Gotowe bibliografie tematyczne / CpG Islands

Gotowa bibliografia na temat „CpG Islands”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "CpG Islands"

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Weitzman, Jonathan B. "CpG islands". Genome Biology 3 (2002): spotlight—20020319–01. http://dx.doi.org/10.1186/gb-spotlight-20020319-01.

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Gebhard, Claudia, Mohammed Sadeh, Dagmar Glatz, Lucia Schwarzfischer, Rainer Spang, Gerhard Ehninger, Christian Thiede, Reinhard Andreesen i Michael Rehli. "Profiling of Aberrant DNA Methylation In AML Reveals Subclasses of CpG Islands with Epigenetic or Genetic Association". Blood 116, nr 21 (19.11.2010): 2498. http://dx.doi.org/10.1182/blood.v116.21.2498.2498.

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Abstract Abstract 2498 CpG islands show frequent and often disease-specific epigenetic alterations during malignant transformation, however, the underlying mechanisms are poorly understood. We used methyl-CpG immunoprecipitation (MCIp) to generate comparative DNA methylation profiles of 30 patients with acute myeloid leukemia for human CpG islands across the genome. DNA methylation profiles across 23.000 CpG islands revealed highly heterogeneous methylation patterns in AML with over 6000 CpG islands showing aberrant de novo methylation in AML. Based on these profiles we selected a subset of 380 CpG islands (covering 15.000 individual CpGs) for detailed fine-mapping analyses of aberrant DNA methylation in 185 patients with AML (50% normal karyotype). We found that a proportion of patients (5/185) displayed a concerted hypermethylation at almost all studied loci, representing the rare CpG island methylator phenotype (CIMP) in AML. Meta analysis of methylation profiling and published ChIP sequencing data separated CpG islands in two groups. A highly correlated subgroup of CpG island regions was strongly associated with histone H3 lysine 27 trimethylation in human hematopoietic progenitor cells, suggesting that disease-related de novo DNA methylation at these CpG islands is linked with polycomb group protein (PcG)-mediated repression. The group of mainly non-PcG target CpG islands showed heterogeneous methylation patterns across patients and unsupervised hierarchical clustering revealed a correlation of methylation profiles with genetic disease markers, including oncofusion proteins as well as CEBPA- and NPM1-mutations. Our study suggests that both epigenetic as well as genetic aberrations may underlay AML-related changes in CpG island DNA methylation states. Disclosures: No relevant conflicts of interest to declare.
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Bender, Christina M., Mark L. Gonzalgo, Felicidad A. Gonzales, Carvell T. Nguyen, Keith D. Robertson i Peter A. Jones. "Roles of Cell Division and Gene Transcription in the Methylation of CpG Islands". Molecular and Cellular Biology 19, nr 10 (1.10.1999): 6690–98. http://dx.doi.org/10.1128/mcb.19.10.6690.

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ABSTRACT De novo methylation of CpG islands within the promoters of eukaryotic genes is often associated with their transcriptional repression, yet the methylation of CpG islands located downstream of promoters does not block transcription. We investigated the kinetics of mRNA induction, demethylation, and remethylation of the p16promoter and second-exon CpG islands in T24 cells after 5-aza-2′-deoxycytidine (5-Aza-CdR) treatment to explore the relationship between CpG island methylation and gene transcription. The rates of remethylation of both CpG islands were associated with time but not with the rate of cell division, and remethylation of thep16 exon 2 CpG island occurred at a higher rate than that of the p16 promoter. We also examined the relationship between the remethylation of coding sequence CpG islands and gene transcription. The kinetics of remethylation of the p16exon 2, PAX-6 exon 5, c-ABL exon 11, andMYF-3 exon 3 loci were examined following 5-Aza-CdR treatment because these genes contain exonic CpG islands which are hypermethylated in T24 cells. Remethylation occurred most rapidly in the p16, PAX-6, and c-ABL genes, shown to be transcribed prior to drug treatment. These regions also exhibited higher levels of remethylation in single-cell clones and subclones derived from 5-Aza-CdR-treated T24 cells. Our data suggest that de novo methylation is not restricted to the S phase of the cell cycle and that transcription through CpG islands does not inhibit their remethylation.
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Du, Xin, Leng Han, An-Yuan Guo i Zhongming Zhao. "Features of Methylation and Gene Expression in the Promoter-Associated CpG Islands Using Human Methylome Data". Comparative and Functional Genomics 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/598987.

