Готові списки джерел за темами / Tissue specific methylation

Добірка наукової літератури з теми "Tissue specific methylation"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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Статті в журналах з теми "Tissue specific methylation"

1

Meng, Wei, Arnab Chakravarti, and Tim Lautenschlaeger. "Methylation-specific high-resolution melting analysis (MS-HRM)-based DNA promoter profiling in paired FFPE bladder cancer samples." Journal of Clinical Oncology 30, no. 5_suppl (February 10, 2012): 315. http://dx.doi.org/10.1200/jco.2012.30.5_suppl.315.

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315 Background: DNA methylation and histone modification are widely studied epigenetic events that can decrease gene expression levels. Promoter hypermethylation has been proposed as a potential diagnostic or prognostic biomarker in various cancers. We studied DNA promoter methylation of 5 cancer-associated genes (MRE11, APX1, ERCC1, RASSF1A and RASSF2A ) in paired FFPE bladder cancer tissues and normal adjacent tissue. The MRE11/Rad50/NBS1 complex serves as a single-strand DNA nuclease which participates in the repair of DNA double-strand breaks and replication errors. APX1 plays a key role in regulating H2O2 levels and H2O2 signaling. DNA repair machinery, ERCC1 protein levels in tumor tissue have been shown to predict response to platinum-based chemotherapy. RASSF1 is thought to be a tumor suppressor gene, while the function of RASSF2 is less well understood. Methods: 16 bladder cancer cases with available paraffin-embedded tumor and matched normal adjacent tissue specimens (32 tissue samples) were analyzed. DNA was extracted by Ambion RecoverAll Total Nucleic Acid Isolation kit. FFPE DNA bisulfite modification was performed using Zymo EZ DNA Methylation Kit. Methylation Specific-High Resolution Melting (MS-HRM) analysis was used to assess methylation status. MS-HRM monitors the melting behavior of PCR amplicons by using a DNA intercalating fluorescent dye. Results: MRE11 and APX1 promoters were not methylated in either cancer or normal adjacent samples. The ERCC1 gene was heavily methylated in 94% (30/32) of all cancer and wild type samples. RASSF1A and RASSF2A promoter methylation was significantly different between cancer and normal adjacent tissue. 50% (8/16) RASSF1A and 25% (4/16) RASSF2A had promoter methylation in cancer tissues, while only 6% (1/16) RASSF1A and 0% (0/16) RASSF2A had promoter methylation in normal adjacent tissues. 69% (11/16) of bladder cancer tissues were positive for RASSF1A or RASSF2A promotor methylation while only 1/16 normal adjacent tissue samples was positive for either promotor methylation. Conclusions: The results show that cancer and non-cancer tissue have different RASSF1A and RASSF2A promoter methylation patterns.
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Herzog, Emilie, Jubby Galvez, Anton Roks, Lisette Stolk, Michael Verbiest, Paul Eilers, Jan Cornelissen, Eric Steegers, and Régine Steegers-Theunissen. "Tissue-specific DNA methylation profiles in newborns." Clinical Epigenetics 5, no. 1 (2013): 8. http://dx.doi.org/10.1186/1868-7083-5-8.

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3

Williams, Ben P., Lindsey L. Bechen, Deborah A. Pohlmann, and Mary Gehring. "Somatic DNA demethylation generates tissue-specific methylation states and impacts flowering time." Plant Cell 34, no. 4 (December 25, 2021): 1189–206. http://dx.doi.org/10.1093/plcell/koab319.

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Abstract Cytosine methylation is a reversible epigenetic modification of DNA. In plants, removal of cytosine methylation is accomplished by the four members of the DEMETER (DME) family of 5-methylcytosine DNA glycosylases, named DME, DEMETER-LIKE2 (DML2), DML3, and REPRESSOR OF SILENCING1 (ROS1) in Arabidopsis thaliana. Demethylation by DME is critical for seed development, preventing experiments to determine the function of the entire gene family in somatic tissues by mutant analysis. Here, we bypassed the reproductive defects of dme mutants to create somatic quadruple homozygous mutants of the entire DME family. dme; ros1; dml2; and dml3 (drdd) leaves exhibit hypermethylated regions compared with wild-type leaves and rdd triple mutants, indicating functional redundancy among all four demethylases. Targets of demethylation include regions co-targeted by RNA-directed DNA methylation and, surprisingly, CG gene body methylation, indicating dynamic methylation at these less-understood sites. Additionally, many tissue-specific methylation differences are absent in drdd, suggesting a role for active demethylation in generating divergent epigenetic states across wild-type tissues. Furthermore, drdd plants display an early flowering phenotype, which involves 5′-hypermethylation and transcriptional down-regulation of FLOWERING LOCUS C. Active DNA demethylation is therefore required for proper methylation across somatic tissues and defines the epigenetic landscape of intergenic and coding regions.
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4

