Relevant bibliographies by topics / CCCDCC

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'CCCDCC'

Author: Grafiati
Published: 11 September 2023

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Journal articles on the topic "CCCDCC"

1

Ahmed, Shereen, Behzad Anwar, and Tabassum Iqbal. "Language Contact: A Study of Syllabic Change of English Borrowed Words in Urdu." International Journal of English Linguistics 8, no. 2 (December 23, 2017): 140. http://dx.doi.org/10.5539/ijel.v8n2p140.

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This paper aims to describe the syllabic changes in those words which Urdu has borrowed from the English language. The changes are observed by exploring the sequence of sounds present in the syllables of English words. The results are presented on the basis of collection of English words taken from Urdu lexicon. The syllable templates that undergo change during the process of Urdu syllabification are: CCV, CVC, CVCC, CCVC, CCVCC, CVVC, CVVVC, CCCV, CCCVC, and CCCVCC. The current study has formulated some specific generalizations and constraints on the basis of which these changes occur. The study has deduced two processes of epenthesis and replacement/substitution which trigger these changes with respect to the phonological rules and phonotactic constraints of the Urdu language.
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Hu, Jie-Li, and Ai-Long Huang. "Dynamics of Hepatitis B Virus Covalently Closed Circular DNA: A Mini-Review." Microorganisms 11, no. 3 (February 27, 2023): 600. http://dx.doi.org/10.3390/microorganisms11030600.

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Eradication of cccDNA is an ideal goal of chronic hepatitis B (CHB) therapy. Understanding the changes in the cccDNA pool during therapy provides a basis for developing CHB treatment strategies. On the other hand, the shift in the balance of the cccDNA pool following therapies allowed researchers to investigate the dynamics of cccDNA. Central to the description of cccDNA dynamics is a parameter called cccDNA half-life. CccDNA half-life is not an intrinsic property of cccDNA molecules, but a description of an observed phenomenon characterized by cccDNA pool decline. Since cccDNA has to be in the nuclei of host cells to function, the half-life of cccDNA is determined by the state and destiny of the host cells. The major factors that drive cccDNA decay include noncytopathic effects and hepatocyte turnover (death and division). In some cases, the determining factor is not the half-life of cccDNA itself, but rather the half-life of the hepatocyte. The main purpose of this review is to analyze the major factors affecting cccDNA half-life and determine the areas requiring further study. In addition, the discrepancy in cccDNA half-life between short-term and long-term nucleot(s)ide analog (NUC) therapy was reported. Hypotheses were proposed to explain the multi-phasic decline of cccDNA during NUC therapy, and a framework based on cccDNA dynamics was suggested for the consideration of various anti-HBV strategies.
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Hsu, Chao-Wei, Yu-De Chu, Ming-Wei Lai, Chih-Lang Lin, Kung-Hao Liang, Yang-Hsiang Lin, and Chau-Ting Yeh. "Hepatitis B Virus Covalently Closed Circular DNA Predicts Postoperative Liver Cancer Metastasis Independent of Virological Suppression." Cancers 13, no. 3 (January 31, 2021): 538. http://dx.doi.org/10.3390/cancers13030538.

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New antiviral therapies against hepatitis B virus (HBV) focus on the elimination of covalently closed circular DNA (cccDNA). However, traditional cccDNA-specific quantitative PCR (qPCR) has a narrow effective range, hindering a reliable comparison between the levels of biopsy-derived cccDNAs. Collaterally, the prognostic role of cccDNA in HBV-related hepatocellular carcinoma (HCC) cannot be clearly defined. Here, we developed a peptide nucleic acid (PNA)-clamping qPCR method to provide a wider range of specific cccDNA quantification (up to 5 logs of effective range). Extrachromosomal DNA was extracted from para-neoplastic tissues for cccDNA quantification. In total, 350 HBV-related HCC patients were included for an outcome analysis. Without differential pre-dilution, cccDNA levels in para-neoplastic liver tissues were determined, ranging from < 2 × 103 to 123.0 × 106 copies/gram. The multivariate linear regression analysis showed that cccDNA was independently correlated with the HBV e antigen (p < 0.001) and serum HBV-DNA levels (p = 0.012). The Cox proportional hazard model analysis showed that cccDNA independently predicted overall survival (p = 0.003) and extrahepatic metastasis-free survival (p = 0.001). In virologically suppressed HCC patients, cccDNA still effectively predicted intrahepatic recurrence-free (p = 0.003) and extrahepatic metastasis-free (p = 0.009) survivals. In conclusion, cccDNA independently predicted postoperative extrahepatic metastasis-free survival.
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Cai, Dawei, Courtney Mills, Wenquan Yu, Ran Yan, Carol E. Aldrich, Jeffry R. Saputelli, William S. Mason, et al. "Identification of Disubstituted Sulfonamide Compounds as Specific Inhibitors of Hepatitis B Virus Covalently Closed Circular DNA Formation." Antimicrobial Agents and Chemotherapy 56, no. 8 (May 29, 2012): 4277–88. http://dx.doi.org/10.1128/aac.00473-12.

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ABSTRACTHepatitis B virus (HBV) covalently closed circular DNA (cccDNA) plays a central role in viral infection and persistence and is the basis for viral rebound after the cessation of therapy, as well as the elusiveness of a cure even after extended treatment. Therefore, there is an urgent need for the development of novel therapeutic agents that directly target cccDNA formation and maintenance. By employing an innovative cell-based cccDNA assay in which secreted HBV e antigen is a cccDNA-dependent surrogate, we screened an in-house small-molecule library consisting of 85,000 drug-like compounds. Two structurally related disubstituted sulfonamides (DSS), termed CCC-0975 and CCC-0346, emerged and were confirmed as inhibitors of cccDNA production, with low micromolar 50% effective concentrations (EC50s) in cell culture. Further mechanistic studies demonstrated that DSS compound treatment neither directly inhibited HBV DNA replication in cell culture nor reduced viral polymerase activity in thein vitroendogenous polymerase assay but synchronously reduced the levels of HBV cccDNA and its putative precursor, deproteinized relaxed circular DNA (DP-rcDNA). However, DSS compounds did not promote the intracellular decay of HBV DP-rcDNA and cccDNA, suggesting that the compounds interfere primarily with rcDNA conversion into cccDNA. In addition, we demonstrated that CCC-0975 was able to reduce cccDNA biosynthesis in duck HBV-infected primary duck hepatocytes. This is the first attempt, to our knowledge, to identify small molecules that target cccDNA formation, and DSS compounds thus potentially serve as proof-of-concept drug candidates for development into therapeutics to eliminate cccDNA from chronic HBV infection.
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Mohd-Ismail, Lim, Gunaratne, and Tan. "Mapping the Interactions of HBV cccDNA with Host Factors." International Journal of Molecular Sciences 20, no. 17 (September 1, 2019): 4276. http://dx.doi.org/10.3390/ijms20174276.

