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Добірка наукової літератури з теми "CNOT3"

Автор: Grafiati

Опубліковано: 14 грудня 2024

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Статті в журналах з теми "CNOT3"

Mittal, Saloni, Akhmed Aslam, Rachel Doidge, Rachel Medica, and G. Sebastiaan Winkler. "The Ccr4a (CNOT6) and Ccr4b (CNOT6L) deadenylase subunits of the human Ccr4–Not complex contribute to the prevention of cell death and senescence." Molecular Biology of the Cell 22, no. 6 (March 15, 2011): 748–58. http://dx.doi.org/10.1091/mbc.e10-11-0898.

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A key step in cytoplasmic mRNA degradation is the shortening of the poly(A) tail, which involves several deadenylase enzymes. Relatively little is known about the importance of these enzymes for the cellular physiology. Here we focused on the role of the highly similar Ccr4a (CNOT6) and Ccr4b (CNOT6L) deadenylase subunits of the Ccr4–Not complex. In addition to a role in cell proliferation, Ccr4a and Ccr4b play a role in cell survival, in contrast to the Caf1a (CNOT7) and Caf1b (CNOT8) deadenylase subunits or the CNOT1 and CNOT3 noncatalytic subunits of the Ccr4–Not complex. Underscoring the differential contributions of the deadenylase subunits, we found that knockdown of Caf1a/Caf1b or Ccr4a/Ccr4b differentially affects the formation of cytoplasmic foci by processing-body components. Furthermore, we demonstrated that the amino-terminal leucine-rich repeat (LRR) domain of Ccr4b influenced its subcellular localization but was not required for the deadenylase activity of Ccr4b. Moreover, overexpression of Ccr4b lacking the LRR domain interfered with cell cycle progression but not with cell viability. Finally, gene expression profiling indicated that distinct gene sets are regulated by Caf1a/Caf1b and Ccr4a/Ccr4b and identified Ccr4a/Ccr4b as a key regulator of insulin-like growth factor–binding protein 5, which mediates cell cycle arrest and senescence via a p53-dependent pathway.

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Elmén, Lisa, Claudia B. Volpato, Anaïs Kervadec, Santiago Pineda, Sreehari Kalvakuri, Nakissa N. Alayari, Luisa Foco, et al. "Silencing of CCR4-NOT complex subunits affects heart structure and function." Disease Models & Mechanisms 13, no. 7 (May 29, 2020): dmm044727. http://dx.doi.org/10.1242/dmm.044727.

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ABSTRACTThe identification of genetic variants that predispose individuals to cardiovascular disease and a better understanding of their targets would be highly advantageous. Genome-wide association studies have identified variants that associate with QT-interval length (a measure of myocardial repolarization). Three of the strongest associating variants (single-nucleotide polymorphisms) are located in the putative promotor region of CNOT1, a gene encoding the central CNOT1 subunit of CCR4-NOT: a multifunctional, conserved complex regulating gene expression and mRNA stability and turnover. We isolated the minimum fragment of the CNOT1 promoter containing all three variants from individuals homozygous for the QT risk alleles and demonstrated that the haplotype associating with longer QT interval caused reduced reporter expression in a cardiac cell line, suggesting that reduced CNOT1 expression might contribute to abnormal QT intervals. Systematic siRNA-mediated knockdown of CCR4-NOT components in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) revealed that silencing CNOT1 and other CCR4-NOT genes reduced their proliferative capacity. Silencing CNOT7 also shortened action potential duration. Furthermore, the cardiac-specific knockdown of Drosophila orthologs of CCR4-NOT genes in vivo (CNOT1/Not1 and CNOT7/8/Pop2) was either lethal or resulted in dilated cardiomyopathy, reduced contractility or a propensity for arrhythmia. Silencing CNOT2/Not2, CNOT4/Not4 and CNOT6/6L/twin also affected cardiac chamber size and contractility. Developmental studies suggested that CNOT1/Not1 and CNOT7/8/Pop2 are required during cardiac remodeling from larval to adult stages. To summarize, we have demonstrated how disease-associated genes identified by GWAS can be investigated by combining human cardiomyocyte cell-based and whole-organism in vivo heart models. Our results also suggest a potential link of CNOT1 and CNOT7/8 to QT alterations and further establish a crucial role of the CCR4-NOT complex in heart development and function.This article has an associated First Person interview with the first author of the paper.

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Zheng, Xiaofeng, Raluca Dumitru, Brad L. Lackford, Johannes M. Freudenberg, Ajeet P. Singh, Trevor K. Archer, Raja Jothi, and Guang Hu. "Cnot1, Cnot2, and Cnot3 Maintain Mouse and Human ESC Identity and Inhibit Extraembryonic Differentiation." STEM CELLS 30, no. 5 (April 9, 2012): 910–22. http://dx.doi.org/10.1002/stem.1070.

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McLenachan, Samuel, Dan Zhang, Janya Grainok, Xiao Zhang, Zhiqin Huang, Shang-Chih Chen, Khine Zaw, et al. "Determinants of Disease Penetrance in PRPF31-Associated Retinopathy." Genes 12, no. 10 (September 28, 2021): 1542. http://dx.doi.org/10.3390/genes12101542.

