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Journal articles on the topic 'Nibrin'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Cerosaletti, Karen, Jocyndra Wright, and Patrick Concannon. "Active Role for Nibrin in the Kinetics of Atm Activation." Molecular and Cellular Biology 26, no. 5 (March 1, 2006): 1691–99. http://dx.doi.org/10.1128/mcb.26.5.1691-1699.2006.

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ABSTRACT The Atm protein kinase is central to the DNA double-strand break response in mammalian cells. After irradiation, dimeric Atm undergoes autophosphorylation at Ser 1981 and dissociates into active monomers. Atm activation is stimulated by expression of the Mre11/Rad50/nibrin complex. Previously, we showed that a C-terminal fragment of nibrin, containing binding sites for both Mre11 and Atm, was sufficient to provide this stimulatory effect in Nijmegen breakage syndrome (NBS) cells. To discriminate whether nibrin's role in Atm activation is to bind and translocate Mre11/Rad50 to the nucleus or to interact directly with Atm, we expressed an Mre11 transgene with a C-terminal NLS sequence in NBS fibroblasts. The Mre11-NLS protein complexed with Rad50, localized to the nucleus in NBS fibroblasts, and associated with chromatin. However, Atm autophosphorylation was not stimulated in cells expressing Mre11-NLS, nor were downstream Atm targets phosphorylated. To determine whether nibrin-Atm interaction is necessary to stimulate Atm activation, we expressed nibrin transgenes lacking the Atm binding domain in NBS fibroblasts. The nibrin ΔAtm protein interacted with Mre11/Rad50; however, Atm autophosphorylation was dramatically reduced after irradiation in NBS cells expressing the nibrin ΔAtm transgenes relative to wild-type nibrin. These results indicate that nibrin plays an active role in Atm activation beyond translocating Mre11/Rad50 to the nucleus and that this function requires nibrin-Atm interaction.

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2

Desai-Mehta, Ami, Karen M. Cerosaletti, and Patrick Concannon. "Distinct Functional Domains of Nibrin Mediate Mre11 Binding, Focus Formation, and Nuclear Localization." Molecular and Cellular Biology 21, no. 6 (March 15, 2001): 2184–91. http://dx.doi.org/10.1128/mcb.21.6.2184-2191.2001.

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ABSTRACT The inherited chromosomal instability disorder Nijmegen breakage syndrome (NBS) results from truncating mutations in theNBS1 gene, which encodes the protein nibrin. Nibrin is part of a nuclear multiprotein complex that also contains the DNA repair proteins Mre11 and Rad50. Upon irradiation, this complex redistributes within the nucleus, forming distinct foci that have been implicated as sites of DNA repair. In NBS cells, nibrin is absent and Mre11 and Rad50 are cytoplasmic. In this study, the interacting domains on nibrin and Mre11 were mapped using the yeast two-hybrid system and expression of epitope-tagged constructs in NBS fibroblasts. Deletion of the carboxy-terminal 101 amino acids of nibrin eliminated its ability to interact with Mre11 and to complement the radiation sensitivity of NBS cells. However, this truncated form of nibrin could localize to the nucleus and form radiation-inducible foci. Expression of a carboxy-terminal 354-amino-acid fragment of nibrin was sufficient to direct the nuclear localization of nibrin, as well as that of Mre11 and Rad50. Despite providing some partial complementation of the radiation-sensitive phenotype, the nibrin-Mre11-Rad50 complexes in these cells were unable to form foci. These results indicate that nibrin directs not only the nuclear localization of the nibrin-Mre11-Rad50 complexes but also radiation-induced focus formation. However, direct interaction between nibrin and Mre11 is required for normal cellular survival postirradiation. Distinct domains of nibrin are required for each of these functions, focus formation, nuclear localization, and Mre11 interaction.

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3

Vissinga, Christine S., Tiong C. Yeo, Sarah Warren, James V. Brawley, Jennifer Phillips, Karen Cerosaletti, and Patrick Concannon. "Nuclear Export of NBN Is Required for Normal Cellular Responses to Radiation." Molecular and Cellular Biology 29, no. 4 (December 15, 2008): 1000–1006. http://dx.doi.org/10.1128/mcb.01131-08.

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ABSTRACT Nijmegen breakage syndrome arises from hypomorphic mutations in the NBN gene encoding nibrin, a component of the MRE11/RAD50/nibrin (MRN) complex. In mammalian cells, the MRN complex localizes to the nucleus, where it plays multiple roles in the cellular response to DNA double-strand breaks. In the current study, sequences in mouse nibrin required to direct the nuclear localization of the MRN complex were identified by site-specific mutagenesis. Unexpectedly, nibrin was found to contain both nuclear localizing signal (NLS) sequences and a nuclear export signal (NES) sequence whose functions were confirmed by mutagenesis. Both nuclear import and export sequences were active in vivo. Disruption of either the NLS or NES sequences of nibrin significantly altered the cellular distribution of nibrin and Mre11 and impaired survival after exposure to ionizing radiation. Mutation of the NES sequence in nibrin slowed the turnover of phosphorylated nibrin after irradiation, indicating that nuclear export of nibrin may function, in part, to downregulate posttranslationally modified MRN complex components after DNA damage responses are complete.

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4

Aracil Avila, Miguel, Antonio Nieto, Adnan Tanovic, Bradley J. Monk, Stanley B. Kaye, Andres Poveda, Thomas J. Herzog, Trilok V. Parekh, Nadia Badri, and Carlos Galmarini. "Exploratory analysis of nibrin in advanced ovarian cancer (AOC) patients treated in the phase III OVA-301 trial." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 5566. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.5566.

