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Academic literature on the topic 'NFE2'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "NFE2"

1

García-Rodríguez, Fernando M., and Nicolás Toro. "Sinorhizobium meliloti nfe (Nodulation Formation Efficiency) Genes Exhibit Temporal and Spatial Expression Patterns Similar to Those of Genes Involved in Symbiotic Nitrogen Fixation." Molecular Plant-Microbe Interactions® 13, no. 6 (June 2000): 583–91. http://dx.doi.org/10.1094/mpmi.2000.13.6.583.

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The nfe genes (nfeA, nfeB, and nfeD) are involved in the nodulation efficiency and competitiveness of the Sinorhizobium meliloti strain GR4 on alfalfa roots. The nfeA and nfeB genes are preceded by functional nif consensus sequences and NifA binding motifs. Here, we determined the temporal and spatial expression patterns of the nfe genes in symbiosis with alfalfa. Translational fusions of the nfe promoters with the gusA gene and reverse transcription-polymerase chain reaction analyses indicate that they are expressed and translated within mature nitrogen-fixing nodules and not during early steps of nodule development. Within the nodules the three nfe genes exhibit a spatial expression pattern similar to that of genes involved in symbiotic nitrogen fixation. We show that nfeB and nfeD genes are expressed not only from their own promoters but also from the upstream nfe promoter sequences. Furthermore, with the use of specific antibodies the NfeB and NfeD proteins were detected within the root nodule bac-teroid fraction. Finally, NfeB was inmunolocalized in the bacteroid cell membrane whereas NfeD was detected in the bacteroid cytoplasm.
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Sanders, Mathijs A., Annelieke Zeilemakers, Jasper Koenders, Remco Hoogenboezem, François Kavelaars, Rob Henderson, Bob Lowenberg, and Peter J. M. Valk. "The Gene Encoding Nuclear Erythroid Factor 2 (NFE2) Is Recurrently Mutated in Acute Myeloid Leukemia." Blood 120, no. 21 (November 16, 2012): 1392. http://dx.doi.org/10.1182/blood.v120.21.1392.1392.

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Abstract Abstract 1392 Background: Acute myeloid leukemia (AML) is a heterogeneous disease characterized by the accumulation of various acquired (cyto)genetic aberrations in the leukemic blasts. Novel state-of-the-art sequencing technologies enable sequencing of complete disease genomes. Methods: We have used Complete Genomics (CG) next-generation sequencing to identify novel recurrent mutations in AML. We have selected a single AML case, WHO: AML with maturation, FAB: M2, karyotype 45X, -Y and a NPM1 mutation. Mutations in FLT3, CEBPA, ASXL1, IDH1, IDH2, NRAS, KRAS and DNMT3A were absent. By whole genome sequencing of the AML and its corresponding remission sample, we identified acquired mutations in the protein coding regions of 31 genes (CG somatic score >0.1), including NPM1 and PTPN11. Results: Interestingly, a frame-shift mutation in the protein coding region of the Nuclear Erythroid Factor 2 (NFE2) transcription factor gene was identified and acquisition of this mutation was confirmed by Sanger sequencing of both AML and remission samples. The complete NFE2 gene of the index AML patient was sequenced but no additional mutation was present, nor was the remaining allele affected by deletions and/or amplifications. The index mutation introduces a premature stop codon (PTC) in the NFE2 gene, upstream of the region encoding the bZIP domain. To investigate if NFE2 would be recurrently mutated in AML, we screened a cohort of 1139 AML cases by denaturing high performance liquid chromatography (dHPLC) analyses for mutations in a 350bp region surrounding the index mutation in the NFE2 gene. We identified NFE2 mutations in 5 additional cases of AML. Subsequently, we screened the complete NFE2 gene in 254 randomly selected AML cases by Roche 454 sequencing. This analysis revealed 8 NFE2 mutant cases in total. These results indicate that approximately 3.5% (8/254) of unselected primary AML cases carry NFE2 mutations. The acquisition of the NFE2 mutations was confirmed by Sanger sequencing of all NFE2mutant AML cases and their corresponding derived T cells. Frame shift mutations upstream of the NFE2 bZIP domain introducing PTCs were present in 6 out of all identified NFE2 mutant cases (n=13). The remaining cases carried non-synonymous NFE2 mutations and a single case an in-frame insertion/deletion. In our cohort of molecularly and clinically well-characterized cohort of AML patients the NFE2 mutations were not associated with any clinical characteristic or any other (cyto)genetic aberration. Discussion: It is currently unclear if the NFE2 mutations would lead to a gain-of-function or a loss-of-function. Nfe2-deficient mice lack circulating platelets and die of hemorrhage; their megakaryocytes showed no cytoplasmic platelet formation. In addition, NFE2 transgenic mice show MPNs, including thrombocytosis, and spontaneous transformation to acute myeloid leukemia. However, the NFE2 mutations did not associate with abnormal platelet counts in the affected AML cases, nor did the AML cases have consistent megakaryocyte abnormalities. Mutant NFE2 is currently functionally studied by introduction into various cell line models and mouse primary bone marrow. Conclusion: In conclusion, we have identified recurrent mutation in the transcription factor gene NFE2 in a subset of AML cases. The exact role of mutant NFE2 is currently being investigated. Disclosures: No relevant conflicts of interest to declare.
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Peeken, Jan C., Jonas S. Jutzi, Julius Wehrle, Christoph Koellerer, Hans F. Staehle, Heiko Becker, Elias Schoenwandt, et al. "Epigenetic regulation of NFE2 overexpression in myeloproliferative neoplasms." Blood 131, no. 18 (May 3, 2018): 2065–73. http://dx.doi.org/10.1182/blood-2017-10-810622.

