Journal articles: 'Nemo'

1

Corn, A. "Nemo." Literary Imagination 9, no. 3 (May 26, 2007): 273. http://dx.doi.org/10.1093/litimag/imm006.

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Plagge, Mark, Christopher D. Carothers, Elsa Gonsiorowski, and Neil Mcglohon. "NeMo." ACM Transactions on Modeling and Computer Simulation 28, no. 4 (October 13, 2018): 1–25. http://dx.doi.org/10.1145/3186317.

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Hsieh, Cheng-Yu, Jieyu Zhang, and Alexander Ratner. "Nemo." Proceedings of the VLDB Endowment 15, no. 13 (September 2022): 4093–105. http://dx.doi.org/10.14778/3565838.3565859.

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Weak Supervision (WS) techniques allow users to efficiently create large training datasets by programmatically labeling data with heuristic sources of supervision. While the success of WS relies heavily on the provided labeling heuristics, the process of how these heuristics are created in practice has remained under-explored. In this work, we formalize the development process of labeling heuristics as an interactive procedure, built around the existing workflow where users draw ideas from a selected set of development data for designing the heuristic sources. With the formalism, shown in Figure 1, we study two core problems of (1) how to strategically select the development data to guide users in efficiently creating informative heuristics, and (2) how to exploit the information within the development process to contextualize and better learn from the resultant heuristics. Building upon two novel methodologies that effectively tackle the respective problems considered, we present Nemo, an end-to-end interactive system that improves the overall productivity of WS learning pipeline by an average 20% (and up to 47% in one task) compared to the prevailing WS approach.

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4

Bates, Jane. "Nemo complex." Nursing Standard 21, no. 19 (January 17, 2007): 27. http://dx.doi.org/10.7748/ns.21.19.27.s35.

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Renouard, Jean-Philippe. "merci nemo." Vacarme 24, no. 3 (2003): 72. http://dx.doi.org/10.3917/vaca.024.0072.

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6

Hay, Ronald T. "Modifiying NEMO." Nature Cell Biology 6, no. 2 (February 2004): 89–91. http://dx.doi.org/10.1038/ncb0204-89.

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7

Smallridge, Rachel. "Understanding NEMO." Nature Reviews Molecular Cell Biology 7, no. 6 (May 17, 2006): 384–85. http://dx.doi.org/10.1038/nrm1944.

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8

Koylass, Nicholas Robert, Elizabeth A. DeRiso, Andrea L. Szymczak-Workman, Angela Montecalvo, Joanne M. Murphy, Maria Cristina Seminario, Lawrence P. Kane, and Stephen C. Bunnell. "Recruitment of NEMO/IKKγ to TCR microclusters during T cell activation." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 184.1. http://dx.doi.org/10.4049/jimmunol.202.supp.184.1.

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Abstract The IκB kinase (IKK) complex mediates the activation of canonical NFκB isoforms following T cell receptor (TCR) ligation. This complex consists of the kinases IKKα and IKKβ and an essential adaptor subunit, the NFκB essential modulator protein (NEMO). Most models suggest that the IKK complex is activated within oligomeric Carma1/Bcl10/Malt1 (CBM) signalosomes. However, we observed that NEMO enters TCR microclusters before CBM complexes are assembled, within ~70 seconds of TCR engagement. NEMO also entered mobile vesicles and in larger membrane-bounded structures (hereafter ‘macroclusters’). The recruitment of NEMO into TCR microclusters is prevented by Src kinase inhibitors and by the catalytic inactivation of ZAP-70, but occurs in the absence of either SLP-76 or Carma1. Further, NEMO fails to co-localize with TCR-induced CBM polymers. Thus, the recruitment of NEMO to the TCR occurs via a CBM-independent mechanism. The deletion the zinc-finger (ZnF) domain of NEMO disables NFκB signaling and eliminates NEMO from microclusters, while preserving NEMO macroclusters. Since the ZnF domain interacts with polyubiquitin chains, we generated point mutations impacting the ubiquitin-binding site in the ZnF domain and two independent sites within the NEMO ubiquitin-binding ‘NUB’ domain. These mutations impair the ability of NEMO to capture K63-linked and/or linear polymers, hinder NFκB signaling, and eliminate NEMO from microclusters without disrupting NEMO macroclusters. These findings suggest that NEMO is rapidly recruited to polyubiquitin chains associated with the TCR, rather than the CBM complex, and that the CBM complex augments IKK-dependent NFκB signaling via a distinct, recruitment-independent mechanism.

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Medunjanin, Senad, Maximilian Putzier, Till Nöthen, Sönke Weinert, Thilo Kähne, Blerim Luani, Werner Zuschratter, and Ruediger C. Braun-Dullaeus. "DNA-PK: gatekeeper for IKKγ/NEMO nucleocytoplasmic shuttling in genotoxic stress-induced NF-kappaB activation." Cellular and Molecular Life Sciences 77, no. 20 (January 13, 2020): 4133–42. http://dx.doi.org/10.1007/s00018-019-03411-y.

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Abstract The transcription factors of the nuclear factor κB (NF-κB) family play a pivotal role in the cellular response to DNA damage. Genotoxic stress-induced activation of NF-κB differs from the classical canonical pathway by shuttling of the NF-κB Essential Modifier (IKKγ/NEMO) subunit through the nucleus. Here, we show that DNA-dependent protein kinase (DNA-PK), an enzyme involved in DNA double-strand break (DSB) repair, triggers the phosphorylation of NEMO by genotoxic stress, thereby enabling shuttling of NEMO through the nucleus with subsequent NF-κB activation. We identified serine 43 of NEMO as a DNA-PK phosphorylation site and point mutation of this serine to alanine led to a complete block of NF-κB activation by ionizing radiation (IR). Blockade of DNA-PK by a specific shRNA or by DNA-PKcs-deficient cells abrogated NEMO entry into the nucleus, as well. Accordingly, SUMOylation of NEMO, a prerequisite of nuclear NEMO, was abolished. Based on these observations, we propose a model in which NEMO phosphorylation by DNA-PK provides the first step in the nucleocytoplasmic trafficking of NEMO.

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Goel, Simran, Rosario Oliva, Sadasivam Jeganathan, Verian Bader, Laura J. Krause, Simon Kriegler, Isabelle D. Stender, et al. "Linear ubiquitination induces NEMO phase separation to activate NF-κB signaling." Life Science Alliance 6, no. 4 (January 31, 2023): e202201607. http://dx.doi.org/10.26508/lsa.202201607.