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CpG islands are typically located in the 5′end of genes and considered as gene markers because they play important roles in gene regulation via epigenetic change. In this study, we compared the features of CpG islands identified by several major algorithms by setting the parameter cutoff values in order to obtain a similar number of CpG islands in a genome. This approach allows us to systematically compare the methylation and gene expression patterns in the identified CpG islands. We found that Takai and Jones’ algorithm tends to identify longer CpG islands but with weaker CpG island features (e.g., lower GC content and lower ratio of the observed over expected CpGs) and higher methylation level. Conversely, the CpG clusters identified by Hackenberg et al.’s algorithm using stringent criteria are shorter and have stronger features and lower methylation level. In addition, we used the genome-wide base-resolution methylation profile in two cell lines to show that genes with a lower methylation level at the promoter-associated CpG islands tend to express in more tissues and have stronger expression. Our results validated that the DNA methylation of promoter-associated CpG islands suppresses gene expression at the genome level.
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Qu, Ying, Andreas Lennartsson, Verena I. Gaidzik, Stefan Deneberg, Sofia Bengtzén, Mohsen Karimi Arzenani, Lars Bullinger, Konstanze Döhner i Sören Lehmann. "Genome-Wide DNA Methylation Analysis Shows Enrichment of Differential Methylation in “Open Seas” and Enhancers and Reveals Hypomethylation in DNMT3A Mutated Cytogenetically Normal AML (CN-AML)". Blood 120, nr 21 (16.11.2012): 653. http://dx.doi.org/10.1182/blood.v120.21.653.653.

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Abstract Abstract 653 DNA methylation is involved in multiple biologic processes including normal cell differentiation and tumorigenesis. In AML, methylation patterns have been shown to differ significantly from normal hematopoietic cells. Most studies of DNA methylation in AML have previously focused on CpG islands within the promoter of genes, representing only a very small proportion of the DNA methylome. In this study, we performed genome-wide methylation analysis of 62 AML patients with CN-AML and CD34 positive cells from healthy controls by Illumina HumanMethylation450K Array covering 450.000 CpG sites in CpG islands as well as genomic regions far from CpG islands. Differentially methylated CpG sites (DMS) between CN-AML and normal hematopoietic cells were calculated and the most significant enrichment of DMS was found in regions more than 4kb from CpG Islands, in the so called open sea where hypomethylation was the dominant form of aberrant methylation. In contrast, CpG islands were not enriched for DMS and DMS in CpG islands were dominated by hypermethylation. DMS successively further away from CpG islands in CpG island shores (up to 2kb from CpG Island) and shelves (from 2kb to 4kb from Island) showed increasing degree of hypomethylation in AML cells. Among regions defined by their relation to gene structures, CpG dinucleotide located in theoretic enhancers were found to be the most enriched for DMS (Chi χ2<0.0001) with the majority of DMS showing decreased methylation compared to CD34 normal controls. To address the relation to gene expression, GEP (gene expression profiling) by microarray was carried out on 32 of the CN-AML patients. Totally, 339723 CpG sites covering 18879 genes were addressed on both platforms. CpG methylation in CpG islands showed the most pronounced anti-correlation (spearman ρ =-0.4145) with gene expression level, followed by CpG island shores (mean spearman rho for both sides' shore ρ=-0.2350). As transcription factors (TFs) have shown to be crucial for AML development, we especially studied differential methylation of an unbiased selection of 1638 TFs. The most enriched differential methylation between CN-AML and normal CD34 positive cells were found in TFs known to be involved in hematopoiesis and with Wilms tumor protein-1 (WT1), activator protein 1 (AP-1) and runt-related transcription factor 1 (RUNX1) being the most differentially methylated TFs. The differential methylation in WT 1 and RUNX1 was located in intragenic regions which were confirmed by pyro-sequencing. AML cases were characterized with respect to mutations in FLT3, NPM1, IDH1, IDH2 and DNMT3A. Correlation analysis between genome wide methylation patterns and mutational status showed statistically significant hypomethylation of CpG Island (p<0.0001) and to a lesser extent CpG island shores (p<0.001) and the presence of DNMT3A mutations. This links DNMT3A mutations for the first time to a hypomethylated phenotype. Further analyses correlating methylation patterns to other clinical data such as clinical outcome are ongoing. In conclusion, our study revealed that non-CpG island regions and in particular enhancers are the most aberrantly methylated genomic regions in AML and that WT 1 and RUNX1 are the most differentially methylated TFs. Furthermore, our data suggests a hypomethylated phenotype in DNMT3A mutated AML. Disclosures: No relevant conflicts of interest to declare.
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Kim, Ki-Bong. "CpG Islands Detector: a Window-based CpG Island Search Tool". Genomics & Informatics 8, nr 1 (31.03.2010): 58–61. http://dx.doi.org/10.5808/gi.2010.8.1.058.

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Macleod, Donald, Robin R. Ali i Adrian Bird. "An Alternative Promoter in the Mouse Major Histocompatibility Complex Class II I-Aβ Gene: Implications for the Origin of CpG Islands". Molecular and Cellular Biology 18, nr 8 (1.08.1998): 4433–43. http://dx.doi.org/10.1128/mcb.18.8.4433.