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Key Points Overexpression of NFE2 in MPNs is associated with H3Y41 phosphorylation by JAK2V617F. JMJD1C is an NFE2 target gene and acts in a positive feedback loop contributing to NFE2 overexpression in MPNs.
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Steiner, Laurie A., Vincent P. Schulz, Yelena Maksimova, Milind Mahajan, David M. Bodine, and Patrick G. Gallagher. "Dynamic CO-Localization of GATA1, NFE2, and EKLF and Changes in Gene Expression During Hematopoiesis." Blood 116, no. 21 (November 19, 2010): 741. http://dx.doi.org/10.1182/blood.v116.21.741.741.

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Abstract Abstract 741 Regulation of lineage choice during the development and differentiation of erythroid cells in hematopoiesis is a complex process. GATA1, NFE2, and EKLF are transcription factors critical for erythropoiesis. Focused studies, including detailed analyses of the human beta globin gene locus and a select group of erythrocyte membrane protein genes, have revealed that these three transcription factors may co-localize at common regulatory sites in erythroid-expressed genes. To address the hypothesis that GATA1, NFE2, and EKLF frequently co-localize on critical regulatory elements responsible for cell-type specific gene expression during erythropoiesis, chromatin immunoprecipitation coupled with ultrahigh throughput sequencing (ChIP-seq) was used to identify sites of GATA1, NFE2, and EKLF occupancy in human primary hematopoietic stem and progenitor cells (HSPCs) and human primary erythroid cells. ChIP was done using CD34+ HSPCs prepared by immunomagnetic bead selection and cultured CD71+/GPA+ erythroid cells (R3/R4 population) using antibodies against GATA1, NF-E2, and EKLF. The MACS algorithm (Zhang et al. Genome Biol, 2008) was used to identify regions of DNA-protein interaction, with a p-value ≤10e-5. Sites identified by MACS were ordered by p-value, and the 7000 sites with the most stringent p-values were selected for further analysis. Sites which occurred within 200bp of each other were treated as a single site. Unexpectedly, sites of GATA1, NFE2, and EKLF occupancy were common in HSPCs, with 6643 GATA1, 6657 NFE2, and 6579 EKLF sites identified, respectively. Sites identified in HSPCs were primarily in enhancers (>1kb from a RefSeq gene; 44% of GATA1, 49% of NFE2, and 51% of EKLF sites) and in introns (32% of GATA1, 34% of NFE2, and 34% of EKLF sites), with only a few sites at proximal promoters (within 1kb of a TSS; 7% of GATA1, 6% of NFE2, and 7% EKLF sites.) In erythroid cells, 6895 GATA1, 6907 NF-E2, and 6874 EKLF sites were identified. For all 3 factors, binding site occupancy varied greatly from that observed in HSPCs. Proximal promoter binding was much more common in erythroid cells than in HSPCs, with 19% of GATA1, 28% of NFE2 and 38% of EKLF sites found at promoters. Binding was frequently found at enhancers (41% of GATA, 38% NFE2, and 32% EKLF sites) and in introns (29% of GATA1, 26% of NFE2, and 21% of EKLF). To gain insight into three factor co-occupancy on a genome-wide scale, GATA1, EKLF, and NFE2 binding sites were compared using the Active Region Comparer (http://dart.gersteinlab. org/). Surprisingly, co-localization of all three factors was common in HSPCs, occurring at 2666 sites (40%, 40% and 45% of GATA1, NFE2, and EKLF sites). Sites of GATA1-NFE2-EKLF co-localization in HSPCs were located primarily at enhancers (51% of sites), in introns (32% of sites), and rarely at proximal promoters (6% of sites). In erythroid cells, co-localization of all three transcription factors was also common, occurring at 2445 sites (35%, 35%, and 36% of GATA1, NFE2, and EKLF sites, respectively). In contrast to HSPCs, sites of GATA1-NFE2-EKLF co-localization in erythroid cells were located primarily at proximal promoters (35% of sites) and enhancers (34% of sites), with co-localization in introns accounting for 20% of sites. A limited subset of sites, 1429 GATA1, 921 NFE2, and 1038 EKLF sites, were present in both HSPC and erythroid cells. Throughout the genome, there were only 233 sites of three factor co-localization in common in both HSPC and erythroid cells. Gene expression in HSPC and erythroid cell was analyzed via RNA hybridization to Illumina HumanHT-12 v3 Expression BeadChip arrays. In erythroid cells, genes with GATA1-NFE2-EKLF co-localization from 5kb upstream to 2kb downstream had significantly higher levels of mRNA expression than genes without GATA1-NFE2-EKLF co-localization (p<2.2e-16). The reverse was observed in HSPCs, where genes with GATA1-NFE2-EKLF co-localization had significantly lower levels of mRNA expression than genes without GATA1-NFE2-EKLF co-localization (p<7.3e-05). These data support the hypothesis that co-localization of GATA1, NFE2, and EKLF is a common finding in hematopoietic cells. Significant differences in factor co-localization and gene expression in HSPC and erythroid cells suggest that this coordinated binding orchestrates different patterns of gene expression during hematopoiesis. Disclosures: No relevant conflicts of interest to declare.
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Rost, Megan S., Ilya Shestopalov, Yang Liu, Andy H. Vo, Catherine E. Richter, Sylvia M. Emly, Francesca G. Barrett, et al. "Nfe2 is dispensable for early but required for adult thrombocyte formation and function in zebrafish." Blood Advances 2, no. 23 (November 30, 2018): 3418–27. http://dx.doi.org/10.1182/bloodadvances.2018021865.