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Retinitis pigmentosa 11 (RP11) is caused by dominant mutations in PRPF31, however a significant proportion of mutation carriers do not develop retinopathy. Here, we investigated the relationship between CNOT3 polymorphism, MSR1 repeat copy number and disease penetrance in RP11 patients and non-penetrant carriers (NPCs). We further characterized PRPF31 and CNOT3 expression in fibroblasts from eight RP11 patients and one NPC from a family carrying the c.1205C>T variant. Retinal organoids (ROs) and retinal pigment epithelium (RPE) were differentiated from induced pluripotent stem cells derived from RP11 patients, an NPC and a control subject. All RP11 patients were homozygous for the 3-copy MSR1 repeat in the PRPF31 promoter, while 3/5 NPCs carried a 4-copy MSR1 repeat. The CNOT3 rs4806718 genotype did not correlate with disease penetrance. PRFP31 expression declined with age in adult cadaveric retina. PRPF31 and CNOT3 expression was reduced in RP11 fibroblasts, RO and RPE compared with controls. Both RP11 and NPC RPE displayed shortened primary cilia compared with controls, however a subpopulation of cells with normal cilia lengths was present in NPC RPE monolayers. Our results indicate that RP11 non-penetrance is associated with the inheritance of a 4-copy MSR1 repeat, but not with CNOT3 polymorphisms.

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Banowska, Lidia. "Ironia, cnota i „strach śmieszności”. (Herbert – Norwid)." Studia Norwidiana 40 (September 13, 2022): 37–56. http://dx.doi.org/10.18290/sn2240.2.

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Artykuł dotyczy związku ironii oraz cnoty w poezji Cypriana Norwida oraz Zbigniewa Herberta jako pojęć kluczowych dla twórczości obu autorów i sytuuje się w obszarze badań nad tradycją norwidowską w pisarstwie autora Pana Cogito. Słynny wiersz Herberta Pan Cogito o cnocie zostaje potraktowany jako studium przypadku. Na podstawie interpretacji tego tekstu autorka stawia tezę, iż obrazową matrycą myślenia Herberta o cnocie była wyobraźnia ironiologiczna autora Quidama, a ironia odsłania się jako jedna z możliwych konkretyzacji cnoty. Podstawę dla budowania obrazowych przedstawień obu pojęć stanowią zabiegi personifikacji alegorii, którym nośność i oryginalność zapewnia dekonwencjonalizujący gest równoczesnej antropomorfizacji, prowadzący do ironizacji w ujęciu obu kobiecych bohaterek. Ważnym wątkiem rozważań jest związek między cnotą i ironią sytuowany w perspektywie kulturowej. Rodzaj relacji między obu pojęciami dobrze oddaje metafora siostrzeństwa: ironia jako siostra prawdy jest zarazem siostrą cnoty. Cnota jako aksjologiczna pamięć kultury warunkuje cywilizacyjny postęp; ironia sytuacji diagnozowanej przez obu twórców polega na odwróceniu znaczeń i wartości, w którym pod pręgierzem drwiny odrzucane jest to, co jedynie gwarantuje rozwój, a pojawiający się w związku z tym lęk przed wyśmianiem wywołuje u większości niechęć do praktykowania cnót – paradoksalnie uniemożliwiając rozwój. Związek między cnotą a ironią polega zatem tutaj na ujawnianiu niewłaściwości takiego biegu spraw; ironia odsłania się tym samym jako odpowiedź na nie-cnotę czasów i ludzi czasy te współtworzących, w degeneracji których istotnym czynnikiem okazuje się odrzucenie „myślenia według wartości”. Tym samym najgłębsza wartość związku obu omawianych pojęć zdaje się polegać na próbie przywrócenia aksjologicznego ładu.

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Díaz-Peña, Roberto, Ana M. Aransay, Beatriz Suárez-Álvarez, Jacome Bruges-Armas, Naiara Rodríguez-Ezpeleta, María Regueiro, Fernando M. Pimentel-Santos, et al. "A high density SNP genotyping approach within the 19q13 chromosome region identifies an association of a CNOT3 polymorphism with ankylosing spondylitis." Annals of the Rheumatic Diseases 71, no. 5 (January 31, 2012): 714–17. http://dx.doi.org/10.1136/annrheumdis-2011-200661.

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ObjectiveTo identify genomic variants in the 19q13 chromosome region associated with ankylosing spondylitis (AS) in human leucocyte antigen (HLA)-B27-positive populations.MethodsHigh-throughput genotyping of 1536 haplotype-tag single nucleotide polymorphisms (SNPs) was performed in 249 patients with AS and 302 healthy controls. Some of the identified associations were validated by genotyping four SNPs in two additional cohorts consisting of 412 cases/301 controls and 144 cases/203 controls. All individuals selected (both cases and controls) were HLA-B27-positive.ResultsTwo markers in two different genes (CNOT3 and LAIR2) showed significant association (p<10−3) with AS. In addition, sliding windows analysis showed association of groups of adjacent SNPs in regions located around CNOT3 (Chr19: 59347459-59356564, p=2.43×10−4 to 6.54×10−4). The associations were validated by genotyping four SNPs from regions located near LAIR2 and CNOT3 genes (rs1055234, rs8111398, rs2287828 and rs4591276) in two additional cohorts. The CNOT3 polymorphism (rs1055234) remained associated with AS (combined p=9.73×10−6). One SNP, located downstream of KIR3DL1, was detected which, tested in combination with HLA-Bw4I80, was associated with AS.ConclusionA novel significant association was detected between SNP rs1055234 and AS susceptibility.

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Szram, Mariusz. "Can humility exist without poverty? A response by Cappadocian Fathers and John Chrysostom." Vox Patrum 62 (September 4, 2014): 505–10. http://dx.doi.org/10.31743/vp.3599.