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5566 Background: Nibrin (p95/NBS1) is a protein with an essential function in DNA double-strand break repair by homologous recombination. Therefore, we have investigated its value as a possible biomarker in patients with AOC by immunohistochemistry (IHC). Methods: IHC staining was performed in 138 samples from a subset of patients that have participated in the phase III OVA-301 trial, in which the combination of trabectedin plus pegylated liposomal doxorubicin (PLD) or PLD alone were randomly administered for advanced disease after failure of platinum-based chemotherapy (Monk 2010; Monk 2012). A computerized image analysis system was used to calculate the total percentage of nibrin-positive cells. Nibrin expression was considered as a continuous variable. The analysis of overall response rate (ORR) and progression-free survival (PFS) was based on independent oncologist assessment. Overall survival (OS) was defined from randomization to death/last contact. All the comparisons had an exploratory nature; an alpha cut-off value of 0.05 (two-sided) was established as statistically significant. Results: For PFS, there was a statistically significant correlation between high levels of nibrin and short PFS (HR = 1.014, 95% CI: 1.004-1.024, p=0.0047). Similarly, for OS, there was a statistically significant correlation between high levels of nibrin and worse OS (HR = 1.009, 95% CI: 1.001-1.017, p = 0.0295). A multivariate analysis showed that high levels of nibrin were independently correlated to a worse PFS (HR = 1.012, 95% CI: 1.002-1.022, p = 0.0147) and to a worse OS (HR = 1.010, 95% CI: 1.002-1.018, p=0.0192). After stratification according to platinum-sensitivity, high nibrin showed a significant correlation with lower ORR (ORR = 1.02, 95% CI: 1.01-1.03, p=0.0009), short PFS and OS values only in the platinum-sensitive patients. Conclusions: The results point out the potential importance of nibrin expression in the clinical outcome of patients with AOC. In particular, high protein expression of nibrin seems to be associated with a worse clinical outcome. Prospective clinical trials evaluating the clinical usefulness of this marker with other standard of care treatments are warranted. Clinical trial information: NCT00113607.

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5

Kracker, S., Y. Bergmann, I. Demuth, P. O. Frappart, G. Hildebrand, R. Christine, Z. Q. Wang, K. Sperling, M. Digweed, and A. Radbruch. "Nibrin functions in Ig class-switch recombination." Proceedings of the National Academy of Sciences 102, no. 5 (January 24, 2005): 1584–89. http://dx.doi.org/10.1073/pnas.0409191102.

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6

Tanzarella, Caterina, Antonio Antoccia, Emanuela Spadoni, Alessandra di Masi, Vanna Pecile, Eliana Demori, Raymonda Varon, Gian Luigi Marseglia, Luciano Tiepolo, and Paola Maraschio. "Chromosome instability and nibrin protein variants in NBS heterozygotes." European Journal of Human Genetics 11, no. 4 (April 2003): 297–303. http://dx.doi.org/10.1038/sj.ejhg.5200962.

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7

Abidi, Fizza, Mervyn Hossein, Saima Akram, and Angabeen Anjum. "Nibrin Double Strand Breakage and its Role in Development of Cancers." Journal of the Pakistan Dental Association 29, no. 02 (May 5, 2020): 94–99. http://dx.doi.org/10.25301/jpda.292.94.

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8

UZUNOGLU, HAKAN, TUGCAN KORAK, EMEL ERGUL, NIHAL UREN, ALI SAZCI, N. ZAFER UTKAN, ERTUĞRUL KARGI, ÇAĞRI TRIYAKI, and OKTAY YIRMIBESOGLU. "Association of the nibrin gene (NBN) variants with breast cancer." Biomedical Reports 4, no. 3 (January 25, 2016): 369–73. http://dx.doi.org/10.3892/br.2016.579.

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9

Gatei, Magtouf, David Young, Karen M. Cerosaletti, Ami Desai-Mehta, Kevin Spring, Sergei Kozlov, Martin F. Lavin, Richard A. Gatti, Patrick Concannon, and KumKum Khanna. "ATM-dependent phosphorylation of nibrin in response to radiation exposure." Nature Genetics 25, no. 1 (May 2000): 115–19. http://dx.doi.org/10.1038/75508.

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10

Erdős, Melinda, Beáta Tóth, Pálma Juhász, Mohamed Mahdi, and László Maródi. "Nijmegen Breakage syndrome." Orvosi Hetilap 151, no. 16 (April 1, 2010): 665–73. http://dx.doi.org/10.1556/oh.2010.28851.

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A Nijmegen–Breakage-szindróma ritka, autoszomális recesszív öröklődésű kórkép, amelyre súlyos kombinált immundeficientia, visszatérő sinopulmonalis fertőzések, a kromoszómainstabilitás és az ionizáló sugárzással szembeni hiperszenzitivitás miatt a malignus betegségek gyakoribb előfordulása, fejlődési rendellenességek, madárarc, progresszív microcephalia, valamint növekedési és mentális retardáció jellemző. A betegség hátterében a DNS-repair-mechanizmusokban fontos szerepet játszó nibrin nevű protein kódolásáért felelős NBS1 gén mutációja áll. A közleményben a szerzők két esetismertetés kapcsán bemutatják a betegség klinikumát, a jellemző laboratóriumi leleteket, és összefoglalják a kórkép molekuláris patomechanizmusával kapcsolatos ismereteket, valamint a kezelés lehetőségeit.

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11

Dave, Jigna H., Hemangini H. Vora, Trupti I. Trivedi, and Nandita R. Ghosh. "Nibrin expression in oral squamous cell carcinoma: association with clinicopathological parameters." Journal of Cancer Metastasis and Treatment 2, no. 11 (November 25, 2016): 436. http://dx.doi.org/10.20517/2394-4722.2015.82.

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12

Salewsky, Bastian, Petra Wessendorf, Daniel Hirsch, Harald Krenzlin, and Martin Digweed. "Nijmegen breakage syndrome: The clearance pathway for mutant nibrin protein is allele specific." Gene 519, no. 2 (May 2013): 217–21. http://dx.doi.org/10.1016/j.gene.2013.02.033.

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13

Bunjevacki, Vera, Nela Maksimovic, Tatjana Damnjanovic, Suzana Cvjeticanin, Ivana Novakovic, Ljiljana Lukovic, Momcilo Ristanovic, Andrija Bogdanovic, and Biljana Jekic. "657del5 mutation of the NBS1 gene in myelodysplastic syndrome." Archives of Biological Sciences 66, no. 3 (2014): 1055–59. http://dx.doi.org/10.2298/abs1403055b.