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AbstractThe NFE2 transcription factor is expressed in multiple hematopoietic lineages with a well-defined role in regulating megakaryocyte biogenesis and platelet production in mammals. Mice deficient in NFE2 develop severe thrombocytopenia with lethality resulting from neonatal hemorrhage. Recent data in mammals reveal potential differences in embryonic and adult thrombopoiesis. Multiple studies in zebrafish have revealed mechanistic insights into hematopoiesis, although thrombopoiesis has been less studied. Rather than platelets, zebrafish possess thrombocytes, which are nucleated cells with similar functional properties. Using transcription activator-like effector nucleases to generate mutations in nfe2, we show that unlike mammals, zebrafish survive to adulthood in the absence of Nfe2. Despite developing severe thrombocytopenia, homozygous mutants do not display overt hemorrhage or reduced survival. Surprisingly, quantification of circulating thrombocytes in mutant 6-day-old larvae revealed no significant differences from wild-type siblings. Both wild-type and nfe2 null larvae formed thrombocyte-rich clots in response to endothelial injury. In addition, ex vivo thrombocytic colony formation was intact in nfe2 mutants, and adult kidney marrow displayed expansion of hematopoietic progenitors. These data suggest that loss of Nfe2 results in a late block in adult thrombopoiesis, with secondary expansion of precursors: features consistent with mammals. Overall, our data suggest parallels with erythropoiesis, including distinct primitive and definitive pathways of development and potential for a previously unknown Nfe2-independent pathway of embryonic thrombopoiesis. Long-term homozygous mutant survival will facilitate in-depth study of Nfe2 deficiency in vivo, and further investigation could lead to alternative methodologies for the enhancement of platelet production.
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Rost, Megan S., Ilya Shestopalov, Yang Liu, Andy H. Vo, Francesca Barrett, David L. Stachura, Leonard I. Zon, and Jordan A. Shavit. "Nfe2 Is Dispensable for Early, but Required for Adult Thrombocyte Formation and Function in Zebrafish." Blood 128, no. 22 (December 2, 2016): 2534. http://dx.doi.org/10.1182/blood.v128.22.2534.2534.

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Abstract The NFE2 transcription factor is expressed in multiple hematopoietic lineages with a well-defined role in regulating megakaryocyte biogenesis and platelet production in mammals. Mice deficient in NFE2 completely lack circulating platelets, causing early lethality due to neonatal hemorrhage. Recent data in mice suggest some differences in embryonic and adult thrombopoiesis, and overexpression of NFE2 in murine bone marrow cells increases megakaryocyte maturation and platelet release, suggesting a role for NFE2 in both early and late megakaryocyte development. Zebrafish have emerged as an excellent model for studying hematopoiesis and thrombopoiesis due to their external development, optical transparency, high fecundity, and conservation of nearly the entire hemostatic system. Rather than platelets, zebrafish possess thrombocytes - nucleated cells believed to be the functional equivalent in mammals. We designed TALENs to target exon 4 of zebrafish nfe2, producing two mutant strains containing either an 8 or 10 base pair deletion, both resulting in a frameshift and null allele. We tracked survival for over one year and found that unlike mammals, zebrafish survive into adulthood in the absence of Nfe2 function with no signs of overt bleeding or lethality. We bred the nfe2 mutation into a transgenic background in which thrombocytes and hematopoietic progenitor cells express green fluorescent protein (Tg(cd41:GFP)) and are characterized by GFPhigh and GFPlow expression, respectively. We performed flow cytometry analysis and found that the percentage of GFPhigh cells (circulating thrombocytes) in the peripheral blood was significantly decreased from 0.67% to 0.2% in homozygous mutants (p < 0.001). In contrast, the percentage of GFPlow cells in the kidney marrow, the site of hematopoiesis in adult zebrafish, was increased from 0.47% to 1.17% in nfe2-/- mutants (p < 0.001). Surprisingly, quantification of circulating thrombocytes in 6 day old nfe2 null zebrafish larvae showed no significant differences from wild type siblings. Finally, we performed colony forming assays on whole kidney marrow lysates to measure the ability of hematopoietic progenitors to differentiate into thrombocytes. Both mutant and wild type adults are capable of producing thrombocytic colonies in the presence of thrombopoietin and erythropoietin. We and others have shown that thrombocytes participate in the formation of induced thrombi upon laser-mediated endothelial injury in zebrafish embryos and larvae. We tested the functionality of nfe2-/- thrombocytes and were surprised to find that wild type and nfe2 null zebrafish larvae form fibrin- and thrombocyte-rich clots in response to endothelial injury at day of life 3 (venous circulation) and 6 (arterial circulation), respectively. Measurement of both the time to occlusion as well as the total number of thrombocytes adhering to the site of injury revealed no significant differences between wild type and nfe2-/- larvae. These data suggest that loss of Nfe2 results in a late block in thrombopoiesis with secondary expansion of thrombocytic precursors, both features that are consistent with mammals. Surprisingly, Nfe2 appears to be dispensable for early embryonic thrombocyte production and function. These results suggest parallels with erythropoiesis, including distinct primitive and definitive pathways of development. This includes the potential for a previously unknown Nfe2-independent pathway of embryonic thrombopoiesis. The long term homozygous mutant survival will also facilitate more in depth study of Nfe2 deficiency in vivo, and further investigation could lead to alternative methodologies for the enhancement of platelet production in vivo or ex vivo. Disclosures Zon: Fate, Inc.: Equity Ownership, Membership on an entity's Board of Directors or advisory committees, Other: Founder; Scholar Rock: Equity Ownership, Membership on an entity's Board of Directors or advisory committees, Other: Founder; Marauder Therapeutics: Equity Ownership, Other: Founder.
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Li, You-Jun, Rachel R. Higgins, Brian J. Pak, Ramesh A. Shivdasani, Paul A. Ney, Michael Archer, and Yaacov Ben-David. "p45NFE2 Is a Negative Regulator of Erythroid Proliferation Which Contributes to the Progression of Friend Virus-Induced Erythroleukemias." Molecular and Cellular Biology 21, no. 1 (January 1, 2001): 73–80. http://dx.doi.org/10.1128/mcb.21.1.73-80.2001.