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The NF-κB essential modulator NEMO is the core regulatory component of the inhibitor of κB kinase complex, which is a critical checkpoint in canonical NF-κB signaling downstream of innate and adaptive immune receptors. In response to various stimuli, such as TNF or IL-1β, NEMO binds to linear or M1-linked ubiquitin chains generated by LUBAC, promoting its oligomerization and subsequent activation of the associated kinases. Here we show that M1-ubiquitin chains induce phase separation of NEMO and the formation of NEMO assemblies in cells after exposure to IL-1β. Phase separation is promoted by both binding of NEMO to linear ubiquitin chains and covalent linkage of M1-ubiquitin to NEMO and is essential but not sufficient for its phase separation. Supporting the functional relevance of NEMO phase separation in signaling, a pathogenic NEMO mutant, which is impaired in both binding and linkage to linear ubiquitin chains, does not undergo phase separation and is defective in mediating IL-1β–induced NF-κB activation.

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11

Wackernagel, Lisa-Marie, Mohsen Abdi Sarabi, Sönke Weinert, Werner Zuschratter, Karin Richter, Klaus Dieter Fischer, Ruediger C. Braun-Dullaeus, and Senad Medunjanin. "IKKγ/NEMO Localization into Multivesicular Bodies." International Journal of Molecular Sciences 23, no. 12 (June 17, 2022): 6778. http://dx.doi.org/10.3390/ijms23126778.

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The NF-κB pathway is central pathway for inflammatory and immune responses, and IKKγ/NEMO is essential for NF-κB activation. In a previous report, we identified the role of glycogen synthase kinase-3β (GSK-3β) in NF-κB activation by regulating IKKγ/NEMO. Here, we show that NEMO phosphorylation by GSK-3β leads to NEMO localization into multivesicular bodies (MVBs). Using the endosome marker Rab5, we observed localization into endosomes. Using siRNA, we identified the AAA-ATPase Vps4A, which is involved in recycling the ESCRT machinery by facilitating its dissociation from endosomal membranes, which is necessary for NEMO stability and NF-κB activation. Co-immunoprecipitation studies of NEMO and mutated NEMO demonstrated its direct interaction with Vps4A, which requires NEMO phosphorylation. The transfection of cells by a mutated and constitutively active form of Vps4A, Vps4A-E233Q, resulted in the formation of large vacuoles and strong augmentation in NEMO expression compared to GFP-Vps4-WT. In addition, the overexpression of the mutated form of Vps4A led to increased NF-κB activation. The treatment of cells with the pharmacologic V-ATPase inhibitor bafilomycin A led to a dramatic downregulation of NEMO and, in this way, inhibited NF-κB signal transduction. These results reveal an unexpected role for GSK-3β and V-ATPase in NF-κB signaling activation.

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12

Hubeau, Marjorie, Flora Ngadjeua, Anne Puel, Laura Israel, Jacqueline Feinberg, Maya Chrabieh, Kiran Belani, et al. "New mechanism of X-linked anhidrotic ectodermal dysplasia with immunodeficiency: impairment of ubiquitin binding despite normal folding of NEMO protein." Blood 118, no. 4 (July 28, 2011): 926–35. http://dx.doi.org/10.1182/blood-2010-10-315234.

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Abstract Nuclear factor-κB essential modulator (NEMO), the regulatory subunit of the IκB kinase complex, is a critical component of the NF-κB pathway. Hypomorphic mutations in the X-linked human NEMO gene cause various forms of anhidrotic ectodermal dysplasia with immunodeficiency (EDA-ID). All known X-linked EDA-ID–causing mutations impair NEMO protein expression, folding, or both. We describe here 2 EDA-ID–causing missense mutations that affect the same residue in the CC2-LZ domain (D311N and D311G) that do not impair NEMO production or folding. Structural studies based on pull-down experiments showed a defect in noncovalent interaction with K63-linked and linear polyubiquitin chains for these mutant proteins. Functional studies on the patients' cells showed an impairment of the classic NF-κB signaling pathways after activation of 2 NEMO ubiquitin-binding–dependent receptors, the TNF and IL-1β receptors, and in the CD40-dependent NF-κB pathway. We report the first human NEMO mutations responsible for X-linked EDA-ID found to affect the polyubiquitin binding of NEMO rather than its expression and folding. These experiments demonstrate that the binding of human NEMO to polyubiquitin is essential for NF-κB activation. They also demonstrate that the normal expression and folding of NEMO do not exclude a pathogenic role for NEMO mutations in patients with EDA-ID.

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13

Zilberman-Rudenko, Jevgenia, Linda Monaco Shawver, Alex W. Wessel, Yongquan Luo, Martin Pelletier, Wanxia Li Tsai, Younglang Lee, et al. "Recruitment of A20 by the C-terminal domain of NEMO suppresses NF-κB activation and autoinflammatory disease." Proceedings of the National Academy of Sciences 113, no. 6 (January 22, 2016): 1612–17. http://dx.doi.org/10.1073/pnas.1518163113.

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Receptor-induced NF-κB activation is controlled by NEMO, the NF-κB essential modulator. Hypomorphic NEMO mutations result in X-linked ectodermal dysplasia with anhidrosis and immunodeficiency, also referred to as NEMO syndrome. Here we describe a distinct group of patients with NEMO C-terminal deletion (ΔCT-NEMO) mutations. Individuals harboring these mutations develop inflammatory skin and intestinal disease in addition to ectodermal dysplasia with anhidrosis and immunodeficiency. Both primary cells from these patients, as well as reconstituted cell lines with this deletion, exhibited increased IκB kinase (IKK) activity and production of proinflammatory cytokines. Unlike previously described loss-of-function mutations, ΔCT-NEMO mutants promoted increased NF-κB activation in response to TNF and Toll-like receptor stimulation. Investigation of the underlying mechanisms revealed impaired interactions with A20, a negative regulator of NF-κB activation, leading to prolonged accumulation of K63-ubiquitinated RIP within the TNFR1 signaling complex. Recruitment of A20 to the C-terminal domain of NEMO represents a novel mechanism limiting NF-κB activation by NEMO, and its absence results in autoinflammatory disease.

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14

Nishikomori, Ryuta, Hiroshi Akutagawa, Kyoko Maruyama, Mami Nakata-Hizume, Katsuyuki Ohmori, Kazunori Mizuno, Akihiro Yachie, et al. "X-linked ectodermal dysplasia and immunodeficiency caused by reversion mosaicism of NEMO reveals a critical role for NEMO in human T-cell development and/or survival." Blood 103, no. 12 (June 15, 2004): 4565–72. http://dx.doi.org/10.1182/blood-2003-10-3655.