Khodosevich, K. V., Yu B. Lebedev, and E. D. Sverdlov. "The Tissue-Specific Methylation of Human-Specific Endogenous Retroviral LTRs." Russian Journal of Bioorganic Chemistry 30, no. 5 (September 2004): 441–45. http://dx.doi.org/10.1023/b:rubi.0000043787.07628.2a.

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Olumi, Aria F., Zongwei Wang, Rongbin Ge, Shulin Wu, Shahin Tabetabaei, and Chin-Lee Wu. "Epigenetic silencing and variable expression of SRD5A2 in specific compartments of human prostate." Journal of Clinical Oncology 34, no. 2_suppl (January 10, 2016): 38. http://dx.doi.org/10.1200/jco.2016.34.2_suppl.38.

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38 Background: The steroid-5α reductase type 2 gene (SRD5A2) and protein play a significant role in the development and growth of prostate tissue. SRD5A2 can be expressed in both the epithelial and stromal compartments of the prostate gland. Previously, we have shown that somatic suppression of SRD5A2 during adulthood is dependent on epigenetic changes associated with methylation of the promoter region of the SRD5A2 gene. Here we determined whether variability of SRD5A2 expression occurs in specific compartments of prostate tissues. Methods: Frozen and formalin-fixed sections of human adult prostate tissue was used. Laser capture microdissection (LCM) was performed to obtain a pure population of epithelial and stromal cells. Approximately 500–600 excised cells were captured, and the methylation pattern of SRD5A2 was determined by DNA methylation pull-down assay kit. The expression of SRD5A2 protein was identified with immunohistochemistry and quantitated by ELISA. Results: In the whole prostate tissue, samples with high SRD5A2 immunoreactivity had much lower levels of SRD5A2 promoter methylation compared to those with low SRD5A2 immunoreactivity. DNA methylation assay for the epithelial compartment closely resembled the findings of the whole prostate tissue. In contrast, the samples from the stromal compartment showed uniform methylation irrespective of the methylation pattern in the epithelial compartment or the whole tissue. The expression of SRD5A2 protein quantitated by ELISA further showed that the variable expression of SRD5A2 is better determined by epithelial compartment expression. Conclusions: Our data suggests that variability of SRD5A2 expression is dependent on the methylation pattern and expression of SRD5A2 in the epithelial compartment and not the stroma. Therefore, if epithelial expression of SRD5A2 is more representative of the whole prostatic tissue expression, then it is logical that SRD5A2 inhibitor’s efficacy is dependent on involution of the epithelial cells. Our findings will have broad implications for the use of 5ARIs in the treatment of BPH and for the chemoprevention of prostate cancer. Grant support: NIH/R01 DK091353
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6

Choi, Joe, and Nam. "Development of Tissue-Specific Age Predictors Using DNA Methylation Data." Genes 10, no. 11 (November 4, 2019): 888. http://dx.doi.org/10.3390/genes10110888.