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ABSTRACT In previous studies, we identified a common site of retroviral integration designated Fli-2 in Friend murine leukemia virus (F-MuLV)-induced erythroleukemia cell lines. Insertion of F-MuLV at the Fli-2 locus, which was associated with the loss of the second allele, resulted in the inactivation of the erythroid cell- and megakaryocyte-specific genep45 NFE2 . Frequent disruption ofp45 NFE2 due to proviral insertion suggests a role for this transcription factor in the progression of Friend virus-induced erythroleukemias. To assess this possibility, erythroleukemia was induced by F-MuLV inp45 NFE2 mutant mice. Sincep45 NFE2 homozygous mice mostly die at birth, erythroleukemia was induced in +/− and +/+ mice. We demonstrate that +/− mice succumb to the disease moderately but significantly faster than +/+ mice. In addition, the spleens of +/− mice were significantly larger than those of +/+ mice. Of the 37 tumors generated from the +/− and +/+ mice, 10 gave rise to cell lines, all of which were derived from +/− mice. Establishment in culture was associated with the loss of the remaining wild-typep45 NFE2 allele in 9 of 10 of these cell lines. The loss of a functional p45NFE2 in these cell lines was associated with a marked reduction in globin gene expression. Expression of wild-typep45 NFE2 in the nonproducer erythroleukemic cells resulted in reduced cell growth and restored the expression of globin genes. Similarly, the expression ofp45 NFE2 in these cells also slows tumor growth in vivo. These results indicate thatp45 NFE2 functions as an inhibitor of erythroid cell growth and that perturbation of its expression contributes to the progression of Friend erythroleukemia.
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Dou, Rui, Xiong Wang, and Jin Zhang. "Prognostic Value and Immune Infiltration Analysis of Nuclear Factor Erythroid-2 Family Members in Ovarian Cancer." BioMed Research International 2022 (January 11, 2022): 1–9. http://dx.doi.org/10.1155/2022/8672258.

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Ovarian cancer (OC) often presents at an advanced stage and is still one of the most frequent causes of gynecological cancer-related mortality worldwide. The nuclear factor erythroid-2 (NFE2) transcription factors include nuclear factor, erythroid 2 like 1 (NFE2L1), NFE2L2, and NFE2L3. NFE2 members bind to the antioxidant-response element (ARE) region and activate the expression of targeted genes. The distinct functions of NFE2 members in OC remain poorly elucidated. Several online bioinformatics databases were applied to determine gene expression, prognosis, mutations, and immune infiltration correlation in OC patients. NFE2L1 and NFE2L2 were decreased in OC, whereas NFE2L3 was increased. NFE2L2 and NFE2L3 were significantly correlated with the clinical stages of OC. High NFE2L1 level was significantly associated with short progression-free survival (PFS) in patients with OC ( HR = 1.18 , P = 0.021 ), while high NFE2L2 expression strongly correlated with long PFS ( HR = 0.77 , P = 0.00067 ). High NFE2L3 expression was associated with better overall survival and postprogression survival in OC. Functional analysis showed that NFE2 members mainly focused on transcription coactivator activities. Genetic alterations of NFE2 members were found in 13% of OC patients, and amplification ranked the top. The expression of NFE2 members was significantly correlated with immune infiltration of CD4+ T cells, CD8+ T cells, B cells, macrophages, and neutrophils in OC. Our study provides novel insights into the roles and prognostic potential of NFE2 family members in OC.
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Pratt, Stephen J., Anna Drejer, Helen Foott, Bruce Barut, Alison Brownlie, John Postlethwait, Yasutake Kato, Masayuki Yamamoto, and Leonard I. Zon. "Isolation and characterization of zebrafish NFE2." Physiological Genomics 11, no. 2 (October 29, 2002): 91–98. http://dx.doi.org/10.1152/physiolgenomics.00112.2001.

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Vertebrate hematopoiesis is regulated by distinct cell-specific transcription factors such as GATA-1 and SCL. Mammalian p45-NFE2 was characterized for its ability to bind the hypersensitive sites of the globin locus control region. NFE2 is a member of a cap’n’collar (CNC) and basic zipper (BZIP) superfamily that regulates gene transcription. It has been implicated in diverse processes such as globin gene expression, oxidative stress, and platelet lineage differentiation. Here, we have isolated the zebrafish ortholog of NFE2. The gene is highly homologous, particularly in the DNA-binding domain. Mapping the zebrafish NFE2 to linkage group 23 establishes a region of chromosomal synteny with human chromosome 12, further suggesting evolutionary conservation. During embryogenesis, the zebrafish gene is expressed specifically in erythroid cells and also in the developing ear. NFE2 expression is lacking in zebrafish mutants that have no hematopoietic cells. An analysis of the sauternes mutant, which carries a mutation in the ALAS-2 gene and thus has defective heme synthesis, demonstrates higher levels of NFE2 expression than normal. This further establishes the block to erythroid differentiation in the sauternes mutant. Our studies demonstrate conservation of the vertebrate genetic program for the erythroid lineage.
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Heuston, Elisabeth F., Jens Lichtenberg, Stacie M. Anderson, Vikram R. Paralkar, Cheryl Keller Capone, Ross C. Hardison, Mitchell J. Weiss, and David M. Bodine. "Differences In The Genome-Wide Epigenetic Signatures Of mRNA and Long Non-Coding RNA Genes In Mouse Erythroblasts and Megakaryocytes." Blood 122, no. 21 (November 15, 2013): 1198. http://dx.doi.org/10.1182/blood.v122.21.1198.1198.