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Abstract X-linked ectodermal dysplasia and immunodeficiency (XL-EDA-ID) is an X-linked recessive disease caused by a mutation in the nuclear factor-κB (NF-κB) essential modulator (NEMO). Here we report an XL-EDA-ID patient with atypical features of very few naive-phenotype T cells and defective mitogen-induced proliferation of peripheral blood mononuclear cells (PBMCs). The patient's NEMO defect was diagnosed by flow cytometric analysis of intracellular NEMO staining. Specific cell lineages (monocytes and neutrophils) expressed reduced levels of NEMO, but 2 populations of T, B, and NK cells were detected with normal and reduced expression of NEMO. Genomic analysis revealed that duplication of a 4.4-kb sequence ranging from intron 3 to exon 6 caused the reduced expression of NEMO. Polymorphism analysis showed that the patient's B- and T-cell lines with reduced and normal expression of NEMO had the same X chromosome, indicating that the somatic mosaicism was not due to fetomaternal transfusion but was most likely due to postzygotic reversion. This XLEDA-ID case adds to our understanding of NEMO biology, indicating that NEMO is critical for T-cell development and/or survival in humans as well as in mice. (Blood. 2004;103:4565-4572)

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Lee, Younglang, Eries Lee, Jevgenia Zilberman-Rudenko, Yong Chen, Marjan Gucek, Richard M. Siegel, and Eric Paul Hanson. "A20 regulates NF-κB activation through K48 linked polyubiquitination of NEMO." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 67.23. http://dx.doi.org/10.4049/jimmunol.198.supp.67.23.

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Abstract Activation of the NF-κB family of transcription factors is related to diverse biological processes, such as development, immune responses, and inflammation. As a result, mutations affecting the NF-κB signaling pathway cause syndromes characterized by immunodeficiency and autoinflammaotory disease. Recently, we identified the C-terminus of NEMO to be a regulator of NF-κB signaling, as a class of NEMO mutations lacking the C-terminus (ΔCT-NEMO) confer gain-of-function properties to the IKK complex due to impaired recruitment of A20 to the TNFR. Here, we investigated details by which A20 recruitment to the TNFR suppresses NF-κB signaling. The C-terminus of NEMO has been previously identified to preferentially recognize K63-linked polyubiquitin that in its unanchored form can mediate NEMO/A20 interaction. We found that the IKK complex containing ΔCT-NEMO forms but not other mutant forms of NEMO exhibit impaired K63 polyubiquitin binding ability. In addition to unanchored K63-lilnked polyubiquitin, we hypothesized that direct polyubiquitination of A20 could enable a functional interaction between A20 and NEMO. Using mass spectroscopy, we identified 4 lysine residues on A20 to be ubiquitination sites. Mutation of these lysines to arginine impaired A20’s ability to suppress TNF induced NF-κB activation. We noted stabilization of NEMO in A20 deficient cells following TNF stimulation. Biochemical studies in Jurkat and 293 cells revealed A20 dependent K48 linked polyubiquitination of NEMO at the TNFR following receptor stimulation. Our data suggest a mechanism of NF-κB regulation in which A20 is directly K63 polyubiquitinated to functionally interacts with NEMO which it targets by K48 linkages proteasomal degradation.

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16

Hewson, Claire. "Nemo, then Dory." Practical Pre-School 2016, Sup186 (July 2016): 7–8. http://dx.doi.org/10.12968/prps.2016.sup186.7.

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Van Epps, Heather L. "Finding NEMO mutations." Journal of Experimental Medicine 203, no. 7 (July 3, 2006): 1620. http://dx.doi.org/10.1084/jem.2037iti3.

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18

Thibodeau, Edward, and Lauren Mentasti. "Who stole Nemo?" Journal of the American Dental Association 138, no. 5 (May 2007): 656–60. http://dx.doi.org/10.14219/jada.archive.2007.0238.

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19

Piattelli, P. "Status of NEMO." Nuclear Physics B - Proceedings Supplements 165 (March 2007): 172–80. http://dx.doi.org/10.1016/j.nuclphysbps.2006.11.026.

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Migneco, E., S. Aiello, M. Ambriola, F. Ameli, I. Amore, M. Anghinolfi, A. Anzalone, et al. "Status of NEMO." Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment 567, no. 2 (November 2006): 444–51. http://dx.doi.org/10.1016/j.nima.2006.05.257.

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21

Weitzman, Jonathan B. "Knocking out NEMO." Molecular Medicine Today 6, no. 9 (September 2000): 339. http://dx.doi.org/10.1016/s1357-4310(00)01763-9.

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Zweiman, Burton, and Marc E. Rothenberg. "NEMO re-found." Journal of Allergy and Clinical Immunology 113, no. 1 (January 2004): 186. http://dx.doi.org/10.1016/j.jaci.2003.10.025.

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CHIARUSI, TOMMASO. "THE NEMO PROJECT." International Journal of Modern Physics A 20, no. 29 (November 20, 2005): 6947–49. http://dx.doi.org/10.1142/s0217751x05030557.

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Since 1998 the NEMO Collaboration started a long term activity to select and characterize an optimal deep-sea site for the installation of a km3 neutrino telescope. In more than 20 sea campaigns, the water and oceanographic properties have been studied. Moreover, an intense program has been performed to study the technical feasibility of a km3 detector and many computer simulations have been made to define a suitable detector architecture. Recently the project NEMO Phase-1 has been funded by INFN and MIUR. It foresees the realization of an underwater laboratory with 3 junction boxes and a couple of instrumented towers according to the design proposed by the NEMO collaboration. The project should be completed by 2006.

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24

Frankel, Laurie. "Finding Nemo (review)." Film & History: An Interdisciplinary Journal of Film and Television Studies 34, no. 1 (2004): 75–76. http://dx.doi.org/10.1353/flm.2004.0016.

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25

van Toor, D. A. G. "Het nemo-teneturbeginsel." Tijdschrift voor Bijzonder Strafrecht & Handhaving 2, no. 1 (April 2016): 28–43. http://dx.doi.org/10.5553/tbsenh/229567002016002001005.

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26

Rider, Elizabeth A. "Nemo on Vacation." Archives of Pediatrics & Adolescent Medicine 159, no. 7 (July 1, 2005): 606. http://dx.doi.org/10.1001/archpedi.159.7.606.

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Distefano, C. "Status of NEMO: results from the NEMO Phase-1 detector." Nuclear Physics B - Proceedings Supplements 190 (May 2009): 109–14. http://dx.doi.org/10.1016/j.nuclphysbps.2009.03.075.

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Sakowicz, Agata, Michalina Lisowska, Lidia Biesiada, Elżbieta Płuciennik, Agnieszka Gach, Magda Rybak-Krzyszkowska, Hubert Huras, et al. "Placental Expression of NEMO Protein in Normal Pregnancy and Preeclampsia." Disease Markers 2019 (January 2, 2019): 1–12. http://dx.doi.org/10.1155/2019/8418379.