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DNA methylation patterns have been shown to change throughout the normal aging process. Several studies have found epigenetic aging markers using age predictors, but these studies only focused on blood-specific or tissue-common methylation patterns. Here, we constructed nine tissue-specific age prediction models using methylation array data from normal samples. The constructed models predict the chronological age with good performance (mean absolute error of 5.11 years on average) and show better performance in the independent test than previous multi-tissue age predictors. We also compared tissue-common and tissue-specific aging markers and found that they had different characteristics. Firstly, the tissue-common group tended to contain more positive aging markers with methylation values that increased during the aging process, whereas the tissue-specific group tended to contain more negative aging markers. Secondly, many of the tissue-common markers were located in Cytosine-phosphate-Guanine (CpG) island regions, whereas the tissue-specific markers were located in CpG shore regions. Lastly, the tissue-common CpG markers tended to be located in more evolutionarily conserved regions. In conclusion, our prediction models identified CpG markers that capture both tissue-common and tissue-specific characteristics during the aging process.
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Pan, Zhangyuan, Xiangyu Wang, Ran Di, Qiuyue Liu, Wenping Hu, Xiaohan Cao, Xiaofei Guo, et al. "A 5-Methylcytosine Site of Growth Differentiation Factor 9 (GDF9) Gene Affects Its Tissue-Specific Expression in Sheep." Animals 8, no. 11 (November 7, 2018): 200. http://dx.doi.org/10.3390/ani8110200.

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Growth differentiation factor 9 (GDF9) plays an important role in the early folliculogenesis of sheep. This study investigated the mRNA expression of ovine GDF9 in different tissues by real-time PCR. GDF9 exhibits significantly higher levels of expression (p < 0.01) in the ovary, relative to other tissues, indicating that its expression is tissue specific. To explore the regulatory mechanism of this tissue-specific expression, the methylation level of one CpG island (−1453 to −1854) of GDF9 promoter in ovary and heart was determined. In this region (−1987 to −1750), only the mC-4 site was present in the Sp4 binding site showed differential methylation between the heart and ovary; with increased (p < 0.01) methylation being observed in the heart. Additionally, the methylation level was negatively correlated with GDF9 mRNA expression (R = −0.75, p = 0.012), indicating that the methylation of this site plays an important role in transcriptional regulation of GDF9. The methylation effect of the mC-4 site was confirmed by using dual-luciferase. Site-directed mutation (methylation) of mC-4 site significantly reduced (p < 0.05) basal transcriptional activity of GDF9 promoter in oocytes. These results imply that methylation of GDF9 promoter CpG island mC-4 site may affect the binding of the Sp4 transcription factor to the GDF9 promoter region in sheep, thereby regulating GDF9 expression and resulting in a tissue-specific expression.
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Yamasaki-Ishizaki, Yoko, Tomohiko Kayashima, Christophe K. Mapendano, Hidenobu Soejima, Tohru Ohta, Hideaki Masuzaki, Akira Kinoshita, et al. "Role of DNA Methylation and Histone H3 Lysine 27 Methylation in Tissue-Specific Imprinting of Mouse Grb10." Molecular and Cellular Biology 27, no. 2 (November 13, 2006): 732–42. http://dx.doi.org/10.1128/mcb.01329-06.

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ABSTRACT Mouse Grb10 is a tissue-specific imprinted gene with promoter-specific expression. In most tissues, Grb10 is expressed exclusively from the major-type promoter of the maternal allele, whereas in the brain, it is expressed predominantly from the brain type promoter of the paternal allele. Such reciprocally imprinted expression in the brain and other tissues is thought to be regulated by DNA methylation and the Polycomb group (PcG) protein Eed. To investigate how DNA methylation and chromatin remodeling by PcG proteins coordinate tissue-specific imprinting of Grb10, we analyzed epigenetic modifications associated with Grb10 expression in cultured brain cells. Reverse transcriptase PCR analysis revealed that the imprinted paternal expression of Grb10 in the brain implied neuron-specific and developmental stage-specific expression from the paternal brain type promoter, whereas in glial cells and fibroblasts, Grb10 was reciprocally expressed from the maternal major-type promoter. The cell-specific imprinted expression was not directly related to allele-specific DNA methylation in the promoters because the major-type promoter remained biallelically hypomethylated regardless of its activity, whereas gametic DNA methylation in the brain type promoter was maintained during differentiation. Histone modification analysis showed that allelic methylation of histone H3 lysine 4 and H3 lysine 9 were associated with gametic DNA methylation in the brain type promoter, whereas that of H3 lysine 27 regulated by the Eed PcG complex was detected in the paternal major-type promoter, corresponding to its allele-specific silencing. Here, we propose a molecular model that gametic DNA methylation and chromatin remodeling by PcG proteins during cell differentiation cause tissue-specific imprinting in embryonic tissues.
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Ząbek, Tomasz, Ewelina Semik, Agnieszka Fornal, Artur Gurgul, and Monika Bugno-Poniewierska. "The Relevance of Methylation Profiles of Equine ITGAL Gene." Annals of Animal Science 16, no. 3 (July 1, 2016): 711–20. http://dx.doi.org/10.1515/aoas-2015-0080.

