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Artículos de revistas sobre el tema "Nemo"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 25 de julio de 2025

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1

Corn, A. "Nemo." Literary Imagination 9, no. 3 (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 (2018): 1–25. http://dx.doi.org/10.1145/3186317.

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3

Hsieh, Cheng-Yu, Jieyu Zhang, and Alexander Ratner. "Nemo." Proceedings of the VLDB Endowment 15, no. 13 (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 Figu

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4

Bates, Jane. "Nemo complex." Nursing Standard 21, no. 19 (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 (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 (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 та ін. "Recruitment of NEMO/IKKγ to TCR microclusters during T cell activation". Journal of Immunology 202, № 1_Supplement (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 ‘macroclust

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9

Medunjanin, Senad, Maximilian Putzier, Till Nöthen та ін. "DNA-PK: gatekeeper for IKKγ/NEMO nucleocytoplasmic shuttling in genotoxic stress-induced NF-kappaB activation". Cellular and Molecular Life Sciences 77, № 20 (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

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10

Goel, Simran, Rosario Oliva, Sadasivam Jeganathan та ін. "Linear ubiquitination induces NEMO phase separation to activate NF-κB signaling". Life Science Alliance 6, № 4 (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

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11

Wackernagel, Lisa-Marie, Mohsen Abdi Sarabi, Sönke Weinert та ін. "IKKγ/NEMO Localization into Multivesicular Bodies". International Journal of Molecular Sciences 23, № 12 (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, w

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12

Hubeau, Marjorie, Flora Ngadjeua, Anne Puel, 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 (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 experime

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13

Zilberman-Rudenko, Jevgenia, Linda Monaco Shawver, Alex W. Wessel та ін. "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, № 6 (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 increas

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14

Nishikomori, Ryuta, Hiroshi Akutagawa, Kyoko Maruyama, 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 (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 we

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15

Lee, Younglang, Eries Lee, Jevgenia Zilberman-Rudenko та ін. "A20 regulates NF-κB activation through K48 linked polyubiquitination of NEMO". Journal of Immunology 198, № 1_Supplement (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

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16

Sakowicz, Agata, Michalina Lisowska, Lidia Biesiada, 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 pla

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17

Velásquez Quiroga, María Alejandra, Cristian Camilo Ballesteros López, Maira Alejandra Puerta Medina, et al. "Neoplasia Endocrina múltiple, una Revisión y Actualización de tema sobre una Entidad de Diagnóstico y Manejo Complejo." Ciencia Latina Revista Científica Multidisciplinar 8, no. 6 (2024): 4856–69. https://doi.org/10.37811/cl_rcm.v8i6.15207.

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Los síndromes de neoplasia endocrina múltiple (NEM) incluyen NEM1, NEM2 (anteriormente NEM2A), NEM3 (anteriormente NEM2B) y el recientemente identificado NEM4. Las presentaciones clínicas son variadas y a menudo se relacionan con la sobreproducción de hormonas específicas. Comprender la genética de cada síndrome ayuda a determinar los plazos de detección. Los tratamientos para cada manifestación dependen de la ubicación, el riesgo de recurrencia o malignidad, el exceso de hormonas y la morbilidad quirúrgica. El manejo multidisciplinario debe incluir genetistas, asesores genéticos, endocrinólog

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18

Mo, Huier, Yinghao Qin, Liying Wan, et al. "Evaluating the Detection of Oceanic Mesoscale Eddies in an Operational Eddy-Resolving Global Forecasting System." Journal of Marine Science and Engineering 11, no. 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)

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19

Rappoport, Nimrod, and Ron Shamir. "NEMO: cancer subtyping by integration of partial multi-omic data." Bioinformatics 35, no. 18 (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 impu

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20

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

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21

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

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22

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

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23

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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24

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

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25

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

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26

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

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27

CHIARUSI, TOMMASO. "THE NEMO PROJECT." International Journal of Modern Physics A 20, no. 29 (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 coup