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Hepatitis B virus (HBV) infection is a major health problem affecting about 300 million people globally. Although successful administration of a prophylactic vaccine has reduced new infections, a cure for chronic hepatitis B (CHB) is still unavailable. Current anti-HBV therapies slow down disease progression but are not curative as they cannot eliminate or permanently silence HBV covalently closed circular DNA (cccDNA). The cccDNA minichromosome persists in the nuclei of infected hepatocytes where it forms the template for all viral transcription. Interactions between host factors and cccDNA are crucial for its formation, stability, and transcriptional activity. Here, we summarize the reported interactions between HBV cccDNA and various host factors and their implications on HBV replication. While the virus hijacks certain cellular processes to complete its life cycle, there are also host factors that restrict HBV infection. Therefore, we review both positive and negative regulation of HBV cccDNA by host factors and the use of small molecule drugs or sequence-specific nucleases to target these interactions or cccDNA directly. We also discuss several reporter-based surrogate systems that mimic cccDNA biology which can be used for drug library screening of cccDNA-targeting compounds as well as identification of cccDNA-related targets.
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Allweiss, Lena, Tassilo Volz, Katja Giersch, Janine Kah, Giuseppina Raffa, Joerg Petersen, Ansgar W. Lohse, et al. "Proliferation of primary human hepatocytes and prevention of hepatitis B virus reinfection efficiently deplete nuclear cccDNA in vivo." Gut 67, no. 3 (April 20, 2017): 542–52. http://dx.doi.org/10.1136/gutjnl-2016-312162.

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ObjectiveThe stability of the covalently closed circular DNA (cccDNA) in nuclei of non-dividing hepatocytes represents a key determinant of HBV persistence. Contrarily, studies with animal hepadnaviruses indicated that hepatocyte turnover can reduce cccDNA loads but knowledge on the proliferative capacity of HBV-infected primary human hepatocytes (PHHs) in vivo and the fate of cccDNA in dividing PHHs is still lacking. This study aimed to determine the impact of human hepatocyte division on cccDNA stability in vivo.MethodsPHH proliferation was triggered by serially transplanting hepatocytes from HBV-infected humanised mice into naïve recipients. Cell proliferation and virological changes were assessed by quantitative PCR, immunofluorescence and RNA in situ hybridisation. Viral integrations were analysed by gel separation and deep sequencing.ResultsPHH proliferation strongly reduced all infection markers, including cccDNA (median 2.4 log/PHH). Remarkably, cell division appeared to cause cccDNA dilution among daughter cells and intrahepatic cccDNA loss. Nevertheless, HBV survived in sporadic non-proliferating human hepatocytes, so that virological markers rebounded as hepatocyte expansion relented. This was due to reinfection of quiescent PHHs since treatment with the entry inhibitor myrcludex-B or nucleoside analogues blocked viral spread and intrahepatic cccDNA accumulation. Viral integrations were detected both in donors and recipient mice but did not appear to contribute to antigen production.ConclusionsWe demonstrate that human hepatocyte division even without involvement of cytolytic mechanisms triggers substantial cccDNA loss. This process may be fundamental to resolve self-limiting acute infection and should be considered in future therapeutic interventions along with entry inhibition strategies.
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Chou, Yu-Chi, King-Song Jeng, Mong-Liang Chen, Hsiao-Hui Liu, Tzu-Ling Liu, Ya-Ling Chen, Yu-Chih Liu, Cheng-po Hu, and Chungming Chang. "Evaluation of Transcriptional Efficiency of Hepatitis B Virus Covalently Closed Circular DNA by Reverse Transcription-PCR Combined with the Restriction Enzyme Digestion Method." Journal of Virology 79, no. 3 (February 1, 2005): 1813–23. http://dx.doi.org/10.1128/jvi.79.3.1813-1823.2005.

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ABSTRACT Virus persistence in chronic hepatitis B patients is due to the sustaining level of covalently closed circular DNA (cccDNA) within the nuclei of infected hepatocytes. In this study, we used a modified 1.3-fold hepatitis B virus (HBV) genome, with a BclI genetic marker embedded in the redundancy region, to examine the transcriptional activity of cccDNA and the effect of the HBx protein on transcriptional regulation. After harvesting total RNA from transfected cells or stable lines, we specifically identified and monitored the transcripts from cccDNA by using reverse transcription-PCR (RT-PCR) combined with the restriction enzyme digestion method. In this approach, we have found that (i) RT-PCR combined with detection of the BclI marker is a highly specific method for distinguishing cccDNA-derived transcripts from the original integrated viral genome, (ii) the transcriptional ability of cccDNA was less efficient than that from the integrated viral genome, and (iii) the transcriptional activity of cccDNA was significantly regulated by the HBx protein, a potential transcription activator. In conclusion, we provided a tool with which to elucidate the transcriptional regulation of cccDNA and clarified the transcriptional regulation mechanism of HBx on cccDNA. The results obtained may be helpful in the development of a clinical intervention for patients with chronic HBV infections.
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Doan, Phuong Thi Bich, Kouki Nio, Tetsuro Shimakami, Kazuyuki Kuroki, Ying-Yi Li, Saiho Sugimoto, Hideo Takayama, et al. "Super-Resolution Microscopy Analysis of Hepatitis B Viral cccDNA and Host Factors." Viruses 15, no. 5 (May 16, 2023): 1178. http://dx.doi.org/10.3390/v15051178.