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AbstractOne of epigenetic features of mammalian genomes is methylation of DNA. This nucleotide modification might exert suppressive effect on gene transcription. We have described putative relevance of methylation of one of immune cells related gene (ITGAL) observed in the set of 11 equine tissues. Comparison between qualitative RT-PCR results and DNA bisulfite sequencing of investigated set of tissues pointed to potential correlations between tissue specific methylation and tissue specific transcription in ITGAL locus. These findings might be important for studies on genetic and epigenetic background of autoimmune disorders in the horse.
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Beri, Silvana, Noemi Tonna, Giorgia Menozzi, Maria Clara Bonaglia, Carlo Sala, and Roberto Giorda. "DNA methylation regulates tissue-specific expression of Shank3." Journal of Neurochemistry 101, no. 5 (June 2007): 1380–91. http://dx.doi.org/10.1111/j.1471-4159.2007.04539.x.

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Дисертації з теми "Tissue specific methylation"

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Dhaliwal, Tarunpreet. "H3K36me3 in Muscle Differentiation: Regulation of Tissue-specific Gene Expression by H3K36-specific Histonemethyltransferases." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23590.

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The dynamic changes in chromatin play a significant role in lineage commitment and differentiation. These epigenetic modifications control gene expression through recruitment of transcription factors. While the active mark H3K4me3 is present around the transcription start site on the gene, the function of the H3K36me3 mark is unknown. A number of H3K36-specific histone methyltransferases (HMTs) have been identified, however the focus of this study is the HMT Hypb. To elucidate the role of H3K36me3 in mediating expression of developmentally-regulated loci, native chromatin immunoprecipitation (N-ChIP) was performed at a subset of genes. Upon differentiation, we observe that H3K36me3 becomes enriched at the 3’ end of several muscle-specific genes. To further investigate the role of H3K36me3 in myogenesis, a lentiviral-mediated knockdown of the H3K36 HMT Hypb was performed in muscle myoblasts using shRNA. Upon Hypb knockdown, we were surprised to observe enhanced myogenesis. N-ChIP was also performed on differentiated Hypb knockdown cell lines in order to look at H3K36me3 enrichment on genes involved in muscle differentiation. N-ChIP data show a drop in H3K36me3 enrichment levels on myogenin and Ckm genes. The possible occupancy of Hypb on the coding regions of muscle-specific genes was experimentally observed by cross-linked chromatin immunoprecipitation (X-ChIP) on differentiated C2C12 cells and subsequently confirmed by X-ChIP on knockdown lines where the occupancy was lost. A model is proposed that links the observed phenotype with H3K36me3.
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Shi, Yuming. "Sex and tissue specific DNA methylation patterns in the house sparrow (Passer domesticus)." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-445070.

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DNA methylation patterns are sex and tissue specific in many species, yet many studies useblood samples, due to its accessibility, to establish links between the DNA methylation anddifferent phenotypes. This raises the question of whether DNA methylation in blood samplesreflect the DNA methylation pattern in other tissues that are more relevant to the phenotypebeing studied. In this research, samples were collected from the brain, blood, liver and gonadof 16 house sparrow (Passer domesticus), half of them were female, while the others weremale. Reduced representation bisulfite sequencing (RRBS) was performed to get themethylation profile in each sample. The result showed a tissue specific methylation profile inthe four investigated tissues, a strong and positive correlation between 0.74 – 0.85 was foundbetween tissues, in which a weaker correlation was found between blood and other tissue. Indifferential methylation analysis, most of the differently methylated sites between sexes werefound in gonads, while the fewest was found in blood, and Z chromosome wasoverrepresented place in all four tissues where the majority of the differently methylated sitesbetween sexes were found. Comparison with the house sparrow genome annotation foundabout half of the differentially methylated sites between sexes were within genes and about 20 % of them were in the exon or coding region of a gene. The result suggested that bloodcould be useful in reflecting the general DNA methylation level in other tissues, but it was nota reliable bioindicator for further detailed study in DNA methylation pattern or in geneontology enrichment pathway analysis.
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3

Daugela, Laurynas [Verfasser]. "Tissue type and Gender Effects on DNA Methylation at specific Loci in Mice / Laurynas Daugela." Bonn : Universitäts- und Landesbibliothek Bonn, 2017. http://d-nb.info/1139118730/34.