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Greccy Ojcowie Kościoła IV w. uznawali zgodnie cnotę pokory za punkt wyjścia na drodze duchowego doskonalenia oraz za matkę wszystkich cnót. W duchu rozwijającego się monastycyzmu podkreślali przede wszystkim ścisły związek pokory z posłuszeństwem jako cnotą najbardziej jej pokrewną. Autor artykułu stara się znaleźć odpowiedź na pytanie, w jaki sposób postrzegali oni relację między pokorą i ubóstwem, mającą głęboką tradycję biblijną. Już w Starym Testamencie ludzie ubodzy (ptoco…) jako znajdujący się w potrzebie byli uważani za szczególnie skromnych i otwartych na pokorne szukanie pomocy u Boga i drugiego człowieka. Ojcowie Kapadoccy i Jan Chryzostom definiowali cnotę pokory jako przypisywanie wszelkiej chwały za dokonane dobre czyny samemu Bogu i niewywyższanie się ponad innych ludzi, nawet największych grzeszników. Zagadnienie związku ubóstwa z tak rozumianą pokorą poruszali komentując przede wszystkim pierwsze z ośmiu błogosławieństw Chrystusa na górze. Z analiz homilii poświęconych tej kwestii przez Grzegorza z Nyssy i Jana Chryzostoma wynikają następujące wnioski: (1) istnieją dwa rodzaje ubóstwa: duchowe i materialne, które są od siebie zależne; (2) istnieje także tzw. „złe ubóstwo”, które oznacza brak podstawowych cnót; jest ono przeszkodą do osiągnięcia cnoty pokory; (3) ubóstwo materialne ułatwia postawę pokory, ale nie wystarcza do osiągnięcia tej cnoty; (4) cnota pokory jest natomiast niemożliwa bez ubóstwa duchowego, które otwiera na Boga; (5) ludzie ubodzy w duchu, których dotyczy pierwsze błogosławieństwo, są synonimem ludzi pokornych.

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Inoue, Takeshi, Masahiro Morita, Atsushi Hijikata, Yoko Fukuda-Yuzawa, Shungo Adachi, Kyoichi Isono, Tomokatsu Ikawa, et al. "CNOT3 contributes to early B cell development by controlling Igh rearrangement and p53 mRNA stability." Journal of Experimental Medicine 212, no. 9 (August 3, 2015): 1465–79. http://dx.doi.org/10.1084/jem.20150384.

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The CCR4–NOT deadenylase complex plays crucial roles in mRNA decay and translational repression induced by poly(A) tail shortening. Although the in vitro activities of each component of this complex have been well characterized, its in vivo role in immune cells remains unclear. Here we show that mice lacking the CNOT3 subunit of this complex, specifically in B cells, have a developmental block at the pro- to pre–B cell transition. CNOT3 regulated generation of germline transcripts in the VH region of the immunoglobulin heavy chain (Igh) locus, compaction of the locus, and subsequent Igh gene rearrangement and destabilized tumor suppressor p53 mRNA. The developmental defect in the absence of CNOT3 could be partially rescued by ablation of p53 or introduction of a pre-rearranged Igh transgene. Thus, our data suggest that the CCR4–NOT complex regulates B cell differentiation by controlling Igh rearrangement and destabilizing p53 mRNA.

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Rodriguez-Gil, Alfonso, Olesja Ritter, Juliane Hornung, Hilda Stekman, Marcus Krüger, Thomas Braun, Elisabeth Kremmer, Michael Kracht, and M. Lienhard Schmitz. "HIPK family kinases bind and regulate the function of the CCR4-NOT complex." Molecular Biology of the Cell 27, no. 12 (June 15, 2016): 1969–80. http://dx.doi.org/10.1091/mbc.e15-09-0629.

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The serine/threonine kinase HIPK2 functions as a regulator of developmental processes and as a signal integrator of a wide variety of stress signals, such as DNA damage, hypoxia, and reactive oxygen intermediates. Because the kinase is generated in a constitutively active form, its expression levels are restricted by a variety of different mechanisms. Here we identify the CCR4-NOT complex as a new regulator of HIPK2 abundance. Down-regulation or knockout of the CCR4-NOT complex member CNOT2 leads to reduced HIPK2 protein levels without affecting the expression level of HIPK1 or HIPK3. A fraction of all HIPK family members associates with the CCR4-NOT components CNOT2 and CNOT3. HIPKs also phosphorylate the CCR4-NOT complex, a feature that is shared with their yeast progenitor kinase, YAK1. Functional assays reveal that HIPK2 and HIPK1 restrict CNOT2-dependent mRNA decay. HIPKs are well known regulators of transcription, but the mutual regulation between CCR4-NOT and HIPKs extends the regulatory potential of these kinases by enabling posttranscriptional gene regulation.

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Głąb, Anna. "Cnota, charakter, dobroć. W nawiązaniu do powieści autobiograficznej Raimonda Gaity Mój ojciec Romulus." Roczniki Filozoficzne 68, no. 1 (March 30, 2020): 49–75. http://dx.doi.org/10.18290/rf20681-3.