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Background. Preeclamptic pregnancies often present an intensified inflammatory state associated with the nuclear activity of NFκB. NEMO is an essential regulator of nuclear factor kappa B (NFκB) in cytoplasmic and nuclear cellular compartments. The aim of the present study is to examine the level and localization of the NEMO protein in preeclamptic and nonpreeclamptic placentas. Methods. The study includes 97 preeclamptic cases and 88 controls. NEMO distribution was analyzed immunohistochemically. Its localization in the nuclear and cytoplasmic fractions, as well as in total homogenates of placental samples, was studied by western blot and ELISA. Results. The western blot and ELISA results indicate a significant difference in NEMO concentration in the total and nuclear fractions between preeclamptic and control samples (p<0.01 and p<0.001, respectively). In the cytoplasmic complement, similar levels of NEMO were found in preeclamptic and control placentas. In addition, immunohistochemical staining revealed that the NEMO protein is mainly localized in the syncytiotrophoblast layer, with controls demonstrating a stronger reaction with NEMO antibodies. This study also shows that the placental level of NEMO depends on the sex of the fetus. Conclusions. The depletion of the NEMO protein in the cellular compartments of placental samples may activate one of the molecular pathways influencing the development of preeclampsia, especially in pregnancies with a female fetus. A reduction of the NEMO protein in the nuclear fraction of preeclamptic placentas may intensify the inflammatory state characteristic for preeclampsia and increase the level of apoptosis and necrosis within preeclamptic placentas.

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Mo, Huier, Yinghao Qin, Liying Wan, Yu Zhang, Xing Huang, Yi Wang, Jianyong Xing, Qinglong Yu, and Xiangyu Wu. "Evaluating the Detection of Oceanic Mesoscale Eddies in an Operational Eddy-Resolving Global Forecasting System." Journal of Marine Science and Engineering 11, no. 12 (December 12, 2023): 2343. http://dx.doi.org/10.3390/jmse11122343.

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In this study, a global analysis and forecasting system at 1/12° is built for operational oceanography at the National Marine Environmental Forecasting Center (NMEFC) by using the NEMO ocean model (NMEFC-NEMO). First, statistical analysis methods are designed to evaluate the performance of sea level anomaly (SLA) forecasting. The results indicate that the NMEFC-NEMO performs well in SLA forecasting when compared with the Mercator-PSY4, Mercator-PSY3, UK-FOAM, CONCEPTS-GIOPS and Bluelink-OceanMAPS forecasting systems. The respective root-mean-squared errors (RMSEs) of NMEFC-NEMO (Mercator PSY4) are 0.0654 m (0.0663 m) and 0.0797 m (0.0767 m) for the lead times of 1 and 7 days. The anomaly correlation coefficients between forecasting and observations exceed 0.8 for the NMEFC-NEMO and Mercator-PSY4 systems, suggesting that the accuracy of SLA predicted using NMEFC-NEMO is comparable to Mercator PSY4 and superior to other forecasting systems. Moreover, the global spatial distribution of oceanic eddies are effectively represented in NMEFC-NEMO when compared to that in the HYCOM reanalysis, and the detection rate reaches more than 90% relative to HYCOM reanalysis. Regarding the strong eddies in the Kuroshio region, the NMEFC-NEMO reproduces the characteristic for anticyclonic and cyclonic eddies merging and splitting alternatively. As for the detective eddies in the Gulf Stream, NMEFC-NEMO effectively represents the spatial distribution of mesoscale eddies from different seasons. The amplitude of oceanic eddies, including both cyclones and anticyclones, were much stronger on 1 July 2019 than 1 January 2019. Overall, NMEFC-NEMO has a superior performance in SLA forecasting and effectively represents the oceanic mesoscale eddies for operational oceanography.

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Rappoport, Nimrod, and Ron Shamir. "NEMO: cancer subtyping by integration of partial multi-omic data." Bioinformatics 35, no. 18 (January 30, 2019): 3348–56. http://dx.doi.org/10.1093/bioinformatics/btz058.

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Abstract Motivation Cancer subtypes were usually defined based on molecular characterization of single omic data. Increasingly, measurements of multiple omic profiles for the same cohort are available. Defining cancer subtypes using multi-omic data may improve our understanding of cancer, and suggest more precise treatment for patients. Results We present NEMO (NEighborhood based Multi-Omics clustering), a novel algorithm for multi-omics clustering. Importantly, NEMO can be applied to partial datasets in which some patients have data for only a subset of the omics, without performing data imputation. In extensive testing on ten cancer datasets spanning 3168 patients, NEMO achieved results comparable to the best of nine state-of-the-art multi-omics clustering algorithms on full data and showed an improvement on partial data. On some of the partial data tests, PVC, a multi-view algorithm, performed better, but it is limited to two omics and to positive partial data. Finally, we demonstrate the advantage of NEMO in detailed analysis of partial data of AML patients. NEMO is fast and much simpler than existing multi-omics clustering algorithms, and avoids iterative optimization. Availability and implementation Code for NEMO and for reproducing all NEMO results in this paper is in github: https://github.com/Shamir-Lab/NEMO. Supplementary information Supplementary data are available at Bioinformatics online.

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Kawai, Tomoki, Ryuta Nishikomori, Kazushi Izawa, Yuuki Murata, Naoko Tanaka, Hidemasa Sakai, Megumu Saito, et al. "Frequent somatic mosaicism of NEMO in T cells of patients with X-linked anhidrotic ectodermal dysplasia with immunodeficiency." Blood 119, no. 23 (June 7, 2012): 5458–66. http://dx.doi.org/10.1182/blood-2011-05-354167.

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Abstract Somatic mosaicism has been described in several primary immunodeficiency diseases and causes modified phenotypes in affected patients. X-linked anhidrotic ectodermal dysplasia with immunodeficiency (XL-EDA-ID) is caused by hypomorphic mutations in the NF-κB essential modulator (NEMO) gene and manifests clinically in various ways. We have previously reported a case of XL-EDA-ID with somatic mosaicism caused by a duplication mutation of the NEMO gene, but the frequency of somatic mosaicism of NEMO and its clinical impact on XL-EDA-ID is not fully understood. In this study, somatic mosaicism of NEMO was evaluated in XL-EDA-ID patients in Japan. Cells expressing wild-type NEMO, most of which were derived from the T-cell lineage, were detected in 9 of 10 XL-EDA-ID patients. These data indicate that the frequency of somatic mosaicism of NEMO is high in XL-ED-ID patients and that the presence of somatic mosaicism of NEMO could have an impact on the diagnosis and treatment of XL-ED-ID patients.

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Mohammed, Badiea Abdulkarem, and Tat-Chee Wan. "Handoff and Route Optimization in Mobile Networks over IEEE 802.16e." International Journal of Mobile Computing and Multimedia Communications 5, no. 2 (April 2013): 32–45. http://dx.doi.org/10.4018/jmcmc.2013040103.