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ABSTRACT Nonmethylated CpG islands are generally located at the 5′ ends of genes, but a CpG island in the mouse major histocompatibility complex class II I-Aβ gene is remote from the promoter and covers exon 2. We have found that this CpG island includes a novel intronic promoter that is active in embryonic and germ cells. The resulting transcript potentially encodes a severely truncated protein which would lack the signal peptide and external β1 domains. The functional significance of the internal CpG island may be to facilitate gene conversion, thereby sustaining the high level of polymorphism seen at exon 2. Deletions of the I-Aβ CpG island promoter reduce transcription and frequently lead to methylation of the CpG island in a transgenic mouse assay. These and other results support the idea that all CpG islands arise at promoters that are active in early embryonic cells.
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Rizwana, R., i P. J. Hahn. "CpG methylation reduces genomic instability". Journal of Cell Science 112, nr 24 (15.12.1999): 4513–19. http://dx.doi.org/10.1242/jcs.112.24.4513.

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Hypomethylation of DNA in tumor cells is associated with genomic instability and has been suggested to be due to activation of mitotic recombination. We have studied the methylation patterns in two 650 kb double minute chromosomes present in two mouse tumor cell lines, resistant to methotrexate. Multiple copies of the double minute chromosomes amplifying the dihydrofolate reductase gene are present in both the cell lines. In one of the cell lines (Mut F), two unmethylated CpG islands in the double minute chromosomes are readily cleaved by methylation-sensitive rare-cutting restriction endonucleases. In the other cell line (Mut C), the cleavage sites in the double minute chromosomes are partially methylated and resistant to cleavage. The double minute chromosomes with the two unmethylated CpG islands undergo rapid dimerization, whereas the double minute chromosomes with the partially methylated CpG islands are unchanged in size for over a year in continuous culture. The partially methylated CpG islands can be demethylated by azacytidine treatment or naturally by extended time in culture, and become sensitive to cleavage with the rare-cutting restriction endonucleases. The Mut C double minute chromosomes, with the newly demethylated CpG islands, but not the double minute chromosomes with the partially methylated CpG islands, undergo deletions and dimerizations. These results suggest a role for CpG island methylation controlling mitotic recombination between and within large DNA molecules.
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Aoto, Saki, Mayu Fushimi, Kei Yura i Kohji Okamura. "Diversification of CpG-Island Promoters Revealed by Comparative Analysis Between Human and Rhesus Monkey Genomes". Mammalian Genome 31, nr 7-8 (9.07.2020): 240–51. http://dx.doi.org/10.1007/s00335-020-09844-2.

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Abstract While CpG dinucleotides are significantly reduced compared to other dinucleotides in mammalian genomes, they can congregate and form CpG islands, which localize around the 5ʹ regions of genes, where they function as promoters. CpG-island promoters are generally unmethylated and are often found in housekeeping genes. However, their nucleotide sequences and existence per se are not conserved between humans and mice, which may be due to evolutionary gain and loss of the regulatory regions. In this study, human and rhesus monkey genomes, with moderately conserved sequences, were compared at base resolution. Using transcription start site data, we first validated our methods’ ability to identify orthologous promoters and indicated a limitation using the 5ʹ end of curated gene models, such as NCBI RefSeq, as their transcription start sites. We found that, in addition to deamination mutations, insertions and deletions of bases, repeats, and long fragments contributed to the mutations of CpG dinucleotides. We also observed that the G + C contents tended to change in CpG-poor environments, while CpG content was altered in G + C-rich environments. While loss of CpG islands can be caused by gradual decreases in CpG sites, gain of these islands appear to require two distinct nucleotide altering steps. Taken together, our findings provide novel insights into the process of acquisition and diversification of CpG-island promoters in vertebrates.
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Mitchell, C. M., T. Zakar, S. D. Sykes, K. G. Pringle i E. R. Lumbers. "141. METHYLATION OF GENES OF THE RENIN ANGIOTENSIN SYSTEM (RAS) IN EARLY HUMAN AMNION". Reproduction, Fertility and Development 22, nr 9 (2010): 59. http://dx.doi.org/10.1071/srb10abs141.

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The renin angiotensin system (RAS) genes angiotensin converting enzyme (ACE), angiotensin II type 1 receptor (AGTR1) and prorenin receptor (ATP6AP2) have CpG islands at their promoters, so these genes may be regulated by CpG island methylation as may the expression of two proteases implicated in prorenin activation (cathepsin D {CTSD} and kallikrein 1 {KLK1}). We measured CpG island methylation of 3 RAS genes and of CTSD and KLK1 in amnion using the Methyl-Profiler assay (SA Biosciences), which discriminates methyl-CpG density between hypermethylated, intermediately methylated and unmethylated CpG islands. DNA from human amnion collected between 10–17.8 weeks gestation, at elective caesarean section and after labour at term was analysed. The bulk (>80%) of CpG islands in all genes examined except for KLK1 was unmethylated and without intermediate methylation throughout gestation, while the rest was hypermethylated. There was no change in methylation density with labour (Table 1). In early gestation KLK1 methylation was greater than ACE, AGTR1 and ATP6AP2 (P < 0.05). KLKI methylation shifted towards the unmethylated state after labour (P < 0.05). There were correlations between methylation of ACE, AGTR1 and ATP6AP2 (P < 0.02) but not between RAS genes and KLKI. This suggests that the 3 RAS genes in amnion are not controlled by CpG island methylation. It is likely, however, that KLK1 is silenced in early gestation amnion partially by CpG island methylation, which is reduced by term. Since Kallikrein 1 can activate prorenin, the methylation status of this gene may regulate RAS activity in amnion during gestation.
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Rozprawy doktorskie na temat "CpG Islands"

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Thomson, John Paterson. "Defining the protein complement of CpG islands". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/4885.