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Denton, Nathan Frederick. "The role of DNA methylation in the regulation of depot-specific gene expression in human adipose tissue." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:2f927c70-edf9-4187-8228-f52dc71c59cf.

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Adipose tissue is not homogenous as individual fat depots display regional variation in their physiological properties. It follows that body fat distribution is increasingly being recognised as a major determinant of metabolic disease risk. At the cellular level, depot-specific properties are exhibited by adipocyte precursors during in vitro culture and persist for many generations, suggesting these cells retain an ‘intrinsic memory’ of their anatomical origin which is epigenetic in nature. A primary aim was to identify depot-specific genes whose expression may be regulated by DNA methylation in adipose precursors. Using two paired preadipocyte cell lines derived from human subcutaneous abdominal and gluteal adipose tissue - to represent upper and lower body fat with their opposing associations with cardiovascular disease and diabetes respectively - depot-specific gene expression and DNA methylation profiles were detected. Furthermore, the expression of certain genes in preadipocytes was found to change in response to treatment with the DNA demethylating agent 5-azacytidine, which suggests DNA methylation may regulate depot-specific gene expression. A secondary aim was to investigate whether glucocorticoids – which are important determinants of body fat distribution – exert their effects through DNA methylation. The synthetic glucocorticoid dexamethasone was found to modulate the expression of some of the differentially expressed genes in preadipocytes, with this effect possibly being mediated by DNA methylation. It has been postulated that depot-specific phenotypes in adipose tissue may arise from developmental differences. Several genes were found to be expressed in a depot-specific fashion during a differentiation time course, suggesting regional variation in adipogenesis may contribute to the generation of depot-specific phenotypes. Overall, the data presented suggests regional variation within subcutaneous white adipose tissue exists and supports the notion that DNA methylation patterns can, in part, determine adipose tissue heterogeneity.
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Antunes, Joana AP. "The Study of Tissue-Specific DNA Methylation as a Method for the Epigenetic Discrimination of Forensic Samples." FIU Digital Commons, 2017. https://digitalcommons.fiu.edu/etd/3676.

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In forensic sciences, the serological methods used to determine which body fluid was collected from the crime scene are merely presumptive or labor intensive since they rely on protein detection or on microscopic identification of cells. Given that certain forensic cases may need the precise identification of a body fluid to determine criminal contact, such is the example of a suspected sexual assault of a minor; certainty in the body fluid of origin may depict a precise picture of the events. The identification of loci that show differences in methylation according to the tissue of origin can aid forensic analysts in determining the origin of a DNA sample. The process of DNA methylation occurs naturally in the genome of living organisms and consists in the presence of a methyl group on the carbon 5 of a cytosine, which is typically followed by a guanine (CpG). Analyzing patterns of DNA methylation in body fluids collected from a crime scene is preferential to the analysis of proteins or mRNA since the same extracted DNA used for STR typing can be used for DNA methylation analysis. We have validated and identified loci able to discriminate blood, saliva, semen and vaginal epithelia. In the current study, we have also established the minimum amount of DNA able to provide reliable results using methodologies such as pyrosequencing and high-resolution melt (HRM) analysis for the different markers identified. Lastly, we performed an alternative bioinformatic analysis of data collected using an array that studied methylation in over 450,000 individual cytosines on the human genome. We were able to sort the locations that showed potentially higher methylation differences between body fluids and investigated over 100 of them using HRM analysis. The results of that study, allowed the identification of three new loci able to distinguish blood and two new loci able to distinguish saliva and vaginal epithelia, respectively. The use of DNA methylation patterns to aid forensic investigations started with a publication in 2010, therefore each small contribution such as this work may, similarly to what occured in the biochemistry field, result in the discovery of a method able to put the technology in the hands of forensic analysts.
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6

Boucaut, Kerry Jane. "Function and regulation of the human serine protease Testisin." Thesis, Queensland University of Technology, 2002.