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Myelodysplastic syndromes (MDS) are clonal hematologic stem cell disorders with an as yet unknown molecular pathology. Genetic instability has been proposed as a cause of MDS. Mutations in the NBS1 gene, whose product nibrin (p95) is involved in DNA damage repair and cell-cycle control, might be associated with an elevated predisposition to the development of MDS. The aim of the study was to examine truncating 5 bp deletion (657del5), the most frequent NBS1 gene mutation in Slavic populations, in MDS patients. Among 71 MDS patients, we found one case that was heterozygous for the NBS1 657del5 mutation. To the best of our knowledge, this is the first report of a NBS1 mutation in MDS.

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14

Cerosaletti, Karen, and Patrick Concannon. "Independent Roles for Nibrin and Mre11-Rad50 in the Activation and Function of Atm." Journal of Biological Chemistry 279, no. 37 (July 1, 2004): 38813–19. http://dx.doi.org/10.1074/jbc.m404294200.

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15

Varon, Raymonda, Christine Vissinga, Matthias Platzer, Karen M. Cerosaletti, Krystyna H. Chrzanowska, Kathrin Saar, Georg Beckmann, et al. "Nibrin, a Novel DNA Double-Strand Break Repair Protein, Is Mutated in Nijmegen Breakage Syndrome." Cell 93, no. 3 (May 1998): 467–76. http://dx.doi.org/10.1016/s0092-8674(00)81174-5.

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16

PLISIECKA-HA?ASA, J., A. DANSONKA-MIESZKOWSKA, A. REMBISZEWSKA, M. BIDZI??SKI, J. STEFFEN, and J. KUPRYJA??CZYK. "Nijmegen breakage syndrome gene (NBS1) alterations and its protein (nibrin) expression in human ovarian tumours." Annals of Human Genetics 66, no. 6 (November 2002): 353–59. http://dx.doi.org/10.1017/s0003480002001227.

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17

PLISIECKA-HALASA, J., A. DANSONKA-MIESZKOWSKA, A. REMBISZEWSKA, M. BIDZINSKI, J. STEFFEN, and J. KUPRYJANCZYK. "Nijmegen breakage syndrome gene (NBS1) alterations and its protein (nibrin) expression in human ovarian tumours." Annals of Human Genetics 66, no. 6 (November 2002): 353–59. http://dx.doi.org/10.1046/j.1469-1809.2002.00122.x.

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18

Dzikiewicz-Krawczyk, A., M. Mosor, D. Januszkiewicz, and J. Nowak. "Impact of heterozygous c.657-661del, p.I171V and p.R215W mutations in NBN on nibrin functions." Mutagenesis 27, no. 3 (November 30, 2011): 337–43. http://dx.doi.org/10.1093/mutage/ger084.

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19

Garcı́a-Pérez, Miguel Angel, Luis M. Allende, Alfredo Corell, Estela Paz-Artal, Pilar Varela, Alberto López-Goyanes, Francisco Garcı́a-Martin, Rosario Vázquez, Amalia Sotoca, and Antonio Arnaiz-Villena. "Role of Nijmegen Breakage Syndrome Protein in Specific T-Lymphocyte Activation Pathways." Clinical Diagnostic Laboratory Immunology 8, no. 4 (July 1, 2001): 757–61. http://dx.doi.org/10.1128/cdli.8.4.757-761.2001.

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ABSTRACT Nijmegen breakage syndrome (NBS) is a genetic disorder characterized by immunodeficiency, microcephaly, and “bird-like” facies. NBS shares some clinical features with ataxia telangiectasia (AT), including increased sensitivity to ionizing radiation, increased spontaneous and induced chromosome fragility, and strong predisposition to lymphoid cancers. The mutated gene that results in NBS codes for a novel double-stranded DNA break repair protein, named nibrin. In the present work, a Spanish NBS patient was extensively characterized at the immunological and the molecular DNA levels. He showed low CD3+-cell numbers and an abnormal low CD4+naive cell/CD4+ memory cell ratio, previously described in AT patients and also described in the present report in the NBS patient. The proliferative response of peripheral blood lymphocytes in vitro to mitogens is deficient in NBS patients, but the possible link among NBS mutations and the abnormal immune response is still unknown.

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20

Horst, Klemens, Silke Ganzera, Wolfgang Kaisers, Johanna Munding, Berenike Flott-Rahmel, Andrea Tannapfel, and Hubert Zirngibl. "Influence of MRE11, RAD50 and NIBRIN protein expression on survival in pancreatic carcinoma after curative resection." Pathology - Research and Practice 209, no. 10 (October 2013): 635–39. http://dx.doi.org/10.1016/j.prp.2013.07.003.

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21

Alster, Olga, Anna Bielak-Zmijewska, Grazyna Mosieniak, Maria Moreno-Villanueva, Wioleta Dudka-Ruszkowska, Aleksandra Wojtala, Monika Kusio-Kobiałka, et al. "The Role of Nibrin in Doxorubicin-Induced Apoptosis and Cell Senescence in Nijmegen Breakage Syndrome Patients Lymphocytes." PLoS ONE 9, no. 8 (August 13, 2014): e104964. http://dx.doi.org/10.1371/journal.pone.0104964.

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22

Fagundes, Marcia R. Z. Kress, Larissa Fernandes, Marcela Savoldi, Steven D. Harris, Maria H. S. Goldman, and Gustavo H. Goldman. "Identification of a Topoisomerase I Mutant, scsA1, as an Extragenic Suppressor of a Mutation in scaANBS1, the Apparent Homolog of Human Nibrin in Aspergillus nidulans." Genetics 164, no. 3 (July 1, 2003): 935–45. http://dx.doi.org/10.1093/genetics/164.3.935.