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Infection with hepatitis B virus (HBV) cannot be cured completely because of the persistence of covalently closed circular DNA (cccDNA). We previously found that the host gene dedicator of cytokinesis 11 (DOCK11) was required for HBV persistence. In this study, we further investigated the mechanism that links DOCK11 to other host genes in the regulation of cccDNA transcription. cccDNA levels were determined by quantitative real-time polymerase chain reaction (qPCR) and fluorescence in situ hybridization (FISH) in stable HBV-producing cell lines and HBV-infected PXB-cells®. Interactions between DOCK11 and other host genes were identified by super-resolution microscopy, immunoblotting, and chromatin immunoprecipitation. FISH facilitated the subcellular localization of key HBV nucleic acids. Interestingly, although DOCK11 partially colocalized with histone proteins, such as H3K4me3 and H3K27me3, and nonhistone proteins, such as RNA Pol II, it played limited roles in histone modification and RNA transcription. DOCK11 was functionally involved in regulating the subnuclear distribution of host factors and/or cccDNA, resulting in an increase in cccDNA closely located to H3K4me3 and RNA Pol II for activating cccDNA transcription. Thus, it was suggested that the association of cccDNA-bound Pol II and H3K4me3 required the assistance of DOCK11. DOCK11 facilitated the association of cccDNA with H3K4me3 and RNA Pol II.
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Yu, Hai-Bo, Sheng-Tao Cheng, Fang Ren, Yong Chen, Xiao-Feng Shi, Vincent Kam Wai Wong, Betty Yuen Kwan Law, et al. "SIRT7 restricts HBV transcription and replication through catalyzing desuccinylation of histone H3 associated with cccDNA minichromosome." Clinical Science 135, no. 12 (June 2021): 1505–22. http://dx.doi.org/10.1042/cs20210392.

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Abstract Chronic hepatitis B virus (HBV) infection is a significant public health burden worldwide. HBV covalently closed circular DNA (cccDNA) organized as a minichromosome in nucleus is responsible for viral persistence and is the key obstacle for a cure of chronic hepatitis B (CHB). Recent studies suggest cccDNA transcription is epigenetically regulated by histone modifications, especially histone acetylation and methylation. In the present study, we identified transcriptionally active histone succinylation (H3K122succ) as a new histone modification on cccDNA minichromosome by using cccDNA ChIP-Seq approach. Silent mating type information regulation 2 homolog 7 (SIRT7), as an NAD+-dependent histone desuccinylase, could bind to cccDNA through interaction with HBV core protein where it catalyzed histone 3 lysine 122 (H3K122) desuccinylation. Moreover, SIRT7 acts cooperatively with histone methyltransferase, suppressor of variegation 3–9 homolog 1 (SUV39H1) and SET domain containing 2 (SETD2) to induce silencing of HBV transcription through modulation of chromatin structure. Our data improved the understanding of histone modifications of the cccDNA minichromosome, thus transcriptional silencing of cccDNA may represent a novel antiviral strategy for the prevention or treatment of HBV infection.
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Marchetti, Alexander L., and Haitao Guo. "New Insights on Molecular Mechanism of Hepatitis B Virus Covalently Closed Circular DNA Formation." Cells 9, no. 11 (November 6, 2020): 2430. http://dx.doi.org/10.3390/cells9112430.

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The chronic factor of the Hepatitis B Virus (HBV), specifically the covalently closed circular DNA (cccDNA), is a highly stable and active viral episomal genome established in the livers of chronic hepatitis B patients as a constant source of disease. Being able to target and eliminate cccDNA is the end goal for a genuine cure for HBV. Yet how HBV cccDNA is formed from the viral genomic relaxed circular DNA (rcDNA) and by what host factors had been long-standing research questions. It is generally acknowledged that HBV hijacks cellular functions to turn the open circular DNA conformation of rcDNA into cccDNA through DNA repair mechanisms. With great efforts from the HBV research community, there have been several recent leaps in our understanding of cccDNA formation. It is our goal in this review to analyze the recent reports showing evidence of cellular factor’s involvement in the molecular pathway of cccDNA biosynthesis.
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Dissertations / Theses on the topic "CCCDCC"

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Mouzannar, Karim. "Identification du récepteur nucléaire des acides biliaires FXR alpha comme facteur proviral pour le virus de l’hépatite B." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1098/document.