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Schilling, Elmar [Verfasser]. "Analysis of tissue-specific & allele-specific DNA methylation / vorgelegt von Elmar Schilling." 2009. http://d-nb.info/1001198832/34.

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Frederick, Armina-Lyn. "Impact of Bodyweight on Tissue-Specific Folate Status, Genome Wide and Gene-Specific DNA Methylation in Normal Breast Tissues from Premenopausal Women." 2018. https://scholarworks.umass.edu/masters_theses_2/639.

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Obesity has reached an epidemic level in the United States. A number of epidemiological studies have established obesity as a critical risk factor for postmenopausal breast cancer (post-BC), whereas a reverse association holds prior to menopause. A significant scientific gap exists in understanding the mechanism(s) underpinning this epidemiological phenomenon, particularly the reverse association between obesity and premenopausal breast cancer (pre-BC). This study aimed to understand how folate metabolism and DNA methylation informs the association between obesity and pre-BC. Fifty normal breast tissue samples were collected from premenopausal women who underwent reduction mammoplasty. We developed and measured the breast tissue folate by a Lactobacillus Casei microbiological assay, and the DNA methylation of LINE-1, a biomarker of genome-wide methylation, and the promoter methylation and gene expression of SFRP1, a tumor suppressor, were measured by pyrosequencing and real-time PCR. We found a high BMI is associated with increased folate level in the mammary tissue, with an increase of 2.65 ng/g of folate per every 5-unit increase of BMI (p < 0.05). The LINE-1 DNA methylation was significantly associated with BMI (p < 0.05), and marginally associated with folate concentration (p = 0.087). For the 8 CpG sites analyzed in the promoter region of the SFRP1 gene, no associations were observed for either BMI or tissue folate (p > 0.05), although a high expression of SFRP1 was observed in subjects with high BMI or high folate (p < 0.05). This study demonstrated that, in premenopausal women, obesity is associated with an increased mammary folate status, genome-wide DNA methylation and SFRP1 gene expression, indicating that the improved folate and epigenetic status is potentially responsible for the reverse association between obesity and pre-BC. More studies are warranted to further understand how obesity mediates pre-BC via altering folate metabolism and DNA methylation.
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Li, Pei-Shan, and 李佩珊. "Comparative Mouse Tissue Epigenomics: Study of the Role of S/MARs and DNA Methylation In Tissue-specific Expression." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/98379793176530258719.

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碩士
國立陽明大學
生化暨分子生物研究所
100
Since the decoding of the human genome, epigenetic regulation has become the major regulatory paradigm towards understanding the relationship between genotype and phenotype. Although much has been learned about the epigenetic regulation of single genes, how the regulation is achieved at genomic level is still not well understood because of the lack of genome-wide data of epigenetic regulation. The aim of my thesis is to use next-generation high throughput sequencing platforms to map the regulatory elements in the mouse tissues and compare the nature of these elements with respect to regulation of tissue-specificity genes. I used micrococcal nuclease to digest tissues nucleus to identify regulatory elements in mouse tissues. Specifically, I analyzed three types of regulatory elements: 1) DNA methylation, 2) nuclear matrix binding sites, and 3) histone modifications. The regulatory element is refined as S/MARs. To study the distribution of S/MARs in different mouse tissues attempt to identify the regulatory elements of tissue-specific genes. Genome-wide mapping of S/MARs in different mouse tissues suggest significant differences in chromosome organization among the five mouse tissues. And different S/MARs distribution with respected to the positions of the genes in different mouse tissues. Liver highly expressed genes have different S/MARs distribution and accompanied with DNA demethylation in the promoter or intragenic regions of S/MARs difference in corresponding genes in brain. Interestingly, exon and intron junction sites of highly expressed genes in liver bind to nuclear matrix at higher frequency than the corresponding genes in brain. By ChIP assay, scaffold/matrix binding proteins at S/MARs together with splicesomes and histone modifications regulate tissue specific gene expression In Summary, the preliminary study shows that there are distinctive epigenetic features among different mouse tissues. The overall nuclear matrix binding sites indicates a distinctive genome organization in the brain as compared to the other four tissues. The differential association of S/MARs, differential CpG methylation as well as distinctive histone modifications in liver specific genes between liver and brain suggest that these epigenetic mechanisms may be needed to achieve tissue-specific expression. And S/MARs can serve as anchor for proteins binding to achieve differential epigenetic modification resulted in differential gene expression. The technique of genome-wide mapping of S/MARs will develop to facilitate the study of regulatory tissue-specific genes expression, further to deduce the logics of biological-context dependent phenotypes variations.
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Cortese, Rene Gabriel [Verfasser]. "Differential DNA methylation profiles modulating phenotypes : regions of tissue-specific DNA methylation and their relation to gene expression, their evolutionary conservation and their application as molecular biomarkers / vorgelegt von Rene Gabriel Cortese." 2008. http://d-nb.info/988368323/34.