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Abstract The Mre11-Rad50-Nbs1 protein complex has emerged as a central player in the human cellular DNA damage response, and recent observations suggest that these proteins are at least partially responsible for the linking of DNA damage detection to DNA repair and cell cycle checkpoint functions. Mutations in scaANBS1, which encodes the apparent homolog of human nibrin in Aspergillus nidulans, inhibit growth in the presence of the antitopoisomerase I drug camptothecin. This article describes the selection and characterization of extragenic suppressors of the scaA1 mutation, with the aim of identifying other proteins that interfere with the pathway or complex in which the ScaA would normally be involved. Fifteen extragenic suppressors of the scaA1 mutation were isolated. The topoisomerase I gene can complement one of these suppressors. Synergistic interaction between the scaANBS1 and scsATOP1 genes in the presence of DNA-damaging agents was observed. Overexpression of topoisomerase I in the scaA1 mutant causes increased sensitivity to DNA-damaging agents. The scsATOP1 and the scaANBS1 gene products could functionally interact in pathways that either monitor or repair DNA double-strand breaks.

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23

Gatti, Richard A. "Ataxia Telangiectasia." Blood 118, no. 21 (November 18, 2011): SCI—7—SCI—7. http://dx.doi.org/10.1182/blood.v118.21.sci-7.sci-7.

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Abstract Abstract SCI-7 Ataxia-telangiectasia (A-T) is the prototype for an expanded group of inherited radiation sensitive disorders that together define the XCIND syndrome: x-ray hypersensitivity, cancer, immunodeficiency, neurological dysfunction, and DNA repair deficiency. Although the clinical radiosensitivity of these disorders can be tested in the clinical laboratory, diagnostic methods remain limited and in need of further validation. Without exception, to date, sensitivity to ionizing radiation appears to be integrally associated with double strand break (DSB) repair defects and lymphoid cancer susceptibility, setting these disorders apart from single strand break repair disorders such as xeroderma pigmentosum. Responding within seconds to DSB damage are ATM kinase, the protein lacking in A-T, and the NMR complex (nibrin, Mre11, and Rad50). The latter three proteins are associated with three additional XCIND disorders (nibrin deficiency [aka nijmegen breakage syndrome], Mre11 deficiency [ATLD], and Rad50 deficiency). ATM kinase activates a myriad of other proteins that 1) halt DNA synthesis, replication, and the progression of the cell cycle; 2) form a complex protein “mesh” to physically stabilize the broken DNA strands; and 3) restore the integrity of the breaks before they unravel to create even larger chromosomal lesions and resulting malignancies. Another ATM-dependent cancer link involves the downregulation of ATM by microRNA-421. MicroRNA-421 is upregulated by the transcription factor N-myc. Despite this, neuroblastomas are not commonly observed in A-T or XCIND patients. Another subset of XCIND-associated disorders lacks proteins the drive the nonhomologous end joining pathway of DNA repair. Several of these diseases present in infancy as B−/T− severe combined immunodeficiency, or SCID, and are frequent candidates for stem cell transplantation. Attempts to ablate existing bone marrow prior to transplantation may further compromise such patients if they are inherently radiosensitive. Thus, attempts to preselect such patients and reduce radiation dosages may improve general post-transplantation survival. While most protein deficiencies can be diagnosed by immunoblots of appropriate cellular fractions, nonfunctional proteins are not detected by this platform. Colony survival assays (CSA) measure the ability of replicating cells (e.g., lymphoblasts or fibroblasts) to survive after exposure to radiation. Although causal proof that CSA can predict clinical radiosensitivity is lacking, the reduced percent survival fraction (i.e., radiosensitivity) of A-T, N-Bromosuccinimide, or Fanconi cell lines can be abrogated by introducing the mutated cognate gene. Other surrogate assays for radiosensitivity include kinetic studies, pre-irradiation and post-irradiation of γ-H2AX or SMC1 phosphorylation. Ultimately, DNA sequencing of a candidate gene can pinpoint the underlying pathogenesis of radiosensitivity in an XCIND disorder. Disclosures: No relevant conflicts of interest to declare.

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24

Wessendorf, Petra, Jan Vijg, André Nussenzweig, and Martin Digweed. "Deficiency of the DNA repair protein nibrin increases the basal but not the radiation induced mutation frequency in vivo." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 769 (November 2014): 11–16. http://dx.doi.org/10.1016/j.mrfmmm.2014.07.001.

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25

Cerosaletti, Karen M., and Patrick Concannon. "Nibrin Forkhead-associated Domain and Breast Cancer C-terminal Domain Are Both Required for Nuclear Focus Formation and Phosphorylation." Journal of Biological Chemistry 278, no. 24 (April 4, 2003): 21944–51. http://dx.doi.org/10.1074/jbc.m211689200.

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26

Romanowska, Anna, Joanna Gajda, Jacek Jassem, Rafał Pęksa, and Renata Zaucha. "Three secondary malignant neoplasms in a childhood cancer survivor positive for nibrin gene mutation – a case report and literature review." Nowotwory. Journal of Oncology 69, no. 2 (August 2, 2019): 65–66. http://dx.doi.org/10.5603/njo.2019.0012.

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27

Monk, Bradley J., Stanley B. Kaye, Andrés Poveda, Thomas J. Herzog, Miguel Aracil, Antonio Nieto, Nadia Badri, Trilok V. Parekh, Adnan Tanović, and Carlos M. Galmarini. "Nibrin is a marker of clinical outcome in patients with advanced serous ovarian cancer treated in the phase III OVA-301 trial." Gynecologic Oncology 132, no. 1 (January 2014): 176–80. http://dx.doi.org/10.1016/j.ygyno.2013.10.032.

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28

Mendez, Gina, Domenica Cilli, Francesco Berardinelli, Mara Viganotti, Paolo Ascenzi, Caterina Tanzarella, Antonio Antoccia, and Alessandra di Masi. "Cleavage of the BRCT tandem domains of nibrin by the 657del5 mutation affects the DNA damage response less than the Arg215Trp mutation." IUBMB Life 64, no. 10 (September 3, 2012): 853–61. http://dx.doi.org/10.1002/iub.1077.