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In higher eukaryotes, the DNA base Cytosine can exist in a variety of modified forms when in the dinucleotide CpG. Although a methylated form tends to dominate within the genome, approximately 1% of all CpG dinucleotides are found unmodified at high densities spanning around 1Kb and tend to co-localise to the 5’ ends of around 60% of annotated gene promoters. These unique DNA sequences are known as CpG islands (CGIs) and their role within the genome to date is largely unknown. Methylation of CGIs in cancers however has been linked to silencing of associated genes implying a role in gene regulation. Furthermore these sites are also interesting as they remain specifically nonmodified within a genome rich in methylated CpG. We set out to better understand the roles for CGIs through the characterisation of any specific CGI binding proteins. Digestion of nuclei with methyl sensitive restriction enzymes facilitates the purification of CGI fragments. Subsequent immunohistochemistry on the CGI chromatin fragments along with ChIP-PCR over several CGIs revealed an enrichment of the “active” histone modifications including H3K4me3, a depletion of the “silencing” marks such as H3K27me3, as well as a group of CGI specific binding factors. These latter proteins contained a domain previously shown to bind to non-methylated CpG dinucleotides (the CXXC domain) and as such were ideal candidates for CGI specific factors, in particular a protein called Cfp1. Genome wide sequencing revealed a striking correlation between Cfp1 and H3K4me3 which were both seen at around 80% of islands. Furthermore, the presence of Cfp1/H3K4me3 at islands tended to have a negative correlation with the presence of chromatin rich in the silencing histone modification H3K27me3. Closer investigation of the Cfp1 protein reveals it to be a true non-methyl CGI binding factor in vivo and shRNA reduction of Cfp1 levels to around 10% of wild type resulted in a precipitous drop in H3K4me3 levels over CGIs without a dramatic reduction in global H3K4me3 levels. As Cfp1 has been shown to be part of the Set1 histone H3K4 methyltransferase complex responsible for this modification, this CXXC protein may be attracting this histone modifying complex and as such represents a method whereby the underlying DNA sequence (CpG) can drive the overlying epigenetic state. This study may go some way to understanding the functional significance of CGIs within the genome.
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Wachter, Elisabeth. "Influence of CpG islands on chromatin structure". Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9369.

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CpG islands (CGIs) are short GC rich sequences with a high frequency of CpGs that are associated with the active chromatin mark H3K4me3. Most occur at gene promoters and are often free of cytosine methylation. Recent work has begun to clarify the functional significance of CGIs with respect to chromatin structure and transcription. In particular, proteins associated with histone-modifying activities, such as Cfp1 and Kdm2a, bind specifically to non-methylated CGIs via their CxxC domains. For example, artificial promoterless CpG-rich sequences integrated at the 3’ UTR of genes recruit Cfp1 and generate novel peaks of H3K4me3 in mouse ES cells without apparent RNA polymerase recruitment. There is also evidence that G+C-rich DNA recruits H3K27me3, a gene silencing mark. In this thesis I am exploring the constraints on DNA sequence and genomic location that are required to impose both H3K4me3 and H3K27me3 at CGI sequences. Showing that the generation of novel peaks of H3K4me3 and H3K27me3 over a promoter-less CpG rich sequence in a gene desert region is independent of it’s location in the genome extends earlier findings. These findings suggest that shared features of the primary DNA sequence at CGIs directly influence chromatin modification. Thus CGIs are not passive footprints of other cellular mechanisms, but play an active role in setting up local chromatin structure. However, the relative contribution of CpG frequency versus G+C content remains unclear. Therefore a sequence was generated that contains low levels of CpGs, comparable to the bulk genome, but has a G+C content similar to that of CGIs (Low CpG / High G+C). When this sequence was inserted into a gene desert neither marks of H3K4me3 or H3K27me3 were formed, indicating the importance of CpGs. Surprisingly, the reverse sequence with a high CpG frequency similar to that of CGIs and a low G+C content similar to that of the bulk genome (High CpG / Low G+C) did not establish H3K4me3 or H3K27me3 either. However, it was found that this sequence becomes heavily methylated in contrast to CGI-like sequences that remained unmethylated when introduced into a gene desert. This finding suggests that a high G+C content is important for keeping CGI-like sequences methylation free. Upon insertion of this High CpG / Low G+C sequence into mouse ES cells that were devoid of the de-novo DNA methyltransferases 3a and 3b (Dnmt3a/3b -/-) both H3K4me3 and H3K27me3 marks were established at the inserted sequence. This discovery confirms the importance of CpGs for setting up local chromatin structure.
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Longman, Dagmar. "Contribution of CpG islands to ubiquitous gene expression". Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/15231.

