

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Kaufmann, Aisling. "The role of the BARD1 BRCT domains in the DNA damage response." Thesis, University of Dundee, 2014. https://discovery.dundee.ac.uk/en/studentTheses/8c8c745f-8b73-420f-b264-2b12334195e7.

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The DNA within a cell is damaged on a continuous basis by both endogenous and exogenous agents. One of the most dangerous types of damage a cell can incur are DNA Double stranded breaks (DSBs) as failure to repair these types of lesions can lead to mutations, cell death and cancer. In order to maintain genome integrity, cells have several different mechanisms to repair various types of DNA damage. BRCA1 is a tumour suppressor gene commonly mutated in many inherited breast and ovarian cancers. BRCA1 is fundamental to the repair to DNA damage especially the faithful repair of DSB by homologous r
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Jhuraney, Ankita. "The Role of BRCT-Containing Proteins BRCA1 and PAXIP1 in Cancer." Scholar Commons, 2015. http://scholarcommons.usf.edu/etd/5819.

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Modular domains of proteins are important in cellular signaling processes. Eukaryotic cells are constantly undergoing DNA damage due to exogenous and endogenous sources of damage. The DNA damage response (DDR) involves a complex network of signaling events mediated by modular domains such as the BRCT (BRCA1 C-terminal) domains. Therefore, proteins containing BRCT domains are important for DNA damage detection and signaling. In this dissertation, we focus on two BRCT-containing proteins BRCA1 and PAXIP1. BRCA1 is a gene that is known to be associated with increased risk of hereditary breast and
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Buchner, Kristina [Verfasser], and Esther [Akademischer Betreuer] Zanin. "Functional characterization of the BRCT domains of the RhoA GEF Ect2 during cell division / Kristina Buchner ; Betreuer: Esther Zanin." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1234911396/34.

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Butcher, Susan Jane. "BRCT domain-containing proteins in Arabidopsis thaliana." Thesis, University of East Anglia, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398496.

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White, Railey. "Selection of a Non-Phosphorylated Peptide Inhibitor of BRCA1’s (BRCT)2 Domain." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/585.

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A growing body of literature suggests Breast Cancer-Associated Protein 1 (BRCA1) is important not only as a cause, but also as a target in the quest for cancer treatment. BRCA1 deficient cells treated with radiation as well as PARP inhibitors and other chemotherapeutics demonstrate a greater sensitivity than cells with wild type BRCA1. Inhibitors of BRCA1 would take advantage of this synthetic lethality and represent a significant advance in cancer treatment as well as an understanding of the biology of DNA repair. Despite significant study of BRCA1 protein and function, it is a large protein
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Zhang, Yan. "PTIP, a novel BRCT domain-containing apoptotic factor that directly promotes cytochrome c release from mitochondria to cytoplasm." Access restricted to users with UT Austin EID, 2001. http://wwwlib.umi.com/cr/utexas/fullcit?p3037036.

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Ho, Jenny Chung-Yee. "Structural and functional analysis of the Rhp9 BRCT domain region and a study of the Pmt3-modificationystem in Schizosaccharomyces pombe." Thesis, University of Sussex, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340815.

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Becker, Emmanuelle. "Prédictions bioinformatiques des propriétés des domaines de reconnaissance peptidique." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2007. http://tel.archives-ouvertes.fr/tel-00553471.

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Les protéines impliquées dans les voies de signalisation sont souvent activées et inactivées par des interactions de faible affinité. En particulier, les domaines protéiques liant spécifiquement de courts fragments protéiques permettent une régulation intra- et inter-moléculaire efficace des domaines catalytiques auxquels ils sont associés. Citons par exemple les domaines FHA ou des tandems BRCT fréquemment impliqués dans les réponses aux dommages de l'ADN. Etant donnée leur importance dans les réseaux d'interactions et dans la signalisation cellulaire, la prédiction par bioinformatique des pr
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Book chapters on the topic "BRCT domains"

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A., Lindsay, and Alba Guarne. "Extending the Interaction Repertoire of FHA and BRCT Domains." In The Mechanisms of DNA Replication. InTech, 2013. http://dx.doi.org/10.5772/51670.