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28

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

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Rider, Elizabeth A. "Nemo on Vacation." Archives of Pediatrics & Adolescent Medicine 159, no. 7 (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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Kawai, Tomoki, Ryuta Nishikomori, Kazushi Izawa, et al. "Frequent somatic mosaicism of NEMO in T cells of patients with X-linked anhidrotic ectodermal dysplasia with immunodeficiency." Blood 119, no. 23 (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 mosai

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Umar, Putra Arif Yanto, M. Dzaky Abdullah, Ghina Luthfiyyah Mobonggi, and Patma Patma. "The effect of adding carrot, turmeric, and pumpkin solution to Nemo (Amphiprion percula) to increase color brightness." South East Asian Marine Sciences Journal 2, no. 2 (2025): 41–46. https://doi.org/10.61761/seamas.2.2.41-46.

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Nemo (Amphiprion percula) are interesting ornamental fish living in anemones' tentacles. The body color of Nemo fish determines Nemo's selling price and the level of consumer demand. However, the fading of color in Nemo often occurs due to internal and external factors that can cause public interest and selling value to decrease. Therefore, it is necessary to research the addition of carrot, turmeric, and pumpkin solutions to Nemo to improve their color. This study aims to increase the brightness of the color in Nemo. The research method was carried out using an experimental method using a Com

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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 (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 NE

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Koylass, Nicholas Robert, Elizabeth DeRiso, Andrea L. Szymczak-Workman та ін. "Polyubiquitin-dependent recruitment of NEMO/IKKγ into T cell receptor signaling microclusters is controlled by IKKβ kinase activity". Journal of Immunology 204, № 1_Supplement (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 r

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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 (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

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Temmerman, Stephane T., Chi A. Ma, Louis Borges, et al. "Impaired dendritic-cell function in ectodermal dysplasia with immune deficiency is linked to defective NEMO ubiquitination." Blood 108, no. 7 (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 ubiqu

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Nakamori, Yoshitaka, Masahiro Emoto, Naofumi Fukuda та ін. "Myosin motor Myo1c and its receptor NEMO/IKK-γ promote TNF-α–induced serine307 phosphorylation of IRS-1". Journal of Cell Biology 173, № 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 N

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Marienfeld, Ralf B., Lysann Palkowitsch та 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, № 24 (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

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Matin, Shababa B., Allison Wallingford, Shicheng Xu, et al. "Feasibility of a Mobile Health Tool for Mothers to Identify Neonatal Illness in Rural Uganda: Acceptability Study." JMIR mHealth and uHealth 8, no. 2 (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

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Braue, Jonathan, Vagishwari Murugesan, Steven Holland та ін. "NF- κB Essential Modulator Deficiency Leading to Disseminated Cutaneous Atypical Mycobacteria". Mediterranean Journal of Hematology and Infectious Diseases 7 (27 грудня 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

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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 tha

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Tarantino, Nadine, Jean-Yves Tinevez, Elizabeth Faris Crowell, et al. "TNF and IL-1 exhibit distinct ubiquitin requirements for inducing NEMO–IKK supramolecular structures." Journal of Cell Biology 204, no. 2 (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 rec

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44

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 (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 am

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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 (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 a

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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.

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Jain, Ashish, Chi Ma, Yongge Zhao та Stephane Temmerman. "Defective nuclear IKKα function in patients with ectodermal dysplasia with immune deficiency (180.19)". Journal of Immunology 188, № 1_Supplement (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 stimulati

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Wang, Dang, Liurong Fang, Yanling Shi, et al. "Porcine Epidemic Diarrhea Virus 3C-Like Protease Regulates Its Interferon Antagonism by Cleaving NEMO." Journal of Virology 90, no. 4 (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 n

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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 (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 S

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Windheim, Mark, Margaret Stafford, Mark Peggie та 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, № 5 (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 tri

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