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Przedmiotem tekstu jest rozróżnienie między dobrocią i cnotą oraz złem i występkiem, wprowadzone przez Hannah Arendt na podstawie lektury powieści Hermanna Melville’a Billy Budd. Rozróżnienie to analizuję, odnosząc się do historii życia Romulusa Gaity, bohatera powieści autobiograficznej Mój ojciec Romulus, której autorem jest australijski etyk Raimond Gaita. W paragrafie 1 zajmuję się ową dystynkcją, wskazując na przewartościowanie takich pojęć, jak cnota i występek w powieści Melville’a oraz jego rozumienie cnoty. Następnie (paragraf 2) staram się odpowiedzieć na pytanie, dlaczego Gaita pisze o swym ojcu, używając kategorii charakteru, a nie cnoty. Dalej (paragraf 3) podejmuję refleksję nad relacją między cnotą, charakterem, dobrocią a chorobą psychiczną Romulusa. Na koniec (paragraf 4) odpowiadam na pytanie, jaki jest metafizyczny fundament, na którym Gaita formułuje przekonanie o wyższości Dobra i dobroci nad cnotą oraz pokazuję, jakie konkrety składają się na przyjmowaną przez Romulusa etykę dobroci.

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Більше джерел

Дисертації з теми "CNOT3"

Martufi, Matteo. "Role of Cnot3 in gene regulation and cell cycle progression." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24778.

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Gene expression is a process that is tightly regulated by many factors. Different genes are transcribed not only in a cell specific manner but are also differentially expressed at different stages of the cell cycle. Cnot3 is part of the CCR4-NOT deadenylation complex, which is involved in the turnover of mRNAs in the cytoplasm and has also been shown to have roles in regulating transcription and cell proliferation and in maintaining ES cell pluripotency. Previous work demonstrated that Cnot3 interacts directly with Aurora B kinase and is phosphorylated by Aurora B in an in vitro assay. Aurora B and Cnot3 co-localise at active gene promoters in resting B cells. Since Aurora B is a cell cycle kinase, I have developed a cell synchronization system to analyse the role of the Cnot3-Aurora B interaction at different stages of the cell cycle in primary B cells. Using this system, I have demonstrated that the interaction between Cnot3 and Aurora B varies during cell cycle progression. In vitro analysis showed that the interaction occurs through the NOT box domain of Cnot3. Mass spectrometry analysis of Cnot3 interactors, performed on nuclear extracts from B cells in the early G1 and G2 phases of the cell cycle, identified interactions with many factors that are known to have roles in transcription regulation and RNA processing. Interaction of Cnot3 with Histone H1 was confirmed using a peptide binding assay, suggesting a potential role in chromatin organization. Cnot3 was also shown to interact with Xrn2, a 5'-3' exoribonuclease that is involved in RNA turnover and termination of transcription. ChIP analysis demonstrated promoter binding of Cnot3 at a number of cell cycle stages. Cnot3 shows cell cycle dependent binding to promoters of a wide range of active genes, including promoters that are not directly involved in cell cycle regulation. Genome wide analysis using ChIP sequencing revealed changes in the binding profiles of Cnot3 at promoters and enhancers during cell cycle progression. A Cnot3 conditional knock out mouse has been generated, which will be used to test the functional importance of these observations.

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Doidge, Rachel L. "The anti-proliferative activity of BTG/TOB proteins is mediated via the Caf1a (CNOT7)/Caf1b (CNOT8) deadenylase enzymes." Thesis, University of Nottingham, 2013. http://eprints.nottingham.ac.uk/13012/.

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The human BTG/TOB protein family comprises six members (BTG1, BTG2/PC3/Tis21, BTG3/Ana, BTG4/PC3B, TOB1/Tob, and TOB2) that display anti-proliferative activity in a number of cell types. They are characterised by a conserved N-terminal BTG domain that mediates interactions with the Caf1a (CNOT7) and Caf1b (CNOT8) deadenylases. It was unclear whether the anti-proliferative activity of the BTG/TOB proteins was mediated through interactions with Caf1a (CNOT7) and Caf1b (CNOT8). To address this we further characterised the amino acid residues located along the BTG2 and TOB1 interaction surface with Caf1a (CNOT7)/Caf1b (CNOT8) to identify residues required for the interaction. We then analysed the role of BTG2 and TOB1 in the regulation of cell proliferation, translation and mRNA abundance using a mutant that is no longer able to interact with Caf1a (CNOT7)/Caf1b (CNOT8). We conclude that the anti-proliferative activity of BTG/TOB proteins is mediated through interactions with the Caf1a (CNOT7) and Caf1b (CNOT8) deadenylase enzymes. We also demonstrate that recruitment of BTG2 and TOB1 to mRNA leads to reduced protein levels and mRNA degradation. Furthermore, we show that the regulation of mRNA abundance and protein levels is dependent on Caf1a (CNOT7)/Caf1b (CNOT8), but does not appear to require other Ccr4-Not components, including the Ccr4a (CNOT6)/Ccr4b (CNOT6L) deadenylases, or the non-catalytic subunits CNOT1 or CNOT3.

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Engel, Camille. "Description phénotypique de formes rares de trouble du développement intellectuel et caractérisation des mécanismes moléculaires impliqués." Electronic Thesis or Diss., Bourgogne Franche-Comté, 2024. http://www.theses.fr/2024UBFCE006.