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To fulfill the need for on-the-move and uninterrupted internet connectivity in Mobile Networks, IETF NEMO working group was created to extend basic end-host mobility support in Mobile IPv6 (MIPv6) protocol. NEMO Basic Support Protocol (NEMO) has been standardized by this group to provide the network mobility support. However, the handover latency in NEMO is high and, the nested tunnels’ problem in the nested NEMO networks is not considered. Many schemes have been proposed to solve these problems by optimizing the handover signaling procedure, and by proposing routing optimization scheme for NEMO. Better optimized signaling procedure is proposed in this paper, and a proposed Routing Optimization scheme as a solution for the lack of the nested tunnels’ problem is proposed as well. Analytical results highlight the importance of the proposed scheme comparing to others are provided, revealing that the proposed scheme has the lowest handover latency and disruption time.

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Koylass, Nicholas Robert, Elizabeth DeRiso, Andrea L. Szymczak-Workman, Angela Montecalvo, Joanne M. Murphy, Maria-Cristina Seminario, Stephen C. Bunnell, and Lawrence P. Kane. "Polyubiquitin-dependent recruitment of NEMO/IKKγ into T cell receptor signaling microclusters is controlled by IKKβ kinase activity." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 80.1. http://dx.doi.org/10.4049/jimmunol.204.supp.80.1.

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Abstract The IkB kinase (IKK) complex coordinates inflammatory responses by activating canonical NFkB downstream of immune receptors. This complex consists of the kinases IKKa/β and the dimeric adaptor subunit NEMO (NFkB essential modulator protein). NEMO mutations cause immunodeficiencies and impair antigen receptor function. Canonical NFkB activation by immunoreceptors, such as the T cell receptor (TCR), requires the assembly of the Carma1/Bcl10/Malt1 (CBM) signalosome. While, functional studies and in vitro interactions, place the IKK complex downstream of the CBM signalosome, the spatial relationship between these complexes has never been observed in intact immune cells. We observed that NEMO is recruited into TCR microclusters and membrane compartments within ~70 seconds of TCR engagement. Point mutations impacting the K63-linked and linear polyubiquitin ubiquitin-binding domains of NEMO selectively impair NEMO recruitment into TCR microclusters. We verified the involvement of these polyubiquitin chains by showing that inhibitors of either the K63-specific Uev1A/Ubc13 ubiquitin E2 ligase or the linear ubiquitin activating complex (LUBAC) prevent NEMO from entering TCR microclusters. To examine whether the entire IKK complex is recruited to the TCR, we co-expressed IKKb chimeras with NEMO. We observed that wild-type (WT), but not kinase-dead, IKKb caused NEMO microclusters to disappear. Similarly, the treatment of cells expressing WT IKKb with inhibitors of IKKβ or its upstream activator, TAK1, restored the recruitment of IKKβ and NEMO into microclusters. These results suggest that the IKK complex is recruited to the TCR via linear- and K63-linked polyubiquitin chains and then dissociates from the TCR via IKKβ activity.

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Rabadi, May M., Sang Jun Han, Mihwa Kim, Vivette D’Agati, and H. Thomas Lee. "Peptidyl arginine deiminase-4 exacerbates ischemic AKI by finding NEMO." American Journal of Physiology-Renal Physiology 316, no. 6 (June 1, 2019): F1180—F1190. http://dx.doi.org/10.1152/ajprenal.00089.2019.

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Peptidyl arginine deiminase-4 (PAD4) catalyzes the conversion of peptidylarginine residues to peptidylcitrulline. We have previously shown that kidney ischemia-reperfusion (I/R) injury increases renal proximal tubular PAD4 expression and activity. Furthermore, kidney PAD4 plays a critical role in ischemic acute kidney injury (AKI) by promoting renal tubular inflammation, neutrophil infiltration, and NF-κB activation. However, the mechanisms of PAD4-mediated renal tubular inflammation and NF-κB activation after I/R remain unclear. Here, we show that recombinant PAD4 preferentially citrullinates recombinant IKKγ [also called NF-κB essential modulator (NEMO)] over recombinant IKKα or IKKβ. Consistent with this finding, PAD4 citrullinated renal proximal tubular cell IKKγ and promoted NF-κB activation via IκBα phosphorylation in vitro. NEMO inhibition with a selective NEMO-binding peptide attenuated PAD4-mediated proinflammatory cytokine mRNA induction in HK-2 cells. Moreover, NEMO inhibition did not affect proximal tubular cell survival, proliferation, or apoptosis, unlike global NF-κB inhibition. In vivo, NEMO-binding peptide treatment protected against ischemic AKI. Finally, NEMO-binding peptide attenuated recombinant PAD4-mediated exacerbation of ischemic AKI, renal tubular inflammation, and apoptosis. Taken together, our results show that PAD4 exacerbates ischemic AKI and inflammation by promoting renal tubular NF-κB activity and inflammation via NEMO citrullination. Targeting NEMO activation may serve as a potential therapy for this devastating clinical problem.

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Temmerman, Stephane T., Chi A. Ma, Louis Borges, Marek Kubin, Shuying Liu, Jonathan M. J. Derry, and Ashish Jain. "Impaired dendritic-cell function in ectodermal dysplasia with immune deficiency is linked to defective NEMO ubiquitination." Blood 108, no. 7 (October 1, 2006): 2324–31. http://dx.doi.org/10.1182/blood-2006-04-017210.

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Abstract Ectodermal dysplasia with immune deficiency (EDI) is caused by alterations in NEMO (nuclear factor [NF]–κB essential modulator). Most genetic mutations are located in exon 10 and affect the C-terminal zinc finger domain. However, the biochemical mechanism by which they cause immune dysfunction remains undetermined. In this report, we investigated the effect of a cysteine-to-arginine mutation (C417R) found in the NEMO zinc finger domain on dendritic cell (DC) function. Following CD40 stimulation of DCs prepared from 2 unrelated patients with the NEMO C417R mutation, we found NEMO ubiquitination was absent, and this was associated with preserved RelA but absent c-Rel activity. As a consequence, CD40 stimulated EDI DCs failed to synthesize the c-Rel–dependent cytokine interleukin-12, had impaired up-regulation of costimulatory molecules, and failed to support allogeneic lymphocyte proliferation in vitro. In contrast, EDI DCs stimulated with the TLR4 ligand lipopolysaccharide (LPS) showed normal downstream NF-κB activity, DC maturation, and NEMO ubiquitination. These findings show for the first time how mutations in the zinc finger domain of NEMO can lead to pathway specific defects in NEMO ubiquitination and thus immune deficiency.