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29

Kocheva, SA, K. Martinova, Z. Antevska-Trajkova, B. Coneska-Jovanova, A. Eftimov, and AJ Dimovski. "T-lymphoblastic leukemia/lymphoma in macedonian patients with Nijmegen breakage syndrome." Balkan Journal of Medical Genetics 19, no. 1 (June 1, 2016): 91–94. http://dx.doi.org/10.1515/bjmg-2016-0012.

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AbstractNijmegen breakage syndrome (NBS) is a rare autosomal recessive chromosomal instability disorder characterized by microcephaly, immunodeficiency, radiosensitivity and a very high predisposition to malignancy. The gene responsible for the disease, NBS1, is located on chromosome 8q21 and encodes a protein called nibrin. After identification of the gene, a truncating 5 bp deletion, 657-661delACAAA, was identified as the disease-causing mutation in patients with the NBS. In this report, we describe two patients with NBS and T-lymphoblastic leukemia/lymphoma in a Macedonian family. To the best of our knowledge, this is the first family with NBS reported from Macedonia. Both children presented with microcephaly, syndactyly and the development of T cell lymphoblastic lekemia/lymphoma at the age of 7 and 10 years, respectively. The molecular analysis of NBS1 genes in our patients showed homozygosity for the 657del5 mutation in the NBS1 gene. The parents were heterozygotes for the 657del5 mutation and they had no knowledge of a consanguineous relationship. The first child was treated with the International Berlin-Frankfurt-Münster (BFM)-Non Hodgkin lymphoma (NHL) protocol and achieved a complete remission that lasted for 21 months. Subsequently, he developed a medullar relapse with hyperleukocytosis and died due to lethal central nervous system (CNS) complications. The second child was treated according to the International Collaborative Treatment Protocol for Children and Adolescents with Acute Lymphoblastic Leukemia 2009 (AIOP-BFM ALL 2009) protocol. Unfortunately, remission was not achieved.

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30

Cilli, Domenica, Cristiana Mirasole, Rosa Pennisi, Valeria Pallotta, Angelo D'Alessandro, Antonio Antoccia, Lello Zolla, Paolo Ascenzi, and Alessandra di Masi. "Identification of the Interactors of Human Nibrin (NBN) and of Its 26 kDa and 70 kDa Fragments Arising from the NBN 657del5 Founder Mutation." PLoS ONE 9, no. 12 (December 8, 2014): e114651. http://dx.doi.org/10.1371/journal.pone.0114651.

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31

García-Perdomo, Herney Andrés, Mailyn Alejandra Bedoya Saldarriaga, and Adalberto Sánchez. "Frequency of Variants in DNA-Repair Genes in a Southwest Colombian Population." Revista Urología Colombiana / Colombian Urology Journal 28, no. 03 (May 23, 2019): 226–33. http://dx.doi.org/10.1055/s-0039-1688964.

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Abstract Objective To describe the frequency of mutations in DNA-repair genes in a southwestern Colombian population. Methods We have designed an observational study, including 162 people from all ages from southwest Colombia. We have extracted and collected their DNA in filters. We have immersed the DNA in a phosphate buffer along with DNeasy package (Thermo Fisher Scientific, Waltham, MA, USA). The preparation process was with the TruSeq Exome Library Prep (Illumina, Inc. San Diego, CA, USA), then the obtained libraries were normalized with TruSeq Rapid Exome (Illumina, Inc. San Diego, CA, USA). We sequenced the full exome and identified the variants associated with 12 genes (ataxia telangiectasia mutated [ATM], BRCA1 DNA repair associated [BRCA1], BRCA2 DNA repair associated [BRCA2], checkpoint kinase 2 [CHEK2], epithelial cell adhesion molecule [EPCAM], homeobox protein Hox-B13 [HOXB13], mutS homolog 1, 2 and 6 [MLH1, MSH2, MSH6], nibrin [NBN], PMS1 homolog 2, mismatch repair system component [PMS2], and tumor protein p53 [TP53]). Descriptive statistics were performed with the R software (The R Foundation for Statistical Computing, Vienna, Austria). Results A total of 7,315,466 pieces of data were sequenced in this population. The most frequently mutated genes were ATM (1,221 pieces of data; 13.2%), BRCA1 (1,178 pieces of data; 12.8%), BRCA2 (1,484 pieces of data; 16.12%), and NBN (965 pieces of data; 10.42%). The most common single nucleotide polymorphisms (SNPs) in these 12 genes were the following: BRCA2 (rs169547, rs206075, rs206076); ATM (rs659243, rs228589); TP53 (rs1625895, rs1042522, rs1642785); PMS2 (rs2228006, rs1805319); NBN (rs709816); and MSH6 (rs3136367) Conclusion The BRCA2, ATM, BRCA1 and NBN DNA-repair genes were the most frequently mutated in this southwestern Colombian Population.

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Rischewski, J., P. v Bismarck, H. Kabisch, G. Janka-Schaub, T. Obser, and R. Schneppenheim. "The common deletion 657del5 in the Nibrin gene is not a major risk factor for B or T cell non-Hodgkin lymphoma in a pediatric population." Leukemia 14, no. 8 (August 2000): 1528–29. http://dx.doi.org/10.1038/sj.leu.2401836.

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MaGee, Karen D. M., Guy Travers, Brian W. Skelton, Massimilliano Massi, Alan D. Payne, and David H. Brown. "Synthesis, Solid-state Structures, Solution Behaviour and Catalysis Studies of Nickel Complexes of Bis(benzimidazolin-2-ylidene)pyridine Pincer Ligands." Australian Journal of Chemistry 65, no. 7 (2012): 823. http://dx.doi.org/10.1071/ch12044.