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The effect of CpG islands on transgene expression was first tested in cultured cells. In transient transfection it was demonstrated that CpG islands do not influence the expression of a transgene when not integrated into the genome. Even when integrated into the genome of cultured cells, CpG islands are not able to confer position-independent, copy number-dependent transgene expression, as confirmed by the analysis of individual cell lines. However, the results from bulk analysis of primary clones suggest that CpG islands improve the level of expression in cultured cells, and increase the proportion of highly expressing clones. Transgenic mice were used to study the effect of CpG islands on the level and pattern of transgene expression in vivo. Unexpectedly, from the nine transgenic lines generated, transgene expression was detected in only one line. In the rest of the lines transgene expression was silenced, and in these cases the transgene was densely methylated. In half of the silenced lines transgenes were found to localise in the pericentromeric chromatin. The results suggest that full size CpG islands used as promoters do not necessarily overcome the negative effects of neighbouring chromatin to give ubiquitous transgene expression independent of the integration site. During the study of stable cell lines it was observed that cells within a clone do not have the same level of transgene expression, and this heterogeneity in expression was not reduced by the presence of the full size CpG island. In order to elucidate this phenomenon, the hypothesis that intraclonal heterogeneity is caused by individual cells switching transgene expression on and off over a period of time was tested. Clones of cells expressing Green Fluorescent Protein (GFP) were monitored at regular time intervals, and in some cells rapid extinction of fluorescence was observed. It was concluded from this result that transgene expression varies with time.
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Brown, David. "Understanding the role of CFP1 at CpG islands". Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:baf2e91a-4417-407a-8938-bbef1f6c411f.

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Vertebrate genomes are punctuated by CpG islands regions, which have an elevated frequency of CpG dinucleotides. CpG islands are associated with over 70% of mammalian promoters suggesting they may contribute to the regulation of transcription. However, despite being discovered over 30 years ago, the function of CpG islands is still not understood. Unlike the majority of the genome, CpG islands are resistant to DNA methylation. This provides a binding site for CFP1 which binds specifically to non-methylated DNA via its zinc-finger CXXC (zf-CXXC) domain. CFP1 is a subunit of the SET1 methyltransferase complex, and is thought to direct the activating histone modification H3K4me3 to CpG islands. Interestingly, CFP1 also contains a PHD domain which is proposed to bind the H3K4me3 mark, potentially producing a feedback loop between H3K4me3 and the SET1 complex. Although the structural basis for discrimination of non-methylated CpGs is known, it is not clear how zf-CXXC proteins distinguish CpG islands amongst the irregular nucleosomal landscape which exists within the nucleus. This thesis is focused on the role of CFP1 in the relationship between CpG islands, SET1 and H3K4me3. To address these questions, it was important to mechanistically dissect the contribution of the PHD and zf-CXXC domains. The proposal that the PHD domain of CFP1 binds selectively to H3K4me3 was confirmed by in vitro experiments, however this study demonstrates that the PHD domain is insufficient for stable interactions with chromatin. Using complementary genome-wide and live cell imaging approaches, the zf-CXXC domain shown to be required for PHD-dependent interactions. Genome-wide snapshots of binding interactions, together with spatial and temporal details, expose a surprising contribution of the SET1 complex to the nuclear mobility of CFP1, providing a new perspective on the role of CFP1 in H3K4 methylation.
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Sertedaki, Amalia. "Study of hypervariable regions and CpG islands in human genomic DNA". Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238783.

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Farcas, Anca Madalina. "KDM2B links recognition of CpG islands to polycomb domain formation in vivo". Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:cc773afe-703c-4b43-a792-7ee7ba333bcd.

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Mammalian genomes are characterised by global and pervasive DNA methylation and this modification is generally thought to be inhibitory to transcription. An exception to this widespread DNA modification are genomic elements called CpG islands (CGI), contiguous regions of non-methylated DNA which encompass the transcription start site of two thirds of mammalian genes. Although CGIs represent the most prominent feature of mammalian promoters, the contribution of these elements to promoter function remains unclear. Work in this study shows that the histone lysine demethylase KDM2B (FBXL10/ JHDM1B) is a nuclear protein which binds specifically to non-methylated CpG dinucleotides and associates with CGI elements genome-wide through its zinc-finger CxxC (ZF-CxxC) DNA binding domain. Furthermore, in mouse embryonic stem cells, biochemical investigation revealed that KDM2B associates with Polycomb group E3 ubiquitin ligase RING1B to form a variant Polycomb repressive complex 1 (PRC1) characterized by the PCGF1 subunit. Considering that KDM2B has clear DNA-binding activity and that CGIs were reported to function as nucleation sites for polycomb repressive complexes, a potential role for KDM2B in mediating PRC1 recruitment to target genes was investigated. Stable depletion studies indicated that KDM2B is required for the normal targeting of RING1B to CGIs and the regulation of expression of a subset of Polycomb-occupied genes. By taking advantage of a genetic ablation system in which the DNA binding domain of KDM2B can be conditionally deleted, results in this thesis reveal that the ability of KDM2B to recognize non-methylated DNA is essential for polycomb domain formation and normal embryonic development. Finally, through the use of a de novo targeting assay, an unexpected PRC2 recruitment pathway was discovered which is dependent on PRC1-mediated H2AK119ub1 deposition. Together this work uncovers a novel mechanism linking KDM2B-dependent recognition of non-methylated DNA with recruitment of Polycomb proteins and provides the framework on which to further investigate the contribution of CGIs to formation of polycomb domains.
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Zheng, Hao. "Prediction and analysis of the methylation status of CpG islands in human genome". Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/43631.