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L’avènement des nouvelles techniques de séquençage a permis d’augmenter de façon considérable le taux diagnostique des troubles du développement intellectuel (TDI) et plus de 2000 gènes impliqués sont aujourd’hui connus. Malgré ces progrès considérables, l’interprétation des variants identifiés par les techniques de séquençage reste parfois difficile et l’histoire naturelle des TDI nouvellement décrits est souvent méconnue. Notre travail a consisté à étudier quatre formes de TDI rares de modes de transmissionvariés sur les plans clinique et génétique afin de mieux comprendre ces affections et les mécanismes qui les sous-tendent. Nous avons d’une part précisé les tableaux cliniques associés aux variations de BRAT1, CNOT3 et MTOR et avons recherché l’existence d’éventuelles corrélations phénotype-génotype pour les variations de ces gènes. D’autre part, nous avons participé à la mise en place d’un test fonctionnel permettant de reclasser les variants de signification incertaine de PQBP1
The advent of new sequencing techniques has dramatically increased the diagnostic rate of intellectual disability (ID), and more than 2,000 genes are currently known to be involved. Despite these considerable progresses, interpreting the variants identified by sequencing methods remains challenging, and the natural history of newly described ID is often poorly understood. To better understand these disorders and their underlying mechanisms, we have studied four rare forms of ID with various inheritance patterns from both clinical and genetic perspectives. On one hand, we defined the clinical pictures associated with variations in BRAT1, CNOT3 and MTOR, and we investigated the existence of any phenotype-genotype correlations. On the other hand, we contributed to the design of a functional test to reclassify PQBP1 variants of uncertain significance

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McFleder, Rhonda L. "Regulation of Local Translation, Synaptic Plasticity, and Cognitive Function by CNOT7." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/915.

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Local translation of mRNAs in dendrites is vital for synaptic plasticity and learning and memory. Tight regulation of this translation is key to preventing neurological disorders resulting from aberrant local translation. Here we find that CNOT7, the major deadenylase in eukaryotic cells, takes on the distinct role of regulating local translation in the hippocampus. Depletion of CNOT7 from cultured neurons affects the poly(A) state, localization, and translation of dendritic mRNAs while having little effect on the global neuronal mRNA population. Following synaptic activity, CNOT7 is rapidly degraded resulting in polyadenylation and a change in the localization of its target mRNAs. We find that this degradation of CNOT7 is essential for synaptic plasticity to occur as keeping CNOT7 levels high prevents these changes. This regulation of dendritic mRNAs by CNOT7 is necessary for normal neuronal function in vivo, as depletion of CNOT7 also disrupts learning and memory in mice. We utilized deep sequencing to identify the neuronal mRNAs whose poly(A) state is governed by CNOT7. Interestingly these mRNAs can be separated into two distinct populations: ones that gain a poly(A) tail following CNOT7 depletion and ones that surprisingly lose their poly(A) tail following CNOT7 depletion. These two populations are also distinct based on the lengths of their 3’ UTRs and their codon usage, suggesting that these key features may dictate how CNOT7 acts on its target mRNAs. This work reveals a central role for CNOT7 in the hippocampus where it governs local translation and higher cognitive function.

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Oliveira, Maria do Socorro Ribeiro de. "Contribuições para comunicação e computação quânticas: análise do PMD e PDL em um sistema de DQC, geração de um estado entrelaçado de quatro modos e uma porta CNOT para qubits de estados coerentes." reponame:Repositório Institucional da UFC, 2013. http://www.repositorio.ufc.br/handle/riufc/10869.

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OLIVEIRA. M. S. R. Contribuições para comunicação e computação quânticas: análise do PMD e PDL em um sistema de DQC, geração de um estado entrelaçado de quatro modos e uma porta CNOT para qubits de estados coerentes. 2013. 60 f. Dissertação (Mestrado em Engenharia de Teleinformática) - Centro de Tecnologia, Universidade Federal do Ceará, Fortaleza, 2013.
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This work presents contributions to the quantum communication and in computation fields. In the area of quantum communication, we analyzed the impacts of the effects of PMD and PDL on the performance of a quantum key distribution system based on BB84 protocol in a fiber optic network. It was presented an analytical expression for the average fidelity as a function of the PMD and PDL parameters which makes possible to analyze the behavior of bit error and secure bit generation rates for a quantum communication system. In the field of quantum computing, we proposed two optical systems based on linear optics for coherent state qubits. The first system is a probabilistic generator of a four-mode-type entangled state with a maximum efficiency of 25%. From this it state was possible to propose a second system that is able to perform a probabilistically CNOT gate. Both proposed systems may be implemented with existing photonics technology. They do not use single-qubit gate or quantum teleportation that are commonly used in quantum information processing using coherent states.
Este trabalho apresenta contribuições para a área quântica, no âmbito da comunicação e da computação. Na área de comunicação quântica, foram analisados os impactos dos efeitos do PMD e PDL no desempenho de sistemas de distribuição quântica de chaves baseados no protocolo BB84, sob uma rede óptica a fibra. É demonstrada uma expressão analítica da fidelidade média em função dos parâmetros de PMD e PDL, o qual torna possível a análise do comportamento das taxas de erro de bit e de geração de bit seguro de um sistema de comunicação quântica. No campo da computação quântica, são propostos dois sistemas ópticos baseados em óptica linear para qubits de estados coerentes. O primeiro consiste em um gerador probabilístico de um tipo de estado entrelaçado de quatro modos com uma eficiência máxima de 25%. A partir desse estado foi possível propor um segundo sistema que é capaz de realizar uma porta CNOT probabilisticamente. Ambos os sistemas propostos são de implementação factível com a tecnologia fotônica existente, não utilizam portas de um qubit nem teleportação quântica, que são recursos comumente empregados em processamento quântico da informação para estados coerentes.