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L'infection par le virus de l'hépatite B (VHB) est un problème de santé publique majeur avec plus de 257 millions de porteurs chroniques dans le monde ayant un risque important de développer une cirrhose et/ou un hépatocarcinome. L'histoire naturelle de l'infection est très différente selon l'âge auquel l'infection est contractée. Alors que chez l'adulte l'infection est spontanément résolutive dans la majorité des cas, la contamination materno-infantile ou en bas âge aboutit le plus souvent à une infection chronique. Le cccDNA est la forme de persistance du génome viral dans les hépatocytes infectés et la base de transcription de tous les ARN viraux. La protéine virale HBx joue un rôle crucial dans le recrutement des facteurs épigénétiques sur le cccDNA et favorise son activité transcriptionnelle. Les traitements actuels à base d'interféron et d'analogues nucléos(t)idiques ne permettent pas l'éradication du cccDNA et leur interruption est presque toujours suivie d'une réactivation de la réplication du virus. De nouvelles molécules thérapeutiques ciblant le cccDNA sont donc nécessaires pour espérer obtenir une cure fonctionnelle chez les patients chroniquement infectés. Il existe des liens étroits entre l'infection par le VHB et le métabolisme des acides biliaires (AB). Ainsi, notre équipe a précédemment montré que le récepteur nucléaire des acides biliaires, le farnesoid X receptor alpha (FXRalpha) se fixe sur deux éléments de réponse présents dans la région Enhancer II - promoteur de Core du génome viral et module son activité transcriptionnelle. De plus, le VHB et les AB entrent en compétition pour le même récepteur d'entrée hépatocytaire NTCP, modifiant la concentration cellulaire des AB avec des conséquences sur la fonction et l'expression de FXRalpha. Enfin, HBx interagit avec FXRalphaet modifie son activité. Au cours de cette thèse nous avons dans un premier temps identifié une régulation réciproque existante entre la réplication du VHB et FXRalpha. Puis nous avons montré in vitro, dans des cellules HepaRG différenciées et des hépatocytes primaires humains, que FXRalphaest un facteur proviral pour le VHB et que les agonistes de FXRalpha inhibent l'expression de l'ensemble des marqueurs viraux de manière dépendante ou indépendante de la protéine virale HBx. Enfin, dans un modèle in vivo de souris C3H/HeN transduites par un vecteur recombinant AAV2/8-VHB, nous avons obtenu l'effet inhibiteur des agonistes de FXRalphamais uniquement chez les souris adultes et pas chez les souris jeunes. Compte tenu de l'évolution de la flore intestinale avec l'âge et de son importance dans le métabolisme des AB, ces résultats suggèrent que le fort taux d'évolution chronique chez les jeunes enfants pourrait être lié à l'immaturité du métabolisme des AB. La mise en évidence d'un lien entre microbiote, métabolisme des AB et infection par le VHB contribuerait grandement à une meilleure compréhension de l'histoire naturelle de cette infection. De plus, l'identification de FXRalphacomme un facteur de l'hôte favorisant l'infection et l'existence de molécules capables de moduler l'activité de FXRalphasuggèrent que FXRalphapourrait constituer une cible thérapeutique intéressante ciblant le cccDNA et permettant d'améliorer le traitement des patients infectés par le VHB
Hepatitis B virus (HBV) infection is a major global health problem with more than 257 million chronic carriers worldwide that remain at significant risk for developing cirrhosis and/or hepatocellular carcinoma. The natural history of infection is very different depending on the age at which the infection is contracted. Whereas in adults most HBV infections spontaneously resolve, in infants and young children they usually result in chronic infection. cccDNA is the molecular form of viral persistence in infected hepatocytes and serves as a transcription template for all viral RNAs. The viral protein HBx plays a crucial role in the recruitment of epigenetic factors to the cccDNA and promotes its transcriptional activity. Currently, interferon and nucleot(s)ide analogues are the first-line agents in the treatment of chronic hepatitis B without allowing eradication of cccDNA and their interruption are almost always followed by a reactivation of the replication of the virus. New therapeutic molecules targeting cccDNA are therefore needed to hope for a functional cure in chronically infected patients. HBV infection and bile acid (BA) metabolism are tightly linked. Therefore, our team has previously shown that the bile acid nuclear receptor, the farnesoid X receptor alpha (FXRalpha) bind to two response elements present in the Enhancer II - Core promoter region of HBV genome and modulate its transcriptional activity. Moreover, HBV and BA compete for the same entry receptor of hepatocytes NTCP and modify BA cell concentration with consequences on the function and expression of FXRalpha. Finally, HBx interacts with FXRalpha and modify its activity. During my PhD. we have first identified a reciprocal regulation between HBV replication and FXRalpha. Second, we have showed in vitro, in HepaRG differentiated cells and in primary human hepatocytes, that FXRalpha is a proviral factor for HBV and that FXRalpha agonists inhibit the expression of all HBV markers in a dependent or independent manner of the viral protein HBx. Finally, in an in vivo model of C3H/HeN mice transduced with a recombinant AAV2/8-HBV vector, we obtained the inhibitory effect of FXRalpha agonists but only in adult and not in young mice. Considering the evolution of the gut flora with age and its importance in the metabolism of BA, these results suggest that the high rate of chronic progression in young children might be related to the immaturity of BA metabolism. The identification of a link between BA metabolism, gut microbiome composition and evolution of HBV infection will represent a big step toward the understanding of HBV natural history. Moreover, the identification of FXRalpha as a proviral factor for HBV and the capacity of FXRalpha ligands to modulate the transcriptional activity of cccDNA suggest that FXR ligands might represent a new class of molecules with the aim to obtain functional cure for HBV infected patients
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竹内, 文彦. "レンチウイルスを用いたＢ型肝炎cccDNA阻害剤の探索." Kyoto University, 2019. http://hdl.handle.net/2433/242927.

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Ofor, Okezie O. "Characterisation of novel protein partners of the CCCTC-binding factor in breast cancer cell lines." Thesis, Anglia Ruskin University, 2015. http://arro.anglia.ac.uk/701472/.

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CTCF is an evolutionally conserved 11-zinc finger protein. It controls multiple cellular functions and is itself partly regulated via poly (ADP-ribosyl)ation (PARylation). Recent evidence suggested that the hypo PARylated isoform was exclusively expressed in breast tumours and low expression levels was associated with worse prognostic features. It also possessed proliferative activity. The exact mechanism by which CTCF exerted its effects in breast cancer is not known. In order to define the interaction between CTCF and proliferation markers, Ki67 and PCNA, colocalisation studies were performed in a panel of five breast cancer cell lines which possessed different hormone receptor / invasive phenotypes. Following co-localisation, co-immunoprecipitation assays and mass spectrometry were carried out to determine whether CTCF was physically bound to either Ki67 or PCNA. To determine whether CTCF directly regulated ERα activity, CTCF plasmid overexpression and siRNA knockdown assays were performed in the hormone receptor positive MCF7 breast cancer cell line. Changes in endogenous expression of ERα were monitored by quantitative polymerase chain reaction (QPCR). CTCF, Ki67 and PCNA were all found to be strongly expressed in breast cancer cell lines though the strength of this expression for CTCF and Ki67 was antibody dependent. CTCF and Ki67 were shown to colocalise in the nucleoli of all breast cancer cell lines while CTCF and PCNA demonstrated nucleolar colocalisation only in the weakly invasive, hormone receptor positive cell lines. Despite colocalisation, there was no physical interaction detected between CTCF and Ki67 / PCNA on coimmunoprecipitation and mass spectrometry in all the cell lines studied suggesting that the proteins did not exist as a functional complex. Three novel CTCF - interacting protein partners (general transcriptional factor 2, glucose regulated protein 78 and the huntingtin interacting protein-1 related) were however discovered. These new protein partners, known to function at least in part via epidermal growth factor receptor (EGFR) signalling in cancer formation, were discovered only in ER positive breast cancer cell lines. Further investigation did not detect a direct regulatory effect of CTCF on ERα expression suggesting that the effect of CTCF on EGFR signalling in breast cancer cell lines did not involve an indirect action on ERα expression.
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Ofor, Okezie O. "Characterisation of novel protein partners of the CCCTC-binding factor in breast cancer cell lines." Thesis, Anglia Ruskin University, 2015. https://arro.anglia.ac.uk/id/eprint/701472/1/Ofor_2015.pdf.