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"BRCT Domain." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_714.

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"CANCER-LINKED MISSENSE MUTATIONS IN THE BRCT DOMAIN OF BRCA1 AND UNCLASSIFIED VARIANTS." In Cancer Biomarkers. CRC Press, 2012. http://dx.doi.org/10.1201/b14318-13.

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Syed, Mahanazuddin, Shaymaa Al-Shukri, Shorabuddin Syed, et al. "DeIDNER Corpus: Annotation of Clinical Discharge Summary Notes for Named Entity Recognition Using BRAT Tool." In Studies in Health Technology and Informatics. IOS Press, 2021. http://dx.doi.org/10.3233/shti210195.

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Named Entity Recognition (NER) aims to identify and classify entities into predefined categories is a critical pre-processing task in Natural Language Processing (NLP) pipeline. Readily available off-the-shelf NER algorithms or programs are trained on a general corpus and often need to be retrained when applied on a different domain. The end model’s performance depends on the quality of named entities generated by these NER models used in the NLP task. To improve NER model accuracy, researchers build domain-specific corpora for both model training and evaluation. However, in the clinical domain, there is a dearth of training data because of privacy reasons, forcing many studies to use NER models that are trained in the non-clinical domain to generate NER feature-set. Thus, influencing the performance of the downstream NLP tasks like information extraction and de-identification. In this paper, our objective is to create a high quality annotated clinical corpus for training NER models that can be easily generalizable and can be used in a downstream de-identification task to generate named entities feature-set.
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Conference papers on the topic "BRCT domains"

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Irminger-Finger, Irmgard, Maxim Pilyugin, and Magdalena Ratajska. "Abstract 2393: The BARD1 BRCT domains are essential for maintenance of telomere integrity." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2393.

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Xiaobing, He, Xie Yan, and Yu Jingjun. "Bi-Material Re-Entrant Triangle Structures Incorporating Tailorable Thermal Expansion and Tunable Poisson’s Ratio." In ASME 2019 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/detc2019-97686.

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Abstract Based on the bi-material triangle lattice material, a new cellular structure: bi-material re-entrant triangle (BRT) is devised to incorporate tailorable coefficient of thermal expansion (CTE) and tunable Poisson’s ratio (PR) properties by replacing the straight base of a triangle with two hypotenuse members. An equation to systematically build the relationship among the external force, the temperature increment and the deformation for the planar lattice material with bounded joints is derived and then embedded into a theoretical model for devised BRT structure. Using master stiffness
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Golubeva, Volha A., Nicholas T. Woods, and Alvaro N. A. Monteiro. "Abstract 3779: Mutational analysis of MCPH1 C-terminal tandem BRCT domain reveals residues essential for cell cycle arrest." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3779.

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Wang, Yifan, Andrea J. Bernhardy, and Neil Johnson. "Abstract A23: BRCA1 mutations in the BRCT domain can be removed through alternative splicing and induce PARP inhibitor resistance." In Abstracts: AACR Special Conference on DNA Repair: Tumor Development and Therapeutic Response; November 2-5, 2016; Montreal, QC, Canada. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3125.dnarepair16-a23.

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Nakamura, Jun, and Xu Tian. "Abstract 2410: Crucial role of the non-BRCT automodification domain of PARP1 in either DNA binding and PARP inhibitor-mediated cell toxicity." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2410.

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Pettan-Brewer, Christina, John Morton, Rebecca Coil, Jorming Goh, and Warren C. Ladiges. "Abstract 2377: Variation in the BRCT1 domain of the DNA repair gene XRCC1 delays invasive breast cancer in mice." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2377.

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Reports on the topic "BRCT domains"

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Songyang, Zhou. A Proteomic Approach to Identify Phosphorylation-Dependent Targets of BRCT Domains. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada487327.

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Songyang, Zhou. A Proteomic Approach to Identify Phosphorylation-Dependent Targets of BRCT Domains. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada458980.

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