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Goubault, de Brugière Timothée. "Methods for optimizing the synthesis of quantum circuits Quantum CNOT Circuits Synthesis for NISQ Architectures Using the Syndrome Decoding Problem Quantum circuits synthesis using Householder transformations Synthesizing quantum circuits via numerical optimization Reuse method for quantum circuit synthesis." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASG018.

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Pour exécuter un algorithme abstrait sur un ordinateur quantique il faut compiler l'algorithme en une séquence d'instructions bas niveau exécutables par le processeur. L'étape de compilation est cruciale car elle détermine la quantité de ressources nécessaire pour l'exécution d'un algorithme ; par conséquent elle se doit d'être optimisée. Dans cette thèse nous nous intéressons à une brique de la compilation~: la synthèse de circuits quantiques à partir d'une spécification abstraite d'un opérateur. Dans un premier temps nous étudions le cas où la matrice unitaire d'un opérateur quantique nous est donnée et nous explorons la minimisation des ressources quantiques et la minimisation des ressources classiques. Même si l'optimisation simultanée de ces deux types de ressources semble difficile, nous proposons de meilleurs compromis améliorant la littérature.Dans un second temps nous nous intéressons à la classe des opérateurs dits linéaires réversibles. Nous nous intéressons cette fois-ci exclusivement à l'optimisation des ressources quantiques et nous améliorons l'état de l'art dans diverses cas de métriques (taille et profondeur du circuit) et de processeurs quantiques (processeurs NISQ, ou à connectivité complète)
To run an abstract algorithm on a quantum computer, the algorithm must be compiled into a sequence of low-level instructions that can be executed by the processor. The compilation step is crucial because it determines the quantity of resources necessary for the execution of an algorithm. Therefore, the compilation stage must be optimized. In this thesis, we are interested in a brick of compilation: the synthesis of quantum circuits from an abstract specification of an operator.First, we study the case where the unitary matrix of a quantum operator is given to us and we explore the minimization of both quantum resources and classical resources. Even if the simultaneous optimization of these two types of resources seems difficult, we propose better compromises improving the literature.Secondly, we are interested in the class of so-called reversible linear operators. This time we are exclusively interested in the optimization of quantum resources and we improve the state of the art in various cases of quantum metrics (circuit size, circuit depth) and processors (NISQ, fully-connected processors)

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Pasquini, Michael. "Computer quantistici a ioni intrappolati." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2021. http://amslaurea.unibo.it/24678/.

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L'obiettivo di questo elaborato è di dare una descrizione generale del funzionamento di un computer quantistico a ioni intrappolati, dal confinamento degli ioni in trappole unidimensionali fino all’implementazione delle porte logiche. Partendo dalla descrizione della trappola ionica di Paul che confina gli ioni tramite un potenziale di tipo armonico, si è poi descritto in che modo è possibile modificare lo stato interno degli ioni tramite l’interazione con il campo elettromagnetico generato da un laser esterno Si è esaminato nel dettaglio quali sono le principali tipologie di gate a singolo qubit e due tipologie di gate CNOT multi-qubit, quella di Cirac-Zoller e quella di Mølmer–Sørensen. Anche in questo caso, sono state descritte le implementazioni di tali gate nel caso specifico di un computer a ioni intrappolati. Nella parte finale viene presentata un’implementazione di un algoritmo quantistico su un processore reale a ioni intrappolati reso disponibile online dalla compagnia IonQ. In particolare sono stati preparati e misurati due tipi di stati quantistici: lo stato di Bell e il più generale stato GHZ.

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Tsai, Dung-Bang, and 蔡東邦. "Optimal Control of CNOT gate." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/17370157583852447562.

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碩士
國立臺灣大學
物理研究所
96
We investigate how pulse-sequences and operation times of elementary quantum gates can be optimized for silicon-based donor electron spin quantum computer architecture, complementary to the original Kane''s nuclear spin proposal. This gate-sequence-optimal or time-optimal quantum gate control in a quantum circuit is in addition to the more conventional concept of optimality in terms of the number of elementary gates needed in a quantum transformation. The optimal control method we use is the so-called gradient ascent pulse engineering (GRAPE) scheme. We focus on the high fidelity controlled-NOT (CNOT) gate and explicitly find the digitized control sequences by optimizing the effective, reduced donor electron spin Hamiltonian, with external controls over the hyperfine A and exchange J interactions. We first try different piecewise constant control steps and numerically calculate the fidelity (error) against the time needed to implement a CNOT gate with stopping criteria of error in the optimizer set to 〖10〗^(-9) in order to economize the simulation time. Here, the error is defined as 1-F, where F is fidelity. The error is less than 〖10〗^(-8) for times longer than 100ns, and it is found that 30 piecewise constant control steps for the CNOT gate operation will be sufficient to meet the required fidelity (error), and the performance would not be improved further with more steps. With operation time t=100ns and stopping criteria of error set to 〖10〗^(-16), we can find that the near time-optimal, high-fidelity CNOT gate control sequence has an error of 〖1.11×10〗^(-16). We then simulate the control sequences of the CNOT gate, obtained from reduced Hamiltonian simulations, with the full spin Hamiltonian. We find the error of about 〖10〗^(-6) which is below the error threshold required for fault-tolerant (〖10〗^(-4)) quantum computation. The CNOT gate operation time of 100ns is 3 times faster than the globally controlled electron spin scheme of 297ns. One of the great advantages of this near optimal-time high fidelity CNOT gate is that the exchange interaction is not required to be strong (the maximum value is J/h=20MHz compared to the typical value of 10.2GHz. This relaxes significantly the stringent distance constraint of two neighboring donor atoms of about 10nm as reported in the original Kane''s proposal to be about 30nm which is within the reach of the current fabrication technology.