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N-Heterocyclic carbene–nickel complexes with five- and four-coordinate geometries [(CNC)NiBr2] and [(CNC)NiBr]X (X = PF6 or BPh4) have been prepared with the pincer ligands 2,6-bis(N-octylbenzimidazolin-2-ylidene)pyridine and 2,6-bis(N-butyl-5,6-dimethoxybenzimidazolin-2-ylidene)pyridine. The addition of the n-octyl substituent significantly extends the solubility of the complexes and has allowed UV-vis solution studies of the complexes in dichloromethane and methanol. The four- and five-coordinate species exist in equilibrium in solution and this equilibrium has been explored by UV-vis studies. The complexes have also been characterized by NMR studies, and single crystal X-ray diffraction studies have been performed on [(CNC)NiBr2] (where CNC = 2,6-bis(N-octylbenzimidazolin-2-ylidene)pyridine) and [(CNC)NiBr]BPh4 (where CNC = 2,6-bis(N-butyl-5,6-dimethoxybenzimidazolin-2-ylidene)pyridine).

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Endrayani, Rini. "REKRUTMEN DAN SELEKSI KARYAWAN DENGAN METODE PENJARINGAN DI LEMBAGA PENDIDIKAN BERDAMPAK TERHADAP KINERJA KARYAWAN DI NIBRAS HOUSE SIDOREJO (STUDI PADA KARYAWAN NIBRAS HOUSE SIDOREJO LAMPUNG TIMUR)." Jurnal Ekonomi Manajemen Sistem Informasi 2, no. 2 (November 30, 2020): 139–47. http://dx.doi.org/10.31933/jemsi.v2i2.378.

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perencanaan MSDM pada suatu perusahaan mempertimbangkan beberapa faktor diantaranya pola rekrutmen, pada Nibras House Sidorejo pola rekrutmen yang digunakan yaitu dengan penjaringan di lembaga pendidikan, rekrutmen pola ini sebagai antisipasi terjadinya : Kurang dipahaminya proses penjualan retail oleh karyawan, karyawan belum terbiasa bekerja di dalam ruangan atau toko dan karyawan belum mampu mengelola toko dengan baik. Dari permasalahan yang terjadi maka Nibras House Sidorejo membuat suatu terobosan dengan melibatkan lembaga pendidikan sebagai partner dalam proses rekrutmen, terobosan metode ini dikenal dengan istilah program Nibras class untuk peserta didik SMK dengan program keahlian Bisnis Daring Pemasaran (BDP). Dari hasil pengamatan dapat dinyatakan bahwa dengan program Nibras class perusahaan mendapat beberapa keuntungan : Mendapatkan karyawan siap kerja di bidang bisnis retail, Hasil program Nibras class memiliki kompetensi tinggi bekerja, Secara psikologis karyawan sudah menyatu dengan perusahaan dalam beberapa tahun dan Perusahaan tidak perlu lagi membuat program rekrutmen karyawan.

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Coutinho, A. R. S., and V. Bordignon. "125 SWINE EMBRYOS WITH HIGH POTENTIAL TO DEVELOP IN VITRO HAVE LESS γH2A.X AND MORE NBS1 PROTEINS." Reproduction, Fertility and Development 22, no. 1 (2010): 221. http://dx.doi.org/10.1071/rdv22n1ab125.

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The developmental potential of embryos produced in vitro is lower than those produced in vivo. The artificial environment and the stressful conditions of culture may affect embryo development through various mechanisms including DNA damage and, consequently, cell death. We hypothesized that the developmental competence of in vitro-cultured embryos is influenced by mechanisms signalling DNA damage and repair processes. Therefore, the aim of the study was to assess these processes by systematic quantification of phosphorylated histone H2A.X (γH2A.X) and p95 or nibrin protein (NSB1) in early- and late-cleaved swine embryos cultured in vitro. Studies from several groups including ours have demonstrated superior in vitro development for early-cleaved (within 24 h of culture) compared with late-cleaved (between 24 and 48 h) embryos. The presence of γH2A.X is associated with the DNA double-strand breaks, and NBS1 is involved in the process of DNA damage repair. These proteins were detected by both immunofluorescence and western blotting. Swine embryos were produced by parthenogenetic activation using in vitro-matured oocytes. Oocyte maturation, activation, and embryo culture were conducted as previously described (Che L et al. 2007 Theriogenology 67 1297-1304). At 24 and 48 h after activation, embryos were categorized as early- and late-cleaved, and were collected for protein detection on D2-3, D4-5, or D6-7 of culture. A minimum of 3 replicates were performed per treatment. The amount of protein in relation to the β-actin at D2-3, D4-5, and D6-7 as revealed by western blotting was 76.4% ± 1.3, 63.3% ± 10.5, and 43.2% ± 11.2 for γH2A.X and 60.2% ± 4.2, 67.3% ± 13.2, and 61.3% ± 6.2 for NBS1, respectively. Comparisons between early and late-cleaved groups were then performed by immunoflorescence detection of both proteins. Differences between groups were verified using Student’s t-test. The average proportion of cells that were positively stained for γH2AX at D2-3, D4-5, and D6-7 of culture was 64.4% ± 2.6 (n = 178) v. 65.92% ± 3.7 (n = 114; P = 0.7), 55.7% ± 2.4 (n = 121) v. 59.8% ± 4.7 (n = 62; P = 0.4) and 29.1% ± 2.1 (n = 137) v. 43.5% ± 3.4 (n = 41; P = 0.001), for early v. late-cleaved embryos. The values for NSB1 staining were 13.9% ± 3.8 (75) v. 3.9% ± 3.0 (34; P = 0.09), 50.5% ± 4.2 (66) v. 35.8% ± 6.0 (33; P = 0.05), and 51.0% ± 4.5 (n = 54) v. 38.2% ± 5.5 (n = 24; P = 0.1). These findings confirm the presence of γH2A.X and NBS1 proteins in swine embryos during all stages of in vitro culture. We further show that early cleaved embryos have a lower proportion of γH2A.X and a higher proportion of NSB1-positive cells compared with late-cleaved embryos. Together, these findings suggest that early cleaved embryos that have a superior capacity for in vitro development are better prepared to repair DNA damage during in vitro culture. Supported by NSERC.

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McCormack, Philip D., April Pattavina, and Paul E. Tracy. "Assessing the Coverage and Representativeness of the National Incident-Based Reporting System." Crime & Delinquency 63, no. 4 (March 16, 2017): 493–516. http://dx.doi.org/10.1177/0011128717694595.