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Nakamori, Yoshitaka, Masahiro Emoto, Naofumi Fukuda, Akihiko Taguchi, Shigeru Okuya, Michiko Tajiri, Makoto Miyagishi, Kazunari Taira, Yoshinao Wada, and Yukio Tanizawa. "Myosin motor Myo1c and its receptor NEMO/IKK-γ promote TNF-α–induced serine307 phosphorylation of IRS-1." Journal of Cell Biology 173, no. 5 (June 5, 2006): 665–71. http://dx.doi.org/10.1083/jcb.200601065.

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Tumor necrosis factor-α (TNF-α) signaling through the IκB kinase (IKK) complex attenuates insulin action via the phosphorylation of insulin receptor substrate 1 (IRS-1) at Ser307. However, the precise molecular mechanism by which the IKK complex phosphorylates IRS-1 is unknown. In this study, we report nuclear factor κB essential modulator (NEMO)/IKK-γ subunit accumulation in membrane ruffles followed by an interaction with IRS-1. This intracellular trafficking of NEMO requires insulin, an intact actin cytoskeletal network, and the motor protein Myo1c. Increased Myo1c expression enhanced the NEMO–IRS-1 interaction, which is essential for TNF-α– induced phosphorylation of Ser307–IRS-1. In contrast, dominant inhibitory Myo1c cargo domain expression diminished this interaction and inhibited IRS-1 phosphorylation. NEMO expression also enhanced TNF-α–induced Ser307–IRS-1 phosphorylation and inhibited glucose uptake. In contrast, a deletion mutant of NEMO lacking the IKK-β–binding domain or silencing NEMO blocked the TNF-α signal. Thus, motor protein Myo1c and its receptor protein NEMO act cooperatively to form the IKK–IRS-1 complex and function in TNF-α–induced insulin resistance.

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Marienfeld, Ralf B., Lysann Palkowitsch, and Sankar Ghosh. "Dimerization of the IκB Kinase-Binding Domain of NEMO Is Required for Tumor Necrosis Factor Alpha-Induced NF-κB Activity." Molecular and Cellular Biology 26, no. 24 (September 25, 2006): 9209–19. http://dx.doi.org/10.1128/mcb.00478-06.

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ABSTRACT Previous studies have demonstrated that peptides corresponding to a six-amino-acid NEMO-binding domain from the C terminus of IκB kinase alpha (IKKα) and IKKβ can disrupt the IKK complex and block NF-κB activation. We have now mapped and characterized the corresponding amino-terminal IKK-binding domain (IBD) of NEMO. Peptides corresponding to the IBD were efficiently recruited to the IKK complex but displayed only a weak inhibitory potential on cytokine-induced NF-κB activity. This is most likely due to the formation of sodium dodecyl sulfate- and urea-resistant NEMO dimers through a dimerization domain at the amino terminus of NEMO that overlaps with the region responsible for binding to IKKs. Mutational analysis revealed different α-helical subdomains within an amino-terminal coiled-coil region are important for NEMO dimerization and IKKβ binding. Furthermore, NEMO dimerization is required for the tumor necrosis factor alpha-induced NF-κB activation, even when interaction with the IKKs is unaffected. Hence, our data provide novel insights into the role of the amino terminus of NEMO for the architecture of the IKK complex and its activation.

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Kormia Dewi, Kadek Novi, and Yana Qomariana. "Realization of Assertive Acts by Nemo in Finding Nemo the Movie." Humanis 25, no. 1 (February 27, 2021): 85. http://dx.doi.org/10.24843/jh.2021.v25.i01.p11.

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This article is focused on the function of assertive act and the delivery strategies used by Nemo in Finding Nemo the movie. The data was collected by using documentation method and note taking technique. The collected data was analyzed by using descriptive qualitative method and was presented using informal method. The theories applied in this article were a theory of illocutionary act proposed by Searle (1976) to classify the functions of assertive act and a theory of delivery strategies proposed by Parker (1986). The result of the analysis showed that there were six functions of assertive act found in Finding Nemo the movie, those are affirming, predicting, claiming, agreeing, informing, and denying. However, there are only three strategies used by Nemo to deliver the messages of his utterances.

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Matin, Shababa B., Allison Wallingford, Shicheng Xu, Natalie Ng, Anthony Ho, Madison Vanosdoll, Peter Waiswa, Alain B. Labrique, and Soumyadipta Acharya. "Feasibility of a Mobile Health Tool for Mothers to Identify Neonatal Illness in Rural Uganda: Acceptability Study." JMIR mHealth and uHealth 8, no. 2 (February 10, 2020): e16426. http://dx.doi.org/10.2196/16426.

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Background A shortage of community health workers to triage sick neonates and poor recognition of neonatal illness by mothers contribute significantly toward neonatal deaths in low- and middle-income countries. Providing low-resource communities with the tools and knowledge to recognize signs of neonatal distress can lead to early care-seeking behavior. To empower and educate mothers to recognize signs of neonatal illness, we developed a neonatal health assessment device consisting of a smartphone app and a wearable sensor (the NeMo system). Objective The aim of this study was to determine if mothers in rural Uganda were willing and able to use the NeMo system during the first week of their infant’s life. We also assessed mothers’ responses to the device’s recommendation to seek care. Methods A total of 20 mothers were enrolled in the study after giving birth in the Iganga District Hospital. Each mother was trained to use the NeMo system to assess her infant for signs of illness before leaving the hospital and was given the NeMo system to use at home for 1 week. Throughout the week, the smartphone tracked the mothers’ usage of NeMo, and the study team visited twice to observe mothers’ ability to use NeMo. Each mother was interviewed at the end of 1 week to gather qualitative feedback on her experience with the NeMo system. Results In total, 18 mothers completed the study; 2 mothers were withdrawn during the week because of extenuating health circumstances. Moreover, 1 day after enrollment and training, 75% (15/20) of mothers used NeMo properly with no mistakes. 3 days after enrollment and training, only 1 mother placed the wearable sensor improperly on her infant. On the final study day, only 1 mother connected the device improperly. Mothers used NeMo an average of 11.67 (SD 5.70) times on their own at home during the 5 full study days. Although the frequency of use per day decreased from day 1 to day 5 of the study (P=.04), 72% (13/18) of mothers used NeMo at least once per day. In total, 64% (9/14) of mothers who received an alert from the NeMo system to seek care for their infants either called the health care professional working with the study team or reused the system immediately and found no danger signs. All 18 mothers agreed or strongly agreed that the NeMo system was easy to use and helped them know when to seek care for their babies. Conclusions NeMo is a feasible and acceptable tool to aid mothers in rural Uganda to assess their infant’s health.

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Braue, Jonathan, Vagishwari Murugesan, Steven Holland, Nishit Patel, Eknath Naik, Jennifer Leiding, Abraham Tareq Yacoub, Carlos N. Prieto-Granada, and John Norman Greene. "NF- κB Essential Modulator Deficiency Leading to Disseminated Cutaneous Atypical Mycobacteria." Mediterranean Journal of Hematology and Infectious Diseases 7 (December 27, 2014): e2015010. http://dx.doi.org/10.4084/mjhid.2015.010.