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CTCF is an evolutionally conserved 11-zinc finger protein. It controls multiple cellular functions and is itself partly regulated via poly (ADP-ribosyl)ation (PARylation). Recent evidence suggested that the hypo PARylated isoform was exclusively expressed in breast tumours and low expression levels was associated with worse prognostic features. It also possessed proliferative activity. The exact mechanism by which CTCF exerted its effects in breast cancer is not known. In order to define the interaction between CTCF and proliferation markers, Ki67 and PCNA, colocalisation studies were performed in a panel of five breast cancer cell lines which possessed different hormone receptor / invasive phenotypes. Following co-localisation, co-immunoprecipitation assays and mass spectrometry were carried out to determine whether CTCF was physically bound to either Ki67 or PCNA. To determine whether CTCF directly regulated ERα activity, CTCF plasmid overexpression and siRNA knockdown assays were performed in the hormone receptor positive MCF7 breast cancer cell line. Changes in endogenous expression of ERα were monitored by quantitative polymerase chain reaction (QPCR). CTCF, Ki67 and PCNA were all found to be strongly expressed in breast cancer cell lines though the strength of this expression for CTCF and Ki67 was antibody dependent. CTCF and Ki67 were shown to colocalise in the nucleoli of all breast cancer cell lines while CTCF and PCNA demonstrated nucleolar colocalisation only in the weakly invasive, hormone receptor positive cell lines. Despite colocalisation, there was no physical interaction detected between CTCF and Ki67 / PCNA on coimmunoprecipitation and mass spectrometry in all the cell lines studied suggesting that the proteins did not exist as a functional complex. Three novel CTCF - interacting protein partners (general transcriptional factor 2, glucose regulated protein 78 and the huntingtin interacting protein-1 related) were however discovered. These new protein partners, known to function at least in part via epidermal growth factor receptor (EGFR) signalling in cancer formation, were discovered only in ER positive breast cancer cell lines. Further investigation did not detect a direct regulatory effect of CTCF on ERα expression suggesting that the effect of CTCF on EGFR signalling in breast cancer cell lines did not involve an indirect action on ERα expression.
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Broja, Tim [Verfasser], and Jörg [Akademischer Betreuer] Petersen. "Untersuchungen der replikativen Aktivität der cccDNA in vivo in ruhenden und proliferierenden Hepatozyten mithilfe des uPA Mausmodelles / Tim Broja. Betreuer: Jörg Petersen." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2012. http://d-nb.info/1023947382/34.

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LENCI, ILARIA. "New strategies on management of hepatitis b virus after liver transplantation: complete and sustained weaning of hbv prophylaxis in a selected cohort of patients transplanted due to hbv-related cirrhosis." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/208923.

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Introduzione: la riattivazione del virus HBV dopo trapianto di fegato è legata alla persistenza del virus sotto forma di DNA covalente chiuso circolare (cccDNA). Abbiamo dunque esaminato la sicurezza della sospensione completa della profilassi anti-HBV in una coorte di pazienti trapiantati negativi per cccDNA intraepatico. Metodi: 30 pazienti HBsAg positivi, HBeAg e HBV-DNA negativi al momento del trapianto, con cccDNA e HBV-DNA intraepatico negativi hanno sospeso le immunoglobuline anti-HBs, continuando la lamivudina, con controlli clinici mensili. Dopo 6 mesi, tutti i pazienti sono stati sottoposti ad una seconda biopsia epatica: solo i pazienti nuovamente negativi per cccDNA e HBV-DNA intraepatico hanno sospeso anche la lamivudina e sono stati seguiti per ulteriori 6 mesi, prima di sottoporsi a nuova biopsia. I pazienti negativi per tutti i marcatori virologici e sierologici di infezione da HBV, su siero e tessuto epatico, sono stati seguiti per un periodo complessivo di 2 anni. Risultati: 25 pazienti sono risultati negativi per cccDNA e HBV-DNA intraepatico in tutte le biopsie epatiche eseguite durante lo studio, in assenza di alcun segno di riattivazione di HBV dopo un follow-up mediano di 25.2 mesi. Cinque pazienti sono diventati HBsAg positivi, 1 dopo la sospensione delle immunoglobuline, 4 dopo la sospensione della lamivudina. Nessuno di questi 5 pazienti ha mostrato eventi clinici rilevanti. Nel primo pazienti, le immunoglobuline sono state prontamente reintrodotte e il paziente è tornato ad essere HBsAg negativo. Degli altri 4 pazienti, solo 1 è rimasto HBsAg positivo, HBV-DNA positivo, con transaminasi moderatamente levate, per cui ha iniziato tenofovir. Gli altri 3 pazienti hanno mostrato invece un HBsAg positività transitoria, seguita in realtà dalla comparsa di un titolo spontaneo anti-HBs, in assenza di alcun trattamento antivirale. Conclusioni: i pazienti con HBV-DNA negativo al momento del trapianto, risultati cccDNA e HBV-DNA negativi su tessuto epatico, possono cautelativamente sospendere la profilassi anti-HBV. Solo una minoranza di questi in realtà ha mostrato ripositivizzazione dell’HBsAg, in assenza di eventi clinicamente rilevanti, andando incontro alcuni a spontaneo sviluppo di anticorpi anti-HBs.
Background and Aim: HBV reactivation after liver transplantation is due to the persistence of covalently closed circular (ccc) DNA. We investigated the safety of HBV prophylaxis withdrawal in transplanted patients negative for intrahepatic total and ccc-DNA. Methods: thirty HBsAg-positive, HBeAg and HBV-DNA-negative patients at transplant, with undetectable intrahepatic total and ccc-DNA underwent HBIG withdrawal and were continued on lamivudine with monthly monitoring. After 6 months, a second liver biopsy was obtained: patients with confirmed total and ccc-DNA negativity also underwent lamivudine withdrawal and were monitored for additional 6 months, when a third biopsy was obtained. Patients negative for all virological assays were followed-up without prophylaxis for up to 2 years. Results: Twenty-five patients had undetectable total and ccc-DNA in all sequential biopsies and did not exhibit HBV reinfection after a median follow-up of 25.2 months following lamivudine withdrawal. Five patients became HBsAg-positive: one early, after HBIG withdrawal,the other 4 after lamivudine withdrawal. None of these had clinically relevant events. In the first patient HBIG were reinstituted with prompt HBsAg negativization. Of the other 4, only one remained HBsAg-positive with detectable HBV-DNA and mild ALT elevation, and was given tenofovir. In the remaining 3, HBsAg positivity was transient and followed by anti-HBs seroconversion. No antiviral treatment was given to these patients. Conclusions: Patients with undetectable HBV viremia at transplant and undetectable intrahepatic total and cccDNA may undergo cautious weaning of prophylaxis. A minority of them experience transient HBsAg positivization, without clinical or virological events, and some undergo spontaneous anti-HBs seroconversion.
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Fournier, Maëlenn. "Implication du gène core dans l'accumulation de l'ADN circulaire clos de façon covalente du virus de l'hépatite B." Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10058/document.