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Tsai, Dung-Bang. "Optimal Control of CNOT gate." 2008. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0001-1507200819593900.

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Lin, Yu-Chen, and 林育楨. "The Role of CNOT4 E3 Ubiquitin ligase in Influenza A virus replication." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/78341434155778519053.

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碩士
國立陽明大學
生命科學系暨基因體科學研究所
102
Abstract Influenza A virus (IAV) is an enveloped RNA virus. Its genome consists of eight single-stranded negative-sense RNAs that encode 12 viral proteins. Each viral RNA segment is packaged with viral nucleoprotein (NP) and RNA-dependent RNA polymerase complex (PB1, PB2 and PA) to form viral ribonucleoprotein (vRNP) complexes. Our previous report showed that NP is a mono-ubiquitinated protein and can be specifically deubiquitinated by cellular deubiquitinase USP11. Ubiquitination of NP could alter the interaction of NP with viral RNA, and USP11 can cleave ubiquitin from NP, thereby reducing the RNA replication efficiency. Given these findings, we attempted to determine which E3 ligase(s) are responsible for NP ubiquitination; we used a small-scale RNAi screen based on candidates derived from RNAi pooled screening. An E3 ubiquitin ligase termed CNOT4 was picked from that screening for follow-up study. We found that expression of virus NP was decreased in a CNOT4 knockdown A549 cell line upon IAV infection. In addition, using CNOT4 knockdown 293T cells, we determined that viral RdRp activity was also inhibited as demonstrated by the minireplicon reporter assay. These findings suggest that CNOT4 may play a role in viral RNA transcription and replication. Interestingly, NP ubiquitination was decreased as evaluated by an in vitro ubiquitin assay in CNOT4 knockdown cells. When overexpressed wobble CNOT4, both NP ubiquitination and viral RdRp activity ware rescued in knockdown cells. Furthermore, when USP11 was co-expressed with CNOT4, the level of ubiquitination of NP was lower as compared with CNOT4 expressed alone. The results indicate that CNOT4 may increase ubiquitination of viral NP protein and enhance viral RdRp activity, and CNOT4 has opposite function with USP11 for IAV replication. Based on current findings, we hypothesize that CNOT4 is an E3 ligase of NP protein.

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Книги з теми "CNOT3"

Zulawski, Andrzej. Cnota. Warszawa: Wydawnictwo Ksiazkowe "Twoj Styl", 2005.

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Lasocińska, Estera. "Cnota sama z mądrością jest naszym żywotem": Stoickie pojęcie cnoty w poezji polskiej XVII wieku. Warszawa: IBL, 2003.

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Marie, Robertson Eleanor. Bezwstydna cnota. Warszawa: Wydawnictwo Amber, 2009.

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Szczypiorski, Andrzej. Grzechy, cnoty, pragnienia. Poznań: Sens, 1997.

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Korolec, Jerzy B. Wolność, cnota, praxis. Warszawa: Wydawn. Instytutu Filozofii i Socjologii Polskiej Akademii Nauk, 2006.

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Rzeszowski, Uniwersytet, ed. Cnoty: Eseje z filozofii kultury. Rzeszów: Wydawnictwo Uniwersytetu Rzeszowskiego, 2016.

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Przybyszewski, Bolesław. Błogosławiona Jadwiga królowa: Zdobna w cnoty. 2nd ed. Kraków: Wydawn. Św. Stanisława B.M. Archidiecezji Krakowskiej, 1996.

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Przybyszewski, Bolesław. Święta Jadwiga Królowa: Zdobna w cnoty. 3rd ed. Kraków: Wydawn. Św. Stanisława BM Archidiecezji Krakowskiej, 1997.

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Witold, Filler, and Lipiński Eryk, eds. Szpilki 1935-1985: Z dziejów cnoty. Warszawa: Krajowa Agencja Wydawnicza, 1985.

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S, Szczepański Marek, Rojek Paulina 1976-, and Wyższa Szkoła Zarządzania i Nauk Społecznych w Tychach., eds. Cnoty i instytucje obywatelskie w społeczności lokalnej. Tychy: Śląskie Wydawnictwa Naukowe, Wyższa Szkoła Zarządzania i Nauk Społecznych w Tychach, 2001.

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Dumitru, Raluca, and Guang Hu. "Maintenance of Human Embryonic Stem Cell Identity and Inhibition of Extraembryonic Differentiation: Role of CNOT1, CNOT2 and CNOT3." In Stem Cells and Cancer Stem Cells, Volume 11, 3–14. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7329-5_1.

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Jain, M., and A. Gupta. "2641 Diamagnetic susceptibility of CNOTl." In Diamagnetic Susceptibility and Anisotropy of Inorganic and Organometallic Compounds, 2691. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-44694-1_2642.

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Just, Bettina. "CNOT – ein Quantengatter auf zwei QBits." In Quantencomputing kompakt, 89–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/978-3-662-61889-9_10.

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Grześkowiak-Krwawicz, Anna. "Cnota – Virtue as Advice for the Commonwealth." In The Political Discourse of the Polish-Lithuanian Commonwealth, 139–68. Other titles: Dyskurs polityczny Rzeczypospolitej Obojga Narodów. English Description: New York, NY : Routledge, 2021. | Series: Routledge research in early modern history: Routledge, 2020. http://dx.doi.org/10.4324/9780367823535-8.