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DNA methylation serves as a major epigenetic modification crucial to the normal organismal development and the onset and progression of complex diseases such as cancer. Computational predictions for DNA methylation profiling serve multiple purposes. First, accurate predictions can contribute valuable information for speeding up genome-wide DNA methylation profiling so that experimental resources can be focused on a few selected while computational procedures are applied to the bulk of the genome. Second, computational predictions can extract functional features and construct useful models of DNA methylation based on existing data, and can therefore be used as an initial step toward quantitative identification of critical factors or pathways controlling DNA methylation patterns. Third, computational prediction of DNA methylation can provide benchmark data to calibrate DNA methylation profiling equipment and to consolidate profiling results from different equipments or techniques. This thesis is written based on our study on the computational analysis of the DNA methylation patterns of the human genome. Particularly, we have established computational models (1) to predict the methylation patterns of the CpG islands in normal conditions, and (2) to detect the CpG islands that are unmethylated in normal conditions but aberrantly methylated in cancer conditions. When evaluated using the CD4 lymphocyte data of Human Epigenome Project (HEP) data set based on bisulfite sequencing, our computational models for predicting the methylation status of CpG islands in the normal conditions can achieve a high accuracy of 93-94%, specificity of 94%, and sensitivity of 92-93%. And, when evaluated using the aberrant methylation data from the MethCancerDB database for aberrantly methylated genes in cancer, our models for detecting the CpG islands that are unmethylated in normal conditions but aberrantly methylated in colon or prostate cancer can achieve an accuracy of 92-93%, specificity of 98-99%, and sensitivity of 92-93%.
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King, Hamish. "Molecular determinants of chromatin accessibility at CpG islands in mouse embryonic stem cells". Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:53ceabe6-40ba-402e-a430-7474eac30f93.

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In eukaryotic cells, transcription factors and polymerases must access DNA in the context of nucleosomes and chromatin. The accessibility of DNA sequences to such trans-acting factors is an important feature of gene regulatory elements, including promoters. In vertebrates, the majority of gene promoters coincide with CpG islands (CGIs), which remain free from DNA methylation and exhibit elevated CpG densities. This hypomethylated and CpG-rich state at CGI promoters is associated not only with transcriptional activity, but also with high levels of chromatin accessibility. However, the causes and consequences of such chromatin accessibility remain unclear. To address this, I have profiled chromatin accessibility in mouse embryonic stem cells (ESCs). In addition to confirming that CGI accessibility is independent of transcriptional activity, I was able to demonstrate that the loss of DNA methylation in ESCs resulted in increased chromatin accessibility at a subset of CpG-rich repetitive elements, suggesting that non-methylated CpG-rich sequences may, at least partially, facilitate open chromatin states. This was supported by preliminary work targeting bacterial CpG-rich sequences into the mouse genome, where they were sufficient to establish novel regions of chromatin accessibility. To examine potential mechanisms by which hypomethylated DNA could serve to promote chromatin accessibility, I profiled chromatin accessibility in mouse ESCs lacking various chromatin-modifying proteins which are normally enriched at CGIs, with the histone demethylases KDM2A/B linked to maintaining open chromatin at CGIs. As an alternative approach to understanding the causes of chromatin accessibility in mouse ESCs, I examined the mechanism by which the pioneer transcription factor OCT4 is able to access previously inaccessible chromatin, and reveal that it requires the chromatin remodeller BRG1 to remodel chromatin and facilitate transcription factor binding at distal regulatory elements. Ultimately, this work provides an insight into some of the molecular determinants of chromatin accessibility in mouse ESCs, although many of the consequences of such chromatin states remain unclear.
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Auchincloss, Catherine Anne. "Investigations into mouse trinucleotide repeat arrays and their putative association with CpG islands". Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/23129.