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La particularité de ce virus de l'hépatite B est la synthèse d'un ADN circulaire clos covalent (ADNccc) qui est la forme de persistance du virus dans la cellule. Cet ADN est maintenu à une copie par cellule en moyenne chez l'homme grâce à un recyclage des nucléocapsides dans le noyau. En effet, durant le cycle viral, les nucléocapsides sont soit redirigées dans le noyau pour former de l'ADNccc, soit enveloppées puis sécrétées pour former de nouveaux virions. Du fait de son maintien au sein de l'hépatocyte, la formation et la régulation de l'ADNccc restent des éléments clés du traitement antiviral. Il a été montré in vitro que l'accumulation de cet ADN était régulée par les protéines d'enveloppe. Lors de l'étude du taux d'ADNccc dans des biopsies de foie de patients coinfectés HIV-HBV chronique, il a été découvert un patient présentant 300 fois plus d'ADNccc intrahépatique que la moyenne de la cohorte. L'objectif de ma thèse a été de comprendre quel était le mécanisme conduisant à cette accumulation d'ADNccc in vivo. Cela nous a permis de mettre en évidence le rôle du gène core dans l'accumulation de l'ADNccc
The feature of hepatitis B virus is the synthesis of a covalently closed circular DNA (cccDNA) which is the persistence form of the virus in cell. cccDNA is maintained to 1 copy per human cell thanks to the recycling of capsids into the nucleus. Indeed, during the viral cycle, capsids are either transported into the nucleus to form cccDNA or enveloped and secreted to form new infectious virions. Because of its maintenance in the hepatocyte, cccDNA formation and regulation are still key elements of antiviral treatment. It has been shown that, in vitro, cccDNA accumulation was regulated by envelope proteins. Upon the study of cccDNA levels in liver biopsies of HIV-HBV co-infected patients, an individual with a cccDNA level 300 fold higher than the average of the cohort was identified. My thesis objective was to understand which is the mechanism leading to the cccDNA accumulation observed in vivo. This allowed us to highlight the role of core gene in cccDNA accumulation
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Lee, Rory Amundson. "Addressing the situation an analysis of the CCCC Chairs' Addresses of the last 11 Years (1998-2008) /." Tallahassee, Florida : Florida State University, 2009. http://etd.lib.fsu.edu/theses/available/etd-07132009-125559/.

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Thesis (M.A.)--Florida State University, 2009.
Advisor: Kathleen Yancey, Florida State University, College of Arts and Sciences, Dept. of Englsih. Title and description from dissertation home page (viewed on Oct. 28, 2009). Document formatted into pages; contains viii, 100 pages. Includes bibliographical references.
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Ren, Shaotang. "Hepatitis B virion and cccDNA formation in primary tupaia hepatocytes and human hepatoma cell lines upon HBV genome transduction with replication defective adenovirus vectors and in vivo infection of tupaias." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=961156007.

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Locatelli, Maëlle. "The histone chaperone HIRA is crucial for the early establishment of hepatitis B virus minichromosome." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1169/document.