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This article examines the coverage of the National Incident-Based Reporting System (NIBRS) as of 2013. We use NIBRS, Uniform Crime Reports (UCR), and Supplementary Homicide Reports to assess the population coverage and index crime coverage of NIBRS. We also examine the correspondence of crime rates between the UCR and agencies that do and do not participate in NIBRS. We found that NIBRS covers 29.3% of the U.S. population and 28% of UCR index crimes. We also found that the crime rates in NIBRS jurisdictions are appreciably lower than jurisdictions that do not participate in NIBRS. As of 2013, therefore, NIBRS data are not representative of the U.S. population, crime counts, or crime rates.

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Rogers, Lee F. "NIBIB." American Journal of Roentgenology 178, no. 2 (February 2002): 273. http://dx.doi.org/10.2214/ajr.178.2.1780273.

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38

De Silvestri, Elena. "L’apparizione del nibbio." Chiasmi International 19 (2017): 371–86. http://dx.doi.org/10.5840/chiasmi20171931.

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39

Shadwick, Joshua T., William R. King, Yan Zhang, Matthew C. Matusiak, and Bradley A. Campbell. "Assessing best practices in crime labs structure, processes, and performance." Policing: An International Journal 42, no. 5 (October 10, 2019): 751–66. http://dx.doi.org/10.1108/pijpsm-12-2018-0181.

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Purpose Forensic crime labs play an important role in the criminal justice system’s response to violent gun crimes in the USA. The purpose of this paper is to describe the methods of firearms analysis including ballistics imaging and proposed best practices for investigating gun crimes. A separate line of research has begun to explore the structure of forensic labs and how structure impacts lab performance. Design/methodology/approach To date, however, proposed best practices in firearms investigation have not been empirically tested within crime labs. The authors address this gap in the literature by using a mediation model examining organizational correlates of a limited number of tasks (identified by Peter Gagliardi’s 13 Critical Tasks) believed to enhance our final dependent measures, forensic crime lab outcomes (NIBIN acquisitions and hits). The authors examine, therefore, the relationship between organizational correlates, collected from a sample of publicly funded labs in the USA, on several of Gagliardi’s tasks and then explore the relationship of those tasks on our outcome variables: NIBIN acquisitions and hits. Findings Results indicate agency size and number of agencies serviced by a lab are significant factors associated with our mediating variables (Gagliardi’s tasks). Communication was identified as a significant task associated with achieving NIBIN acquisitions and hits. In general, this study underscores the importance of communication between labs and other institutional constituents for increasing ballistics imaging outputs. Furthermore, findings provide partial support for Gagliard’s tasks, by highlighting the role of enhanced communication on organization-based performance outcomes. Originality/value This study is the first to examine the mediating effect of Gagliardi’s tasks on the organizational performance of ballistics imaging systems within crime labs. In addition, this study examines the influence of organizational correlates on these mediating tasks.

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Liu, Liying, Yutao Xing, I. L. C. Merino, D. F. Franceschini, I. G. Solórzano, and E. Baggio-Saitovitch. "Magnetic properties of superconducting phases NiBi and NiBi3 formed during pulsed laser deposition of Ni-Bi films." Journal of Magnetism and Magnetic Materials 514 (November 2020): 167275. http://dx.doi.org/10.1016/j.jmmm.2020.167275.

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41

Seo, Jae-Won, Ji-Young Hwang, and Ueon Sang Shin. "Ionic liquid-doped and p-NIPAAm-based copolymer (p-NIBIm): extraordinary drug-entrapping and -releasing behaviors at 38–42 °C." RSC Adv. 4, no. 51 (2014): 26738–47. http://dx.doi.org/10.1039/c4ra03736g.

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Takeuchi, Daisuke, Yoshi-aki Tojo, and Kohtaro Osakada. "Synthesis of a Ni Complex Chelated by a [2.2]Paracyclophane-Functionalized Diimine Ligand and Its Catalytic Activity for Olefin Oligomerization." Molecules 26, no. 9 (May 5, 2021): 2719. http://dx.doi.org/10.3390/molecules26092719.

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A diimine ligand having two [2.2]paracyclophanyl substituents at the N atoms (L1) was prepared from the reaction of amino[2.2]paracyclophane with acenaphtenequinone. The ligand reacts with NiBr2(dme) (dme: 1,2-dimethoxyethane) to form the dibromonickel complex with (R,R) and (S,S) configuration, NiBr2(L1). The structure of the complex was confirmed by X-ray crystallography. NiBr2(L1) catalyzes oligomerization of ethylene in the presence of methylaluminoxane (MAO) co-catalyst at 10–50 °C to form a mixture of 1- and 2-butenes after 3 h. The reactions for 6 h and 8 h at 25 °C causes further increase of 2-butene formed via isomerization of 1-butene and formation of hexenes. Reaction of 1-hexene catalyzed by NiBr2(L1)–MAO produces 2-hexene via isomerization and C12 and C18 hydrocarbons via oligomerization. Consumption of 1-hexene of the reaction obeys first-order kinetics. The kinetic parameters were obtained to be ΔG‡ = 93.6 kJ mol−1, ΔH‡ = 63.0 kJ mol−1, and ΔS‡ = −112 J mol−1deg−1. NiBr2(L1) catalyzes co-dimerization of ethylene and 1-hexene to form C8 hydrocarbons with higher rate and selectivity than the tetramerization of ethylene.

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43

Mackie, P., and F. Sim. "Fake news, facts and Nibiru." Public Health 153 (December 2017): A1—A2. http://dx.doi.org/10.1016/j.puhe.2017.10.011.

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44

Kim, Sam Woong, Song I. Kang, Da Hye Shin, Se Yun Oh, Chae Won Lee, Yoonyong Yang, Youn Kyoung Son, et al. "Potential of Cell-Free Supernatant from Lactobacillus plantarum NIBR97, Including Novel Bacteriocins, as a Natural Alternative to Chemical Disinfectants." Pharmaceuticals 13, no. 10 (September 23, 2020): 266. http://dx.doi.org/10.3390/ph13100266.