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Abstract The ENCODE project has demonstrated that epigenetic signatures, including DNA methylation and transcription factor (TF) occupancy, define gene expression. However, ENCODE was constructed using static cells that were not capable of further differentiation. We hypothesize that specific epigenetic profiles are associated with erythroid and megakaryocytic differentiation. To test this hypothesis, we isolated primary erythroblasts (EBs) and megakaryocytes (Megs) from mouse bone marrow by flow cytometry and prepared: 1) DNA for genome-wide methylation analysis using MBD2 Methyl-Seq; 2) RNA for both RNA-Seq analysis and microarray analysis of novel and annotated lncRNA expression levels; and 3) chromatin for genome-wide chromatin immunoprecipitation (ChIP-Seq) analysis of occupancy by the TFs GATA1 and NFE2. We developed the web-based high-throughput sequencing tool suite SigSeeker (http://sigseeker.org) to predict regions of methylation and TF occupancy across the genome. High-confidence methylation, GATA1, and NFE2 profiles, represented by the intersection of two independent EB and Meg biological replicates, are shown in Table 1. Of the approximate 100,000 methylated regions in EBs and Megs, 45% were shared between the two cell types. Unlike methylation, GATA1 and NFE2 occupancy showed strong cell type-specific profiles, with most GATA1 occupied sites (79%) being EB-specific, and most NFE2 occupied sites (72%) being Meg-specific. While 26% of EB-specific GATA1 peaks were co-occupied by NFE2, co-occupancy by GATA1 and NFE2 in Megs was rare (0.6%). We developed a second web-based tool called SBR (http://sbrblood.msseeker.org) to correlate ChIP-Seq and Methyl-Seq profiles with RNA-Seq and lncRNA transcriptional data sets. Almost 95% of RefSeq (coding) genes with methylation in the promoter regions were not expressed. Fewer than 5% of methylated RefSeq promoters also had TF occupancy. Unlike promoters, the bodies of RefSeq genes had a high degree of overlap between methylation and TF binding. In EBs, 38% of RefSeq genes with GATA1 occupancy in the body were methylated. Of genes with this profile, 81% were transcriptionally silent. In Megs, 42% of RefSeq genes with NFE2 occupancy in the body were methylated. However, 80% of these Meg-specific genes were transcriptionally active. In contrast to RefSeq genes, lncRNA genes have a different signature. More than 85% of EB-expressed lncRNA promoters are methylated and ∼25% of these promoters are occupied by GATA1 and/or NFE2. Over 90% of EB-expressed lncRNA gene bodies occupied by GATA1 and/or NFE2 are methylated. In contrast less than 10% of Meg-expressed lncRNA promoters are methylated and ∼only 2% of these promoters are occupied by NFE2. However, 90% of Meg-expressed lncRNA gene bodies occupied by GATA1 and/or NFE2 are methylated. Ingenuity IPA analysis of the transcriptional profiles associated with different epigenetic signatures revealed differentially regulated cellular pathways. In EBs, GATA1 occupancy in the promoters of silent genes was associated with cardiovascular (p≤ 10-7) and nervous system development (p≤ 10-7). In Megs, NFE2 promoter occupancy was associated with active genes involved in nucleic acid metabolism (p≤ 10-3) and nervous system development (p≤ 10-5). Genes expressed in both EBs and Megs were involved in transcription (p≤ 10-6), cell cycle progression (p≤ 10-5), and decreased hypoplasia (p≤ 10-20). GATA1 and NFE2 co-occupied genes expressed in both EBs and Megs were associated with suppression of bone-related (p≤ 10-6) and neuron-related transcripts (p≤ 10-8). In summary, we show that TF occupancy and methylation significantly overlap in RefSeq gene bodies, but not in promoters. These profiles have revealed that GATA1 occupancy, independent of NFE2 co-occupancy, correlates with EB-specific transcriptional silencing, whereas Meg-specific transcriptional activation is associated with NFE2 occupancy. In contrast, over 90% active and TF-occupied lncRNA (both novel and previously annotated) gene bodies are methylated. These epigenetic correlations will be important for future studies assessing the regulation of mRNAs and lncRNAs. Disclosures: No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "NFE2"

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AMARU, CALZADA ARIEL. "Mechanism of action of Histone Deacetylase inhibitor. Givinostat in Chronic Myeloproliferative neplasm." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/44363.

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We investigated the mechanism of action of the histone deacetylase inhibitor Givinostat (GVS) in Janus kinase 2 (JAK2)V617F myeloproliferative neoplasm (MPN) cells. GVS inhibited colony formation and proliferation and induced apoptosis at doses two- to threefold lower in a panel of JAK2V617F MPN compared to JAK2 wild- type myeloid leukemia cell lines. By global gene expression analysis, we observed that GVS modulated 293 common genes in the JAK2V617F cell lines HEL and UKE1. In particular, the hematopoietic transcription factors NF-E2 and C-MYB were downmodulated by the drug specifically in JAK2V617F cells at both the RNA and protein level. GVS had a direct effect on the NF-E2 promoters, as demonstrated by specific enrichment of associated histone H3 acetylated at lysine 9. Modulation by GVS of NF-E2 was also observed in freshly isolated CD34+ cells from MPN patients, and was accompanied by inhibition of their proliferation and differentiation toward the erythroid lineage. We conclude that GVS acts on MPN cells through dual JAK2-STAT 5-extracellular signal- regulated kinase 1/2 inhibition and downmodulation of NF-E2 and C-MYB transcription. In the second part of the thesis we investigated whether clinically achievable concentrations of the histone deacetylase (HDAC) inhibitors givinostat and hydroxyurea induce synergistic cytotoxicity in Jak2V617F cells in vitro and through which possible mechanism. The results suggest that combined treatment with givinostat and hydroxyurea is a potential strategy for the management of Jak2V617F myeloproliferative neoplasms.
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Ellingsen, Rikke. "Nonlinear Isogeometric Analysis vs NFEA of Tubular Joints." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for konstruksjonsteknikk, 2013. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-21878.