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Le virus de l'hépatite B (HBV) infecte de manière chronique 240 millions de personnes dans le monde, et est la principale cause de carcinome hépatocellulaire. Actuellement, les traitements standards permettent une suppression virale à long terme, mais ne sont pas capables d'éliminer complètement le virus, en raison de la persistance de l'ADN circulaire et clos de façon covalente (ADNccc). Ce minichromosome viral réside dans le noyau des hépatocytes infectés, grâce à sa structure chromatinienne. En effet, lors de l'infection d'un hépatocyte, l'ADN viral partiellement double brin (ADN relâché circulaire (rc)) est libéré dans le noyau, où il est réparé et enveloppé par des protéines histones, afin de former une structure d'épisome chromatinisé. Les mécanismes conduisant à la formation ainsi qu'à la chromatinisation de l'ADNccc sont encore largement inconnus, et leur élucidation constituerait une première étape vers l'identification de nouvelles cibles thérapeutiques, susceptibles d'altérer la persistance de l'ADNccc. Dans ce but, nous avons étudié le rôle des facteurs hôtes de réparation de l'ADN, et des voies d'assemblage des nucléosomes, dans la formation de l'ADNccc, à des stades précoces (entre 30 minutes et 72 heures) de l'infection, dans des lignées cellulaires d'HepG2-NTCP, ainsi que dans des hépatocytes primaires humains. Nous nous sommes particulièrement concentrés sur la protéine chaperone d'histones, HIRA, qui est connue pour déposer le variant d'histone 3.3 (H3.3) sur l'ADN cellulaire d'une manière indépendante de la réplication et en association avec le remaniement des nucléosomes pendant la transcription et la réparation de l'ADN. Nous avons été capables de détecter l'ADNccc dans la fraction nucléaire des hépatocytes dès 30 minutes et 24 heures post-infection, par qPCR et Southern Blotting (SB), respectivement. L'extinction de HIRA par ARN interférent (siARN) avant l'inoculation du virus, a conduit à une forte diminution de l'accumulation de l'ADNccc (à la fois par qPCR et Southern Blot), qui était indépendante de la protéine HBx (en utilisant un virus HBx-défectueux). Les niveaux d'ADNrc sont restés stables, indiquant soit une éventuelle transition de l'ADNrc en ADNccc incomplète, ou retardée. L'analyse par immunoprécipitation de la chromatine a montré que HIRA était liée à l'ADNccc dès 30 minutes après infection, et que son recrutement était concomitant avec le dépôt de l'histone H3.3, ainsi que la liaison de la protéine de capside du HBV (HBc). Après 24 heures d'infection, une augmentation de la liaison de H3.3 et de l'ARN polymérase II sur l'ADNccc a été observée, en corrélation avec l'initiation de la transcription de l'ARN viral de 3.5 kb. Par des expériences de co-immunoprécipitation et de test de proximité entre protéines (PLA), nous avons montré que HIRA était capable d'interagir avec HBc dans des hépatocytes infectés et dans une lignée cellulaire HepaRG exprimant HBc de manière inductible. En conclusion, nos résultats suggèrent que la chromatinisation de l'ADN viral entrant est un événement très précoce, nécessitant l'histone chaperone HIRA. Bien que HBx ne soit pas requis pour ce processus, HBc pourrait jouer un rôle majeur, suggérant que l'interaction entre HIRA et HBc pourrait représenter une nouvelle cible thérapeutique à étudier
Hepatitis B virus (HBV) chronically infects 240 million people worldwide and is the major cause of hepatocellular carcinoma (HCC). Currently standard-of-care treatments can achieve longterm viral suppression, but are not able to completely eliminate the virus, due to the persistence of the covalently closed circular DNA (cccDNA). cccDNA, the viral minichromosome, resides in the nucleus of infected hepatocytes by virtue of its chromatin structure. Indeed, upon entry into hepatocytes, the partially double stranded viral DNA (relaxed circular (rc)DNA) is released into the nucleus, where it is repaired and wrapped by histones to form an episomal chromatinized structure. The mechanisms leading to cccDNA formation and chromatinization are still largely unknown and their elucidation would be a first step toward the identification of new therapeutic targets to impair cccDNA persistence. To this aim, we investigated the role of host factors belonging to DNA repair and nucleosome assembly pathways in cccDNA formation at early time points (i.e. between 30 minutes and 72 hours) post-infection in both HepG2-NTCP cell line and Primary Human Hepatocytes (PHH). We particularly focused on the histone chaperone Hira, which is known to deposit histone variant 3.3 (H3.3) onto cellular DNA in a replication-independent manner and in association to nucleosome reshuffling during transcription and DNA repair. We were able to detect cccDNA in the nuclear fraction of hepatocytes as early as 30 minutes and 24h post-infection, by qPCR and Southern Blotting (SB), respectively. Knock-down of Hira by RNA interference before virus inoculation led to a strong decrease in cccDNA accumulation (both in qPCR and SB) which was independent from HBx protein expression (using an HBx defective virus). rcDNA levels remained stable, indicating either a possible incomplete or delayed rcDNA to cccDNA transition. Chromatin Immunoprecipitation analysis showed that Hira was bound to cccDNA already at 2 hours post-infection and that its recruitment was concomitant with the deposition of histone H3.3 and the binding of HBV capsid protein (HBc). After 24 hours of infection, an increase of H3.3 and Pol2 binding on cccDNA was observed, correlating with the initiation of the transcription of the 3.5 kb RNA. By Co-Immunoprecipitation and Proximity Ligation Assay experiments, we showed that Hira was able to interact with HBc in infected hepatocytes and in a HepaRG cell line expressing HBc in an inducible manner. Altogether, our results suggest that chromatinization of incoming viral DNA is a very early event, requiring the histone chaperone Hira. While HBx is not required for this process, HBc could play a major role, suggesting that the interaction between Hira and HBc could represent a new therapeutic target to be investigated
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Books on the topic "CCCDCC"

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Maria, Guerrieri Anna, ed. Ewangelium De uirginibus in CCCC 303. Napoli: Istituto Universitario Orientale, 1988.

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Conference on College Composition and Communication (U.S.), ed. CCCC bibliography of composition and rhetoric. Carbondale, IL: Southern Illinois University Press, 1990.

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Brown, Wendell S. A study of the CCCCS pressure field and its relation to circulation. [California]: U.S. Dept. of the Interior, Minerals Management Service, 1990.

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Moteetee, M. M. ACSI-CCCD project in Lesotho: 1989 management information systems report. [Maseru?]: African Child Survival Initiative, Combatting Childhood Communicable Diseases, 1990.

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H, Roen Duane, ed. Views from the center: The CCCC chairs' addresses 1977-2005. Boston: Bedford/St.Martin's, 2006.

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R, Sims Brenda, Conference on College Composition and Communication (U.S.). Committee on Technical Communication., and National Council of Teachers of English. Committee on Technical Communication., eds. Studies in technical communication: Proceedings of the 1990 CCCC and NCTE meetings ; Brenda R. Sims, editor ; sponsored by CCCC and NCTE Committees on Technical Communication. [Denton, Tex.]: University of North Texas Press, 1990.

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cccccc. 7800, 1990.

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Cccc. Independently Published, 2021.

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Tauchnitz, Bernhard Freiherr Von. Five Centuries of the English Language and Literature: Volume CCCCC of the Tauchnitz Ed. Creative Media Partners, LLC, 2021.

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Chapleau, Wilfred. Casualty Care for Civil Disturbances (CCCD). International PreHospital Medicine Institute, 2022.