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The recent pandemic of coronavirus disease 2019 (COVID-19) has increased demand for chemical disinfectants, which can be potentially hazardous to users. Here, we suggest that the cell-free supernatant from Lactobacillus plantarum NIBR97, including novel bacteriocins, has potential as a natural alternative to chemical disinfectants. It exhibits significant antibacterial activities against a broad range of pathogens, and was observed by scanning electron microscopy (SEM) to cause cellular lysis through pore formation in bacterial membranes, implying that its antibacterial activity may be mediated by peptides or proteins and supported by proteinase K treatment. It also showed significant antiviral activities against HIV-based lentivirus and influenza A/H3N2, causing lentiviral lysis through envelope collapse. Furthermore, whole-genome sequencing revealed that NIBR97 has diverse antimicrobial peptides, and among them are five novel bacteriocins, designated as plantaricin 1 to 5. Plantaricin 3 and 5 in particular showed both antibacterial and antiviral activities. SEM revealed that plantaricin 3 causes direct damage to both bacterial membranes and viral envelopes, while plantaricin 5 damaged only bacterial membranes, implying different antiviral mechanisms. Our data suggest that the cell-free supernatant from L. plantarum NIBR97, including novel bacteriocins, is potentially useful as a natural alternative to chemical disinfectants.

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Maio, Michele, Ester Fonsatti, Arianna Burigo, and Giorgio Parmiani. "The Italian Network for Tumor Biotherapy (NIBIT). Sharing Visions, Goals and Efforts at European Level." Tumori Journal 94, no. 2 (March 2008): 179–81. http://dx.doi.org/10.1177/030089160809400208.

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In the context of the Scientific Week 2008 of the Organisation of the European Cancer Institutes, the Italian Network for Tumor Biotherapy (NIBIT), within its initiatives sponsored by Alleanza Contro il Cancro, the Italian Network of Comprehensive Cancer Centers has contributed to organize the Workshop of the European Networks for bio-immunotherapy of tumors. Representatives from the Nordic Center of Excellence for the Development of Anti-Tumor Vaccines (Sweden), the German Network of Immunotherapy of Tumors (Germany), the Biotherapy Development Association and NIBIT gathered to present their organization and ongoing scientific activities, as well as to identify common strategies and shared efforts to push the field of cancer bio-immunotherapy forward at a European level. This article briefly summarizes the history and objectives of NIBIT, along with the actions so far taken by the Network.

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46

Eisenberg, Paul D. "Ex Nihilismo Nibil Fit." International Studies in Philosophy 19, no. 2 (1987): 45–50. http://dx.doi.org/10.5840/intstudphil198719249.

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Nagy, Edward C. "Update on NIBIB Appropriations." Academic Radiology 9, no. 7 (July 2002): 870–73. http://dx.doi.org/10.1016/s1076-6332(03)80366-5.

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Harrington, Donald P. "Priority Setting, NIBIB Style." Journal of the American College of Radiology 2, no. 12 (December 2005): 1033–34. http://dx.doi.org/10.1016/j.jacr.2005.09.003.

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49

Cowie, Bradley E., and David J. H. Emslie. "M–H–BR3 and M–Br–BR3 interactions in rhodium and nickel complexes of an ambiphilic phosphine–thioether–borane ligand." Canadian Journal of Chemistry 96, no. 5 (May 2018): 484–91. http://dx.doi.org/10.1139/cjc-2017-0758.

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Reaction of [Rh(μ-Cl)(CO)(TXPB)] (1; TXPB = 2,7-di-tert-butyl-5-diphenylboryl-4-diphenylphosphino-9,9-dimethylthioxanthene) with NaBH4 yielded square planar [Rh(μ-H)(CO)(TXPB)] (2) in which the hydride ligand bridges between rhodium and the borane unit of TXPB. The Rh–H, Rh–B, and Rh–Cipso distances are short at 1.84(5), 2.456(6), and 2.568(5) Å, respectively, whereas the B–H bond, 1.59(6) Å, falls at the longer end of the usual range. Compound 2 is compared with the previously reported series of rhodium TXPB complexes: [RhX(CO)(TXPB)] {X = F (3), Cl (1), Br (4), I (5)}. Compound 4 in this series features the only crystallographically characterized example of an M–Br–BR3 interaction, and to expand this area, [NiBr(μ-Br)(TXPB)] (6) was prepared via the reaction of [NiBr2(dme)2] (dme = 1,2-dimethoxyethane) with TXPB. An X-ray crystal structure of light purple 6 revealed a square-planar geometry with a strong B–Br interaction {B–Br = 2.311(6) Å; ∑(C–B–C) = 344.5(7)°}. An 11B NMR chemical shift of 23 ppm was observed for 6, indicating that an appreciable B–Br interaction is maintained in solution. No signals were observed in the 31P{1H} NMR spectrum at room temperature, whereas a broadened 31P signal was observed at −20 °C, evolving into a sharp singlet at −67 °C. This behaviour suggests that at room temperature, square planar 6 exists in equilibrium with a paramagnetic tetrahedral isomer, present at a level below that detectable through Evans magnetic measurements.

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Bober, Mariusz, Jacek Senkara, and Bogdan Wendler. "Persistence of the thin layers of transition metal carbides in contact with liquid NiBSi alloy." Welding Technology Review 93, no. 1 (February 27, 2021): 5–12. http://dx.doi.org/10.26628/wtr.v93i1.1128.

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The article presents the results of study on interaction between the liquid NiBSi alloy and solid, thin, micrometer-range layers of transition metal carbides of IVB - VIB groups of the periodic table. The reactive magnetron sputtering method was adopted to deposit of these layers on molybdenum substrates. Carbide layers are destroyed in contact with liquid alloy by dissolving, intensified by the penetration of the liquid along the coating - substrate interface. The strong interaction between liquid NiBSi and both the carbide ceramics and the refractory metal substrate was revealed. The effect intensity differs somewhat for both tested carbide groups: IVB (relatively fast) and VIB (less intense).

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