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In 2005, Hughes et al. introduced the isogeometric analysis. One purpose was to eliminate the conversion between geometry model and analysis model in finite element analyses. NURBS (Non-Uniform Rational B-Splines) were adopted as shape functions and the isoparametric concept was utilized, resulting in the above mentioned analysis method.In this thesis, the differences between traditional finite element analysis and isogeometric analysis have been examined through nonlinear analyses of a gap K-joint subjected to prescribed displacements. The K-joint has been modelled both with solid and thin shell elements in Abaqus/Standard and with solid elements in IFEM. It has been focused on obtaining a mesh of similar refinement for both of the methods to easier be able to compare the results.The results show, as expected, that the thin shell element representation is unsuitable for a three dimensional stress state as around the intersection of the braces and the chord. The analyses with solid elements show a dependence on the continuity of the shape functions. The continuity in an isogeometric analysis is Cp-1 over element borders for basis functions of degree p. In traditional finite element analysis the continuity for solid elements is only C0. This results in differences in the differentiated variables like stresses and strain. Also the calculation of derived values, such as the von Mises stress and principal stresses, has shown to generate differences in the results because this is done differently in Abaqus/Standard and IFEM. The computational time for the isogeometric analyses is higher than for the traditional finite element analyses, and increasing with increasing degree of basis functions because the continuity affects the average bandwidth of the global matrices, and must also be included in the discussions.The conclusion is that more analysis results are needed to be able to make a substantiated conclusion as to which analysis method that is preferable for analyzing a gap K-joint.Regarding which method that is more accurate or conservative, the findings are not consequent.
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Dahmani, Younes. "Uttryck av Nfr2 och dess kliniska roll i klarcellig njurcancer." Thesis, Umeå universitet, Biomedicinsk laboratorievetenskap, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-58605.

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Chesney, James R., Nicholas J. Speciale, and Anil K. Agrawal. "Design of the TOPEX-NFEP Utilizing the Functional Component Approach." International Foundation for Telemetering, 1989. http://hdl.handle.net/10150/614728.

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International Telemetering Conference Proceedings / October 30-November 02, 1989 / Town & Country Hotel & Convention Center, San Diego, California
TOPEX/POSEIDON is a joint American/French Ocean Topography Experiment undertaken by the National Aeronautics and Space Administration (NASA) and Center National d'Etudes Spatiales (CNES) to acquire, process and verify altimetric sea surface height data so that mean and variable geotropic surface currents of the world's oceans can be mapped. This paper describes the functions and the architecture of the proposed front end to the Telemetry, Command and Communication System (TCCS) used for monitoring the spacecraft health, real time analysis required for supporting satellite analysis, collecting the telemetry data, and commanding the satellite. The system uses specialized hardware developed (herewith called as NFEP) at Goddard Space Flight Center to offload the Host processing and to support the data acquisition in a stand alone mode even in case of failure of the Host machine. The NFEP utilizes the semi-custom and custom very large scale integration (VLSI) devices, microprocessor control, and programmable logic designed to provide a generic NASA Communication (NASCOM) block processing and telemetry frame synchronization.
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Bruder, Carl E. G. "Genetic analysis of neurofibromatosis type 2 (NF2) patients and NF2-associated tumors with emphasis on chromosome 22 deletions /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4370-2/.

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Vahldiek, Kai-Felix. "Allelverluste bei Neurofibromatose Typ 2 (NF2) assoziierten Meningeomen." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=965649512.

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Klungsupya, P. "Nucleotide excision repair of the plasmid borne NFA2 gene in Saccharomyces cerevisiae." Thesis, Swansea University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.637808.

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The role of transcription in repair of UV-induced CPD was investigated in the Saccharomyces cerevisiae MFA2 gene. MFA2 mutants were constructed for cloning into a yeast artificial chromosome (YAC) by deletion of either the 22nt TATA box sequences (T2ΔMFA2) or 55nt Mcm1 binding site (MΔMFA2) from its promoter. In vivo transcription analysis using eGFP reporter system reveals a 10-fold reduction in transcription activity for the T2ΔMFA2 a cells compared to the WTMFA2 a cells. This reduced transcription level is very close to the level found in α cells where MFA2 is inactive. A 7-fold reduction in transcription activity was found for MΔMFA2 in both a and α cells. This result indicates the deletion of the MBS eliminates Mcm1/α2-mediated MFA2 repression in α cells dramatically reduced MFA2 expression in a cells. Among 13 CPDs found in the promoter region, three CPDs are increasingly induced following the deletion of the TATA box and MBS sequences. However, their repair rates are not affected. Analysis of NER was performed on individual CPDs in both the transcribed (TS) and non-transcribed (NTS) strands by comparison between the YAC-borne MFA2 and the endogenous gene for each construct. The endogenous MFA2 in YAC strains harbouring the WTMFA2 and MΔMFA2 constructs, exhibit an identical repair profile. This suggests no genetic variation occurs within the isogenic strain harbouring the three promoter element deletion constructs. The repair results on the TS indicate the fastest rate with t50% of 1.5 hr for some CPDs in the transcription region of the transcribed strand of the WTMFA2.
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Vigorito, Christian. "Implementazione di algoritmi di stima della distanza con segnali a bassa frequenza." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amslaurea.unibo.it/3534/.

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L’obiettivo di questo lavoro di tesi è stato quello di definire degli algoritmi in grado di comprendere le prestazioni raggiungibili dalla tecnica NFER alternativa in termini di ranging e accuratezza e, di conseguenza, dedurre se il sistema sia utilizzabile o meno.
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Schmid, M. C. "The role of focal adhesion kinase (FAK) in NF2 -/- turmourigenesis." Thesis, Exeter and Plymouth Peninsula Medical School, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701076.