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A mouse CpG island library was screened for all 10 classes of trinucleotide repeat. Sequence analysis of 89 positive clones revealed that only 32% represented CpG islands, compared to 67% of randomly derived clones. These data implied that trinucleotide repeats are under represented in mouse CpG islands. Where possible PCR primers were designed to amplify these repeats from the mouse genome. The variability of 51 repeat arrays was assessed by their PCR amplification from a panel of sixteen mouse strains. Trinucleotide repeats that exhibited length variability between C57BL/6J and Mus spretus (34/51) were mapped using a relevant interspecific backcross panel. These repeats were then screened by PCR as 'candidates' for causing mouse mutant phenotypes mapping to similar genomic regions. Two complex trinucleotide repeat arrays, which mapped to an identical region of chromosome 7, were found to be expanded in frizzy DNA. Further analysis indicated that neither repeat expansion was the underlying mutation responsible for this phenotype. A transgenic study was also carried out to explore the putative relationship between CpG islands and trinucleotide repeat instability. An expanded human Myotonic Dystrophy repeat was cloned into two similar transgenic constructs, one known to retain its native CpG island properties, and the other mutated to confer non island transgene status. Once transgenic mice had been produced, the methylation of the transgene was assessed by PCR and Southern blot. The introduction of the trinucleotide repeat and a small amount of flanking DNA appears to have complicated the predicted methylation of these transgenic constructs. The stability of the trinucleotide repeat arrays was followed through several generations of mice by fluorescent PCR analysis. Moderate trinucleotide repeat instability was observed in the majority of transgenic lines, with a strong bias towards repeat contraction and instability through the female germline. This instability did not appear associated with transgene CpG island status, as defined by methylation.
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Wong, David J. S. "Methylation of the p16 CpG island during neoplastic progression /". Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/5074.

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Książki na temat "CpG Islands"

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Vavouri, Tanya, i Miguel A. Peinado, red. CpG Islands. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7768-0.

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Sidiropoulos, Michael. Tumor-specific loss of human kallikrein 10 (KLK10/NES-1) by CpG Island hypermethylation in breast, ovarian and prostate cancers. Ottawa: National Library of Canada, 2003.

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Vavouri, Tanya, i Miguel A. Peinado. CpG Islands: Methods and Protocols. Springer New York, 2019.

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Vavouri, Tanya, i Miguel A. Peinado. CpG Islands: Methods and Protocols. Springer New York, 2018.

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Immunobiology of bacterial CpG-DNA. Berlin: Springer, 2000.

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(Editor), Neil A. Winegarden, i PhD Mark Takahashi (Editor), red. Promoter and CpG Island Microarrays (Nuts & Bolts series). Dna Press, 2005.

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Jones, Peter A. Dna Methylation And Cancer (Current Topics in Microbiology & Immunology). Redaktor Peter A. Jones. SPRINGER-VERLAG, 2000.

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The Scope and the Content of the Sri Lankan Constitution: Perspectives of Opinion Leaders (Tamil). International IDEA, the Edinburgh Centre for Constitutional Law; The Centre for Policy Alternatives (Sri Lanka), 2022. http://dx.doi.org/10.31752/idea.2022.3.

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The Scope and the Content of the Sri Lankan Constitution: Perspectives of Opinion Leaders comprises a summary of findings that assesses the knowledge, attitudes and perceptions of leaders from the four main ethnic communities (Sinhala, Tamil, Up Country Tamil and Muslim) across the island. These leaders included religious leaders, government officials, office holders of community-based organizations, teachers and school principals. The assessment adapted and applied International IDEA’s constitutional performance assessment methodology to collect these leaders’ perceptions on the constitutional text and realities on current constitution, the Presidency, human rights and the nature of political and economic order. The Constitutional Performance Assessment was undertaken through a partnership between the Centre for Policy Alternatives (CPA), the International Institute for Democracy and Electoral Assistance (International IDEA) and the Edinburgh Centre for Constitutional Law (ECCL).
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The Scope and the Content of the Sri Lankan Constitution: Perspectives of Opinion Leaders (Sinhala). International IDEA, the Edinburgh Centre for Constitutional Law; The Centre for Policy Alternatives, 2022. http://dx.doi.org/10.31752/idea.2022.2.

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The Scope and the Content of the Sri Lankan Constitution: Perspectives of Opinion Leaders comprises a summary of findings that assesses the knowledge, attitudes and perceptions of leaders from the four main ethnic communities (Sinhala, Tamil, Up Country Tamil and Muslim) across the island. These leaders included religious leaders, government officials, office holders of community-based organizations, teachers and school principals. The assessment adapted and applied International IDEA’s constitutional performance assessment methodology to collect these leaders’ perceptions on the constitutional text and realities on current constitution, the Presidency, human rights and the nature of political and economic order. The Constitutional Performance Assessment was undertaken through a partnership between the Centre for Policy Alternatives (CPA), the International Institute for Democracy and Electoral Assistance (International IDEA) and the Edinburgh Centre for Constitutional Law (ECCL).
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Apostolico, Alberto, Maxime Crochemore i Kunsoo Park. Combinatorial Pattern Matching: 16th Annual Symposium, CPM 2005, Jeju Island, Korea, June 19-22, 2005, Proceedings. Springer London, Limited, 2005.

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Części książek na temat "CpG Islands"

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Plass, Christoph. "CpG Islands". W Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_1361-2.