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Meuli, Giulia, Mathias Soeken, and Giovanni De Micheli. "SAT-based {CNOT, T} Quantum Circuit Synthesis." In Reversible Computation, 175–88. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99498-7_12.

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Just, Bettina. "CNOT: A Quantum Gate on Two Qubits." In Quantum Computing Compact, 83–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-65008-0_10.

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Wong, Hiu Yung. "Quantum Gate Introduction: NOT and CNOT Gates." In Introduction to Quantum Computing, 133–41. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-36985-8_15.

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Felloni, Sara, and Giuliano Strini. "An Error Model for the Cirac-Zoller cnot Gate." In Lecture Notes of the Institute for Computer Sciences, Social Informatics and Telecommunications Engineering, 210–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11731-2_25.

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Niemann, Philipp, Luca Müller, and Rolf Drechsler. "Finding Optimal Implementations of Non-native CNOT Gates Using SAT." In Reversible Computation, 242–55. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-79837-6_15.

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Cheng, Xueyun, Mingqiang Zhu, Xiang Li, and Zhijin Guan. "Nearest Neighbor Synthesis of CNOT Circuit Based on Matrix Transformation." In Advances in Natural Computation, Fuzzy Systems and Knowledge Discovery, 150–56. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-89698-0_16.

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Тези доповідей конференцій з теми "CNOT3"

Wang, Hanyu, Jason Cong, and Giovanni De Micheli. "Quantum State Preparation Using an Exact CNOT Synthesis Formulation." In 2024 Design, Automation & Test in Europe Conference & Exhibition (DATE), 1–6. IEEE, 2024. http://dx.doi.org/10.23919/date58400.2024.10546633.

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Choure, Kamalkishor, Manisha Prajapat, Ankur Saharia, Anton V. Bourdine, Oleg Morozov, Ivan K. Meshkov, Manish Tiwari, and Ghanshyam Singh. "Silicon nitride ring resonators based all-optical CNOT logic gate." In Optical Technologies for Telecommunications 2023, edited by Oleg G. Morozov, Albert C. Sultanov, and Anton V. Bourdine, 37. SPIE, 2024. http://dx.doi.org/10.1117/12.3026516.

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Hinton, Chris, and Madeleine Belisle. "cNOTE." In ACM SIGGRAPH 2006 Art gallery. New York, New York, USA: ACM Press, 2006. http://dx.doi.org/10.1145/1178977.1179101.

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Wang, Qianke, Jun Liu, Dawei Lyu, and Jian Wang. "Experimental Demonstration of A Spatial Mode Quantum Gate Assisted by Diffractive Deep Neural Networks." In CLEO: QELS_Fundamental Science. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleo_qels.2022.ff3j.4.

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We demonstrate a quantum controlled-NOT (CNOT) gate operating on spatial modes of single photons. The CNOT gate is implemented by a series of spatially separated phase plates generated by diffractive deep neural networks (D2NNs).

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Chen, Yanzhu, Linghua Zhu, Nicholas J. Mayhall, Edwin Barnes, and Sophia E. Economou. "How Much Entanglement Do Quantum Optimization Algorithms Require?" In Quantum 2.0. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/quantum.2022.qm4a.2.

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ADAPT-QAOA, a novel problem-tailored version of quantum approximate optimization algorithm, speeds up convergence using entangling operators while reducing the total number of CNOTs. We explore how much entanglement is required to speed up optimization algorithms.

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Ashhab, Sahel, Naoki Yamamoto, Fumiki Yoshihara, and Kouichi Semba. "Numerical analysis of quantum circuits for state preparation and unitary operator synthesis." In Quantum 2.0. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/quantum.2023.qm4b.7.

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We use numerical optimal-control-theory techniques to calculate the number of CNOT gates needed to perform quantum state preparation and unitary operator synthesis. Our approach pro-vides new results and previously inaccessible insight.

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Domínguez-Serna, F. A. "A CNOT Proposal for Temporal-Mode Qubits Based on the Difference Frequency Generation Process." In Frontiers in Optics. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/fio.2023.jtu5a.53.

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Multiple proposals exist for implementing quantum operations on light-based qubits. We propose a nonlinear optics approach using the Difference Frequency Generation process for probabilistic CNOT gates in color qubits, analogous to polarization-based operations [1].

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Lukac, Martin, Kamila Abdiyeva, and Michitaka Kameyama. "CNOT-Measure Quantum Neural Networks." In 2018 IEEE 48th International Symposium on Multiple-Valued Logic (ISMVL). IEEE, 2018. http://dx.doi.org/10.1109/ismvl.2018.00040.

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García-Escartín, Juan Carlos, Pedro Chamorro-Posada, and Alexander Lvovsky. "Optical CNOT gates with Quantum Interrogation." In QUANTUM COMMUNICATION, MEASUREMENT AND COMPUTING (QCMC): Ninth International Conference on QCMC. AIP, 2009. http://dx.doi.org/10.1063/1.3131358.

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Vishwakarma, Soumya, Jerelyn P. Premjit, S. Balakrishnan, and R. Manoov. "Qiskit Simulation of CNOT Equivalent Circuits." In 2023 International Conference on Quantum Technologies, Communications, Computing, Hardware and Embedded Systems Security (iQ-CCHESS). IEEE, 2023. http://dx.doi.org/10.1109/iq-cchess56596.2023.10391294.

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