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Johnson, Kristen C. (Kristen Carrie) 1976. "Analysis of the function of the Nf2 tumor suppressor protein, Merlin." Thesis, Massachusetts Institute of Technology, 2003. http://hdl.handle.net/1721.1/29763.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2003.
Vita.
Includes bibliographical references.
The Neurofibromatosis type 2 tumor suppressor gene (NF2) is mutated in inherited and sporadically occurring central nervous system tumors. The NF2 encoded protein, merlin, shares close sequence similarity in its amino-terminal domain to members of the band 4.1 family of membrane-cytoskeletal linkers. Similarities between merlin and this family suggest a role for merlin in regulating cytoskeletal function. Thus, NF2 may be a novel type of tumor suppressor gene that mediates its tumor suppressor function through interactions with the actin cytoskeleton. However, the molecular and cellular functions of this tumor suppressor gene were largely unknown when the work described here began. Mutational analysis of Nf2 in flies has lead to the identification of a dominant-negative allele, which harbors mutations in the amino-terminal domain of the protein. The work presented here demonstrates that expression of a murine analog of this amino-terminal mutant of Nf2 (termed, Nf2BBA) leads to complete transformation of NIH3T3 fibroblasts in culture. Cells that express Nf2BBA display disruptions of the actin cytoskeleton, lack of contact inhibition of growth, and anchorage-independent growth. In addition, Nf2-deficient mouse embryo fibroblasts (MEFs) exhibited similar contact inhibition and cell-matrix adhesion defects to Nf2BBA expressing cells. Nf2BBA cells continue to cycle under normal growth inhibitory conditions, such as serum withdrawal, and exhibit high levels of the cell cycle regulator, cyclin D1. Elevated levels of cyclin D1 are necessary for cellular transformation following Nf2BBA expression. Nevertheless, the exact mechanism by which Nf2BBA results in cellular transformation remains elusive. Recently published studies have revealed that merlin may regulate members of the RhoGTPase
(cont.) family, as absence of Nf2 expression in fibroblasts leads to many phenotypes reminiscent of overactive Rac, such as increased membrane ruffling and increased activity of the c-jun N- terminal kinase (JNK). Our work has extended to the analysis of the role of merlin in the regulation of the Rac pathway. Using rat schwannoma cells and N2-deficient MEFs, we have demonstrated that merlin exerts its inhibitory effects downstream of Rac, through a direct interaction with the p21 activated kinase, Pak. We demonstrate that in the absence of merlin, Pak is active and hyperphosphorylated, and, conversely, when merlin is overexpressed, Pak activity is diminished. The N-terminal half of merlin binds to the functionally conserved Rac/Cdc42 interaction binding (CRIB) domain of Pak. Several models for merlin regulation of Pak activity will be discussed. Finally, the identification of Pak as a kinase that is misregulated in the absence of NF2 may lead to possible avenues for therapeutic intervention.
by Kristen C. Johnson.
Ph.D.
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Books on the topic "NFE2"

1

National Foundation for Educational Research in England and Wales. NFER research. Slough: NFER., 1990.

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Belletto, René. L'E nfer. Paris: P.O.L., 1986.

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National Foundation for Educational Research in England and Wales. NFER research sheets. Slough: NFER, 1988.

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National Foundation for Educational Research in England and Wales., ed. NFER research sheet. Slough: NFER, 1988.

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National Foundation for Educational Research in England and Wales., ed. NFER current projects. Slough: NFER., 1988.

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Wales, National Foundation for Educational Research in England and. NFER research information sheets. Slough: NFER, 1998.

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National Foundation for Educational Research. NFER research information sheets. Slough: NFER, 1998.

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Peace Corps (U.S.). Information Collection and Exchange and Center for Field Assistance and Applied Research (Peace Corps), eds. Nonformal education (NFE) manual. Washington, D.C: Peace Corps, 2004.

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Griffiths, Jeffrey L. NFER: The first fifty years, 1946-1996. Slough: National Foundation for Educational Research, 2003.

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Agency, Training, and National Foundation for Educational Research in England and Wales., eds. Working together: Consortium links in TVEI (NFER) : summary. London: Training Agency, 1989.

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Book chapters on the topic "NFE2"

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Froehlich, Stephan J., Carlo A. Lackerbauer, Guenter Rudolph, Jan Rémi, Soheyl Noachtar, Werner J. Heppt, Annette Cryer, et al. "NF2." In Encyclopedia of Molecular Mechanisms of Disease, 1475. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6418.

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Mishra, Sanjaya, and Pradeep K. Misra. "Open, Distance, and Digital Non-formal Education in Developing Countries." In Handbook of Open, Distance and Digital Education, 1–17. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-0351-9_21-1.

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AbstractNon-formal education contributes significantly to improve the literacy and livelihoods of individuals. Its significance becomes much more in developing countries where 70% of the world population lives. However, population densities, geographical diversities, and varied socioeconomic conditions in many developing countries make it difficult to offer need-based non-formal education (NFE) to all. Fortunately, open, distance, and digital education (ODDE) has emerged as a viable approach to offer quality non-formal education programs at a minimal cost. Research reveals that proper and effective use of ODDE to offer NFE changes the lives of many citizens in developing countries and may help these countries achieve the Sustainable Development Goals. This chapter presents in its first section an overview of the use of ODDE for supporting NFE initiatives in the developing world and identifies issues and challenges faced. The next section of the chapter outlines theoretical insights and findings of valued publications regarding the use of ODDE for offering NFE. The final section provides the strategies for making the best and optimum use of ODDE to make NFE accessible to all eligible and willing ones in developing countries.
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Mishra, Sanjaya, and Pradeep K. Misra. "Open, Distance, and Digital Non-formal Education in Developing Countries." In Handbook of Open, Distance and Digital Education, 337–53. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-2080-6_21.

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AbstractNon-formal education contributes significantly to improve the literacy and livelihoods of individuals. Its significance becomes much more in developing countries where 70% of the world population lives. However, population densities, geographical diversities, and varied socioeconomic conditions in many developing countries make it difficult to offer need-based non-formal education (NFE) to all. Fortunately, open, distance, and digital education (ODDE) has emerged as a viable approach to offer quality non-formal education programs at a minimal cost. Research reveals that proper and effective use of ODDE to offer NFE changes the lives of many citizens in developing countries and may help these countries achieve the Sustainable Development Goals. This chapter presents in its first section an overview of the use of ODDE for supporting NFE initiatives in the developing world and identifies issues and challenges faced. The next section of the chapter outlines theoretical insights and findings of valued publications regarding the use of ODDE for offering NFE. The final section provides the strategies for making the best and optimum use of ODDE to make NFE accessible to all eligible and willing ones in developing countries.
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Mota, Mateus, Rajeev S. Samant, and Lalita A. Shevde. "Merlin (NF2)." In Encyclopedia of Signaling Molecules, 3089–100. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101780.