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NF- κB essential modulator (NEMO) is a kinase integral to the macrophage TNF-α pathway, which leads to the intracellular destruction of Mycobacteria species. Defects in the NEMO pathway lead to a spectrum of diseases, including but not limited to ectodermal dysplasia, Mendelian susceptibility to mycobacterial diseases, and incontinentia pigmenti. In addition, paucity of NEMO can lead to the inability to mount a proper immune response against opportunistic pyogenic and mycobacterial infections, leading to dissemination to various organ systems. This manuscript will discuss the numerous clinical manifestations of NEMO deficiency, the differential diagnosis for atypical mycobacterial infections in immunocompetent adults, and feature a case report of rare isolated susceptibility to disseminated atypical mycobacteria due to a mutation in the first exon of the NEMO gene.

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Yuan, Jian Guo, Hao Li, and Qing Ping He. "Study on the NEMO Protocol Technologies in WSN." Advanced Materials Research 271-273 (July 2011): 399–403. http://dx.doi.org/10.4028/www.scientific.net/amr.271-273.399.

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In the wireless sensor network (WSN), how the Network Mobility(NEMO) protocol application scheme is better combined with the WSN is studied to meet the demand of network group mobility. A virtual mobile WSN condition with NEMO is constructed in the simulation tool NS-2, and the comparative simulation analysis with the Mobile Internet Protocol V6 (MIPv6) in the energy consumption and the node switching time is performed. The simulation result shows that the energy consumptions of major mobile nodes are far lower than those of MIPv6 in the NEMO, with the increase of nodes, the switching time that NEMO requires has a very little growth and is almost constant. Therefore, the NEMO is superior to the MIPv6 for the mobility support in the WSN.

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Tarantino, Nadine, Jean-Yves Tinevez, Elizabeth Faris Crowell, Bertrand Boisson, Ricardo Henriques, Musa Mhlanga, Fabrice Agou, Alain Israël, and Emmanuel Laplantine. "TNF and IL-1 exhibit distinct ubiquitin requirements for inducing NEMO–IKK supramolecular structures." Journal of Cell Biology 204, no. 2 (January 20, 2014): 231–45. http://dx.doi.org/10.1083/jcb.201307172.

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Nuclear factor κB (NF-κB) essential modulator (NEMO), a regulatory component of the IκB kinase (IKK) complex, controls NF-κB activation through its interaction with ubiquitin chains. We show here that stimulation with interleukin-1 (IL-1) and TNF induces a rapid and transient recruitment of NEMO into punctate structures that are anchored at the cell periphery. These structures are enriched in activated IKK kinases and ubiquitinated NEMO molecules, which suggests that they serve as organizing centers for the activation of NF-κB. These NEMO-containing structures colocalize with activated TNF receptors but not with activated IL-1 receptors. We investigated the involvement of nondegradative ubiquitination in the formation of these structures, using cells deficient in K63 ubiquitin chains or linear ubiquitin chain assembly complex (LUBAC)-mediated linear ubiquitination. Our results indicate that, unlike TNF, IL-1 requires K63-linked and linear ubiquitin chains to recruit NEMO into higher-order complexes. Thus, different mechanisms are involved in the recruitment of NEMO into supramolecular complexes, which appear to be essential for NF-κB activation.

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Mo, H. E., Y. H. Qin, Z. Q. Zu, and Y. Zhang. "Evaluation of the global ocean forecast system in NMEFC with the IV-TT class4 metrics." Journal of Physics: Conference Series 2486, no. 1 (May 1, 2023): 012026. http://dx.doi.org/10.1088/1742-6596/2486/1/012026.

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Abstract Based on the IV-TT Class4 metrics, this paper comprehensively evaluates the forecasting performance of the National Marine Environment Forecast Center High-resolution Global Ocean Forecasting System (hereinafter referred to as NMEFC-NEMO) on sea surface temperature (SST), sea level anomaly (SLA) and temperature-salinity profiles. The RMSE of NMEFC-NEMO for SST and SLA over forecast length has the smallest error among the international operational systems, which are 0.45°C and 0.07m, respectively. The forecast accuracy of NMEFC-NEMO temperature and salt profile RMSE is in the middle among the operational systems, with the values of 0.69°C and 0.24 PSU. In the profile forecast, the error of NMEFC-NEMO is slightly larger than other systems at 50-100 m depth, which is related to the fact that NMEFC-NEMO does not assimilate ARGO temperature and salinity directly. In addition, with respect to the forecast skill scores, NMEFC-NEMO has a positive climatology skill scores for both SST and SLA, and the persistence skill scores for SST is better than that for SLA.

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Tan, Xiao Long, Wen Bin Wang, and Yu Qin Yao. "Optimization and Improvements of NEMO Routing Algorithm." Applied Mechanics and Materials 644-650 (September 2014): 1871–74. http://dx.doi.org/10.4028/www.scientific.net/amm.644-650.1871.

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Next generation Internet network mobility management is an urgent and challenging research area. With the development of wireless technology, mobile network research gets more and more attention. NEMO protocol is presented based on mobile IPv6, it not only ensures the continuity of communication when subnet move, but also makes the mobility transparently for the subnet. NEMO technology application can more adapt to the development requirements of the next generation mobile communication network. This paper first introduced the NEMO technology and the existing NEMO routing optimization scheme. Then analyzed and compared the performance of each schemes in the data path and package message overhead.

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Jain, Ashish, Chi Ma, Yongge Zhao, and Stephane Temmerman. "Defective nuclear IKKα function in patients with ectodermal dysplasia with immune deficiency (180.19)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 180.19. http://dx.doi.org/10.4049/jimmunol.188.supp.180.19.

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Abstract Ectodermal dysplasia with immune deficiency (EDI) is an immunological and developmental disorder caused by alterations in the gene encoding NF-κB essential modulator (NEMO; also known as IκB kinase γ subunit [IKKγ]). Missense mutations in the gene encoding NEMO are associated with reduced signal-induced nuclear translocation of NF-κB proteins, resulting in defective expression of NF-κB target genes. Here, we report 2 unrelated male patients with EDI, both of whom have normal NEMO coding sequences, but exhibit a marked reduction in expression of full-length NEMO protein. TLR4 stimulation of APCs from these patients induced normal cytoplasmic activation and nuclear translocation of NF-κB. However, cells deficient in full-length NEMO were defective in expression of NF-κB-regulated cytokines, such as IL-12, suggesting a downstream defect in chromatin accessibility for NF-κB transcription factors. TLR4-stimulated APCs from the patients were defective in IKKα-dependent H3 histone phosphorylation at the IL-12 promoter and recruitment of NF-κB heterodimers RelA and cRel to the promoter. Expression of a super-active form of IKKα restored IL-12 production in a NEMO knockdown human monocytic cell line following LPS treatment. Our findings suggest that NEMO regulates the nuclear function of IKKα and offer new insights into the mechanisms underlying diminished NF-κB signaling in patients with EDI.