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Plass, Christoph. "CpG Islands". W Encyclopedia of Cancer, 1224–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_1361.

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Antequera, Francisco, i Adrian Bird. "CpG Islands". W DNA Methylation, 169–85. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_8.

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Antequera, Francisco, i Adrian Bird. "CpG Islands: A Historical Perspective". W Methods in Molecular Biology, 3–13. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7768-0_1.

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Mendizabal, Isabel, i Soojin V. Yi. "Diversity of Human CpG Islands". W Handbook of Nutrition, Diet, and Epigenetics, 265–80. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-55530-0_67.

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Mendizabal, Isabel, i Soojin V. Yi. "Diversity of Human CpG Islands". W Handbook of Nutrition, Diet, and Epigenetics, 1–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-31143-2_67-1.

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Ferreira, Humberto J., i Manel Esteller. "CpG Islands in Cancer: Heads, Tails, and Sides". W Methods in Molecular Biology, 49–80. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7768-0_4.

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Afreixo, Vera, Carlos A. C. Bastos, João M. O. S. Rodrigues i Raquel M. Silva. "Identification of DNA CpG Islands Using Inter-dinucleotide Distances". W Communications in Computer and Information Science, 162–72. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20352-2_11.

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Liu, Wei, Hanwu Chen i Ling Chen. "Identifying CpG Islands in Genome Using Conditional Random Fields". W Lecture Notes in Computer Science, 309–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-31588-6_40.

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Bird, A., P. Lavia, D. MacLeod, S. Lindsay, M. Taggart i W. Brown. "Mammalian Genes and Islands of Non-Methylated CpG-Rich DNA". W Human Genetics, 182–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71635-5_18.

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Streszczenia konferencji na temat "CpG Islands"

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Previti, Christopher, Oscar Harari i Coral del Val. "Mining and Predicting CpG islands". W 2007 IEEE International Fuzzy Systems Conference. IEEE, 2007. http://dx.doi.org/10.1109/fuzzy.2007.4295540.

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Lan, Man, Yu Xu, Lin Li, Fei Wang, Ying Zuo, Yuan Chen, Chew Lim Tan i Jian Su. "CpG-discover: A machine learning approach for CpG islands identification from human DNA sequence". W 2009 International Joint Conference on Neural Networks (IJCNN 2009 - Atlanta). IEEE, 2009. http://dx.doi.org/10.1109/ijcnn.2009.5178863.

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Rushdi, Ahmad, i Jamal Tuqan. "A New DSP-Based Measure for CPG Islands Detection". W 2006 IEEE 12th Digital Signal Processing Workshop & 4th IEEE Signal Processing Education Workshop. IEEE, 2006. http://dx.doi.org/10.1109/dspws.2006.265486.

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Kakumani, R., M. O. Ahmad i V. Devabhaktuni. "Identification of CpG islands in DNA sequences using matched filters". W 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6091490.

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Raghavendra, B. S., i A. S. Bopardikar. "Identification of CpG islands in DNA sequences using supervised classification". W 2011 IEEE International Conference on Bioinformatics and Biomedicine Workshops (BIBMW). IEEE, 2011. http://dx.doi.org/10.1109/bibmw.2011.6112519.

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Yalcin, Dicle, i Hasan H. Otu. "Comparative analysis of human and mouse CpG islands using dbCGI". W 2017 IEEE International Conference on Electro Information Technology (EIT). IEEE, 2017. http://dx.doi.org/10.1109/eit.2017.8053357.

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Spontaneo, Leah, i Nick Cercone. "Correlating CpG islands, motifs, and sequence variants in human chromosome 21". W 2010 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2010. http://dx.doi.org/10.1109/bibm.2010.5706584.

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Liu, Bingchuan, Jiajia Chen i Bairong Shen. "Computationally Comparative Analysis of CpG Islands in Human Bidirectional and Unidirectional Promoters". W 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5518272.

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Carson, Matthew B., Robert Langlois i Hui Lu. "Mining knowledge for the methylation status of CpG islands using alternating decision trees". W 2008 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2008. http://dx.doi.org/10.1109/iembs.2008.4650033.

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Hung, Tsai-Hsien, Chih-Jie Shen, Chuan-Mu Chen i Kowit Yu Chong. "Abstract 4914: Methylation profiling of CpG islands in multiple drug resistant cell line". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4914.

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Raporty organizacyjne na temat "CpG Islands"

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Belinsky, S. A., S. B. Baylin i J. J. Issa. Methylation of the estrogen receptor CpG island distinguishes spontaneous and plutonium-induced tumors from nitrosamine-induced lung tumors. Office of Scientific and Technical Information (OSTI), grudzień 1995. http://dx.doi.org/10.2172/381813.

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Belinsky, Steven. Critical Role for Aberrant CpG Island Methylation in the Evolution and Progression of Breast Cancer: Characterization of Known Genes and Identification of Novel Genes. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2001. http://dx.doi.org/10.21236/ada397409.

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