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Book chapters on the topic "CCCDCC"

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Cavinato, Joseph L. "CCCC." In Supply Chain and Transportation Dictionary, 49–84. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4591-0_3.

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Klenova, Elena, Dmitri Loukinov, and Victor Lobanenkov. "CCCTC-Binding Factor." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_902-2.

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Klenova, Elena, Dmitri Loukinov, and Victor Lobanenkov. "CCCTC-Binding Factor." In Encyclopedia of Cancer, 837–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_902.

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Xia, Yuchen, Daniela Stadler, Chunkyu Ko, and Ulrike Protzer. "Analyses of HBV cccDNA Quantification and Modification." In Methods in Molecular Biology, 59–72. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6700-1_6.

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Vishal, Ramola, Mishra Saurabh, Singh R.K., and Chauhan D.S. "CCCDBA Based Implementation of Voltage Mode ThirdOrder Filters." In Lecture Notes of the Institute for Computer Sciences, Social Informatics and Telecommunications Engineering, 185–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-35615-5_27.

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Hailfinger, Carl-Daniel, Kerstin Lemke-Rust, and Christof Paar. "CCCiCC: A Cross-Core Cache-Independent Covert Channel on AMD Family 15h CPUs." In Smart Card Research and Advanced Applications, 159–75. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-42068-0_10.

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Vishal, Ramola, Mishra Saurabh, Singh R.K., and Chauhan D.S. "CCCDBA Based Implementation of Sixth Order Band Pass Filter." In Lecture Notes of the Institute for Computer Sciences, Social Informatics and Telecommunications Engineering, 217–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-35615-5_31.

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Bartholomae, David. "Freshman English, Composition, and CCCC." In Writing on the Margins, 299–311. New York: Palgrave Macmillan US, 2005. http://dx.doi.org/10.1007/978-1-4039-8439-5_19.

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Sharma, Jyoti, Ritambhara, and Avireni Srinivasulu. "A Novel CNFET-Based CCCDTA and Its Application as a Schmitt Trigger." In Advances in Smart Grid Automation and Industry 4.0, 93–101. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-7675-1_9.

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Bloom, Kristie, Abdullah Ely, and Patrick Arbuthnot. "A T7 Endonuclease I Assay to Detect Talen-Mediated Targeted Mutation of HBV cccDNA." In Methods in Molecular Biology, 85–95. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6700-1_8.

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Conference papers on the topic "CCCDCC"

1

Sen Li, Jinguang Jiang, Xifeng Zhou, and Zeyu Zhang. "A novel current-mode versatile filter employing CCCDCC and MO-OTA." In 2013 IEEE 10th International Conference on ASIC (ASICON 2013). IEEE, 2013. http://dx.doi.org/10.1109/asicon.2013.6812026.

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Prasad, Sagar Surendra, Sadaf Tasneem, Bindu Priyadarshini, and Rajeev Kumar Ranjan. "Electronic Tunable Bi-Quad Filter Using MO-CCCDTA." In 2021 Fourth International Conference on Electrical, Computer and Communication Technologies (ICECCT). IEEE, 2021. http://dx.doi.org/10.1109/icecct52121.2021.9616870.

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Singh, Damyanti, and Neeta Pandey. "Realization of Single CCCDTA based incremental/decremental type Memconductance Emulator." In 2019 International Symposium on Advanced Electrical and Communication Technologies (ISAECT). IEEE, 2019. http://dx.doi.org/10.1109/isaect47714.2019.9069680.

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Lamun, Panit, Pattarapong Phasukkit, Montree Kumngern, and Kobchai Dejhan. "A new mixed-mode quadrature oscillator using a single CCCDTA." In 2011 8th International Conference on Electrical Engineering/Electronics, Computer, Telecommunications and Information Technology (ECTI-CON 2011). IEEE, 2011. http://dx.doi.org/10.1109/ecticon.2011.5947791.

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Calaminus, Moritz, Katja Giersch, Tassilo Volz, Andrea Pirosu, Marc Lütgehetmann, Maura Dandri, and Lena Allweiss. "Therapeutic shutdown of HBV transcripts promotes reappearance of the SMC5/6 complex and cccDNA silencing in vivo without affecting posttranslational modifications of cccDNA-bound histones." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740816.

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Jaikla, Winai, and Montree Siripruchyanan. "Current Controlled CDTA (CCCDTA) Based- Novel Floating and Grounded Inductance Simulators." In 2006 International Symposium on Communications and Information Technologies. IEEE, 2006. http://dx.doi.org/10.1109/iscit.2006.340062.

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Karnjanakrajang, Ekkarat, Roungsan Chaisricharoen, and Boonruk Chipipop. "All differential-pair CMOS current-controlled current differencing transconductance amplifier (CCCDTA)." In 2010 International Symposium on Intelligent Signal Processing and Communications Systems (ISPACS 2010). IEEE, 2010. http://dx.doi.org/10.1109/ispacs.2010.5771617.

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Lahiri, Abhirup, Abhinav Misra, and Kinshuk Gupta. "Novel current-mode quadrature oscillators with explicit-current-outputs using CCCDTA." In 2009 19th International Conference Radioelektronika (RADIOELEKTRONIKA). IEEE, 2009. http://dx.doi.org/10.1109/radioelek.2009.5158722.

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Kumngern, Montree. "New current-mode first-order allpass filter using a single CCCDTA." In 2011 International Symposium on Integrated Circuits (ISIC). IEEE, 2011. http://dx.doi.org/10.1109/isicir.2011.6131972.

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Krutz, Daniel E., and Emad Shihab. "CCCD: Concolic code clone detection." In 2013 20th Working Conference on Reverse Engineering (WCRE). IEEE, 2013. http://dx.doi.org/10.1109/wcre.2013.6671332.

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Reports on the topic "CCCDCC"

1

Lee, Jin-Hee. Epigenetic Alterations Associated with CCCTC-Binding Factor Deregulation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada568608.

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Lee, Jin-Hee. Epigenetic Alterations Associated With CCCTC-Binding Factor Deregulation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada599572.

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Bhusari, Sachin. Epigenetic Alterations Associated With CCCTC-Binding Factor Deregulation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada549128.

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