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Mota, Mateus, Rajeev S. Samant, and Lalita A. Shevde. "Merlin (NF2)." In Encyclopedia of Signaling Molecules, 1–11. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101780-1.

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Lang, Stefan M., and Peter C. Lockemann. "Das NF2-Modell." In Datenbankeinsatz, 97–118. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-57782-6_5.

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Buhl, Ralf M., H. Maximilian Mehdorn, and Peter A. Winkler. "NF2/Multiple Meningiomas." In Meningiomas, 555–64. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84628-784-8_59.

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Evans, D. Gareth R. "Neurofibromatosis Type 2 (NF2)." In Neurofibromatoses in Clinical Practice, 47–70. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-629-0_2.

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Armstrong, Carol L. "Neurofibromatosis Type 2 (NF2)." In Encyclopedia of Clinical Neuropsychology, 1–2. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_134-2.

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Armstrong, Carol L. "Neurofibromatosis Type 2 (NF2)." In Encyclopedia of Clinical Neuropsychology, 2404–5. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_134.

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Conference papers on the topic "NFE2"

1

Kauffman, Sean, and Sebastian Fischmeister. "Event stream abstraction using nfer." In ICCPS '19: ACM/IEEE 10th International Conference on Cyber-Physical Systems. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3302509.3313327.

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Johnson, Gregory M., Heiko Stegmann, and Andreas Rummel. "Zero Channel Bias Determination of Device Turn-On and the Seebeck Effect in Nanoprobing." In ISTFA 2022. ASM International, 2022. http://dx.doi.org/10.31399/asm.cp.istfa2022p0262.

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Abstract In prior work, it was demonstrated that information about device turn-on can be obtained in a nanoprobing setup which involves no applied bias across the channel. This was performed on nFET logic devices in 7 nm technology and attributed to the Seebeck effect, or heating from the SEM beam. In this work, the experiments are continued to both nFET and pFET devices and on both 22 nm and 5 nm devices. Further discussion about the opportunities and evidence for Seebeck effect in nanoprobing are discussed.
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Musa, Safuri. "Factors that Affect the Sustainability of Litercay Education Program." In 3rd NFE Conference on Lifelong Learning (NFE 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/nfe-16.2017.48.

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Anugrah Putra, Chandra. "Use of Multimedia Learning Technology Based Graphical User Interface (GUI)." In 3rd NFE Conference on Lifelong Learning (NFE 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/nfe-16.2017.1.

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Rahmat Pramudia, Joni, Sardin Sardin, Nike Kamarubiani, and Muhammad Irfan Hilmi. "Model Management Activity Community Learning Center (Clc) Based on Local Wisdom to Improve Quality of Nonformal Education Service." In 3rd NFE Conference on Lifelong Learning (NFE 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/nfe-16.2017.10.

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Dwi Lestari, Gunarti. "Nonformal Education Ideas on Mahakam Ulu Community as The Extension Area of West Kutai District." In 3rd NFE Conference on Lifelong Learning (NFE 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/nfe-16.2017.11.

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Robandi, Babang, Dharma Kesuma, Arie Rakhmat Riyadi, and Teguh Ibrahim. "The Profile of Critical Consciousness of Indonesia University of Education Students'on Educational Phenomenon (A Phenomenological Study of Paulo Freire's Pedagogy)." In 3rd NFE Conference on Lifelong Learning (NFE 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/nfe-16.2017.12.

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Indra Syahdewa, Budi. "Contribution of Nonformal Education (NFE) in Improving English Performance." In 3rd NFE Conference on Lifelong Learning (NFE 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/nfe-16.2017.13.

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Hidayat, Dayat. "Entrepreneurial Learning by Community-Based Participation through Optimization of Local Potential Development in Karawang." In 3rd NFE Conference on Lifelong Learning (NFE 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/nfe-16.2017.14.

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Heryanto, Nunu. "Empowerment of Group Role to Develop Learning Independency of Farmers in Farming Business (Lifelong Learning Case of Farmers Group in Pagerwangi Village Lembang Subregency West Bandung Regency)." In 3rd NFE Conference on Lifelong Learning (NFE 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/nfe-16.2017.15.

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Reports on the topic "NFE2"

1

Pulst, Stefan M. NF2 in Hrs-Mediated Signal Transduction. Fort Belvoir, VA: Defense Technical Information Center, November 2001. http://dx.doi.org/10.21236/ada400523.

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Pulst, Stefan M. Mouse Models of HRS-NF2 Interaction. Fort Belvoir, VA: Defense Technical Information Center, January 2006. http://dx.doi.org/10.21236/ada456920.

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Pulst, Stefan M. NF2 in Hrs-Mediated Signal Transduction. Fort Belvoir, VA: Defense Technical Information Center, November 2003. http://dx.doi.org/10.21236/ada427555.

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Pulst, Stefan M. NF2 in Hrs-Mediated Signal Transduction. Fort Belvoir, VA: Defense Technical Information Center, November 2002. http://dx.doi.org/10.21236/ada411657.

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Pulst, Stefan M. NF2 in Hrs-Mediated Signal Transduction. Fort Belvoir, VA: Defense Technical Information Center, November 2000. http://dx.doi.org/10.21236/ada391835.

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Koffend, J. B., Carrol E. Gardner, Raymond F. Heifner, and III. Kinetics of the H2-NF2 System,. Fort Belvoir, VA: Defense Technical Information Center, September 1985. http://dx.doi.org/10.21236/ada161220.

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Slattery, William H., and III. Neurofibromatosis Type 2 (NF2) Natural History Consortium. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada434786.

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Slattery, William H., and III. Neurofibromatosis Type 2 (NF2) Natural History Consortium. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada414115.

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Baia, Gilson S. Combinatorial Therapy Approaches for NF2-Deficient Meningiomas. Fort Belvoir, VA: Defense Technical Information Center, June 2012. http://dx.doi.org/10.21236/ada567130.

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Baia, Gilson S. Combinatorial Therapy Approaches for NF2-Deficient Meningiomas. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada584501.

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