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Wang, Dang, Liurong Fang, Yanling Shi, Huan Zhang, Li Gao, Guiqing Peng, Huanchun Chen, Kui Li, and Shaobo Xiao. "Porcine Epidemic Diarrhea Virus 3C-Like Protease Regulates Its Interferon Antagonism by Cleaving NEMO." Journal of Virology 90, no. 4 (December 9, 2015): 2090–101. http://dx.doi.org/10.1128/jvi.02514-15.

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ABSTRACTPorcine epidemic diarrhea virus (PEDV) is an enteropathogenic coronavirus causing lethal watery diarrhea in piglets. Since 2010, a PEDV variant has spread rapidly in China, and it emerged in the United States in 2013, posing significant economic and public health concerns. The ability to circumvent the interferon (IFN) antiviral response, as suggested for PEDV, promotes viral survival and regulates pathogenesis of PEDV infections, but the underlying mechanisms remain obscure. Here, we show that PEDV-encoded 3C-like protease, nsp5, is an IFN antagonist that proteolytically cleaves the nuclear transcription factor kappa B (NF-κB) essential modulator (NEMO), an essential adaptor bridging interferon-regulatory factor and NF-κB activation. NEMO is cleaved at glutamine 231 (Q231) by PEDV, and this cleavage impaired the ability of NEMO to activate downstream IFN production and to act as a signaling adaptor of the RIG-I/MDA5 pathway. Mutations specifically disrupting the cysteine protease activity of PEDV nsp5 abrogated NEMO cleavage and the inhibition of IFN induction. Structural analysis suggests that several key residues outside the catalytic sites of PEDV nsp5 probably impact NEMO cleavage by modulating potential interactions of nsp5 with their substrates. These data show that PEDV nsp5 disrupts type I IFN signaling by cleaving NEMO. Previously, we and others demonstrated that NEMO is also cleaved by 3C or 3C-like proteinases of picornavirus and artertivirus. Thus, NEMO probably represents a prime target for 3C or 3C-like proteinases of different viruses.IMPORTANCEThe continued emergence and reemergence of porcine epidemic diarrhea virus (PEDV) underscore the importance of studying how this virus manipulates the immune responses of its hosts. During coevolution with its hosts, PEDV has acquired mechanisms to subvert host innate immune responses for its survival advantage. At least two proteins encoded by PEDV have been identified as interferon (IFN) antagonists, papain-like protease (PLP) and N protein. Here, we report that the PEDV nsp5 gene, which encodes the 3C-like protease of PEDV, is another IFN antagonist. Mechanistically, the cysteine protease activity of PEDV nsp5 mediates proteolysis of NEMO, the key adaptor for IFN synthesis, and NEMO is cleaved at glutamine 231 (Q231). The new molecular details and determinants impacting NEMO scission by PEDV nsp5 delineated in this study are fundamental to our understanding of critical virus-host interactions that determine PEDV pathogenesis.

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Yogi Priyandana Adi Saputra, I. Gede Made, Pande Ketut Sudiarta, and Gede Sukadarmika. "ANALISIS HASIL DRIVE TEST MENGGUNAKAN SOFTWARE G-NET DAN NEMO DI JARINGAN LTE AREA DENPASAR." Jurnal SPEKTRUM 5, no. 2 (December 19, 2018): 216. http://dx.doi.org/10.24843/spektrum.2018.v05.i02.p27.

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The development of technology is connected with customer needs for the speed and stability of LTE network access. Ensuring the quality of the LTE network can be done by measuring using the drive test method in the service area. The test drive must be equipped with software such as Nemo Handy and G-Net Track Pro. Nemo Handy is a professional drive test software that is widely used by providers, while G-Net Track Pro is a drive test software that was previously applied in the learning process at the campus. So that the measurement results using Nemo Handy and G-Net Track Pro for RSRP, RSRQ and SINR parameters need to be compared to performance. From the comparison of RSRP between measurements with theoretical stated Nemo Handy measurement results are closer than G-Net Track Pro. For example, the difference between RSRP in the PURADEMAK eNodeB for Nemo Handy was 5.96 dBm and the G-Net Track Pro was 9.4 dBm. This is due to the weakness of the G-Net Track Pro device that does not have the PCI locking feature as in Nemo Handy so that at some point the measurement cannot be compared.

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Windheim, Mark, Margaret Stafford, Mark Peggie, and Philip Cohen. "Interleukin-1 (IL-1) Induces the Lys63-Linked Polyubiquitination of IL-1 Receptor-Associated Kinase 1 To Facilitate NEMO Binding and the Activation of IκBα Kinase." Molecular and Cellular Biology 28, no. 5 (January 7, 2008): 1783–91. http://dx.doi.org/10.1128/mcb.02380-06.

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ABSTRACT Interleukin 1 (IL-1) has been reported to stimulate the polyubiquitination and disappearance of IL-1 receptor-associated kinase 1 (IRAK1) within minutes. It has been thought that the polyubiquitin chains attached to IRAK1 are linked via Lys48 of ubiquitin, leading to its destruction by the proteasome and explaining the rapid IL-1-induced disappearance of IRAK1. In this paper, we demonstrate that IL-1 stimulates the formation of K63-pUb-IRAK1 and not K48-pUb-IRAK1 and that the IL-1-induced disappearance of IRAK1 is not blocked by inhibition of the proteasome. We also show that IL-1 triggers the interaction of K63-pUb-IRAK1 with NEMO, a regulatory subunit of the IκBα kinase (IKK) complex, but not with the NEMO[D311N] mutant that cannot bind K63-pUb chains. Moreover, unlike wild-type NEMO, the NEMO[D311N] mutant was unable to restore IL-1-stimulated NF-κB-dependent gene transcription to NEMO-deficient cells. Our data suggest a model in which the recruitment of the NEMO-IKK complex to K63-pUb-IRAK1 and the recruitment of the TAK1 complex to TRAF6 facilitate the TAK1-catalyzed activation of IKK by the TRAF6-IRAK1 complex.

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Franco, Arturo. "Nemo propheta in patria." rita_, no. 9 (2018): 8–9. http://dx.doi.org/10.24192/2386-7027(2018)(v9)(00).

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Nemchenko, Andriy, and Joseph A. Hill. "NEMO Nuances NF-κB." Circulation Research 106, no. 1 (January 8, 2010): 10–12. http://dx.doi.org/10.1161/circresaha.109.211185.

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Journal articles on the topic 'Nemo'

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