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Частини книг з теми "Tissue specific methylation"

1

Razin, Aharon. "Tissue Specific DNA Methylation Patterns: Biochemistry of Formation and Possible Role." In Biological Methylation and Drug Design, 127–37. Totowa, NJ: Humana Press, 1986. http://dx.doi.org/10.1007/978-1-4612-5012-8_11.

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Liu, Xiaoming, and Canxia Xu. "DNA Methylation Analysis of Human Tissue-Specific Connexin Genes." In Methods in Molecular Biology, 21–36. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3664-9_2.

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Antunes, Joana, Kuppareddi Balamurugan, George Duncan, and Bruce McCord. "Tissue-Specific DNA Methylation Patterns in Forensic Samples Detected by Pyrosequencing®." In Methods in Molecular Biology, 397–409. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2715-9_27.

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Milne, Trudy J. "A Protocol for the Determination of the Methylation Status of Gingival Tissue DNA at Specific CpG Islands." In Methods in Molecular Biology, 299–306. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6685-1_17.

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Konate, Moumouni, Mike J. Wilkinson, Benjamin T. Mayne, Eileen S. Scott, Bettina Berger, and Carlos M. Rodríguez López. "Atlas of Age- and Tissue-Specific DNA Methylation during Early Development of Barley (Hordeum vulgare)." In DNA Methylation Mechanism. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.90886.

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Postiglioni, Alicia, Rody Artigas, Andrs Iriarte, Wanda Iriarte, Nicols Grasso, and Gonzalo Rinc. "Could Tissue-Specific Genes be Silenced in Cattle Carrying the Rob(1;29) Robertsonian Translocation?" In DNA Methylation - From Genomics to Technology. InTech, 2012. http://dx.doi.org/10.5772/34007.

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Asting, Annika, Helena Carén, Marianne Andersson, Christina Lönnroth, Kristina Lagerstedt, and Kent Lundholm. "COX-2 Gene Expression in Colon Cancer Tissue Related to Regulating Factors and Promoter Methylation Status." In Specific Gene Expression and Epigenetics, 29–50. Apple Academic Press, 2014. http://dx.doi.org/10.1201/b16680-4.

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"COX-2 Gene Expression in Colon Cancer Tissue Related to Regulating Factors and Promoter Methylation Status." In Specific Gene Expression and Epigenetics, 59–80. Apple Academic Press, 2014. http://dx.doi.org/10.1201/b16680-8.

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Hoivik, EA, T. Bjanesoy, S. Witso, and M. Bakke. "Tissue Specific Methylation of Intronic Enhancers in the Gene Encoding Steroidogenic Factor 1." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–110—P1–110. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p3.p1-110.

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Campanile, Gianluigi, Giuseppe Fanelli, Chiara Fabbri, Alessandro Serretti, and Julien Mendlewicz. "Epigenetics and aetiology of mental illness." In Oxford Textbook of Social Psychiatry, edited by Dinesh Bhugra, Driss Moussaoui, and Tom J. Craig, 41–48. Oxford University PressOxford, 2022. http://dx.doi.org/10.1093/med/9780198861478.003.0005.

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Abstract Over the last few decades, considerable progress has been achieved in understanding the aetiology of mental illness and its biological underpinnings. Genetic factors have been shown to play a substantial role, although genetics alone are not able to explain fully the heritability of these diseases. Epigenetic mechanisms, such as DNA methylation, histone modifications, and RNA interference, modulate tissue-specific gene expression and have been proven to be involved in the aetiopathogenesis of psychiatric disorders. Numerous epidemiological studies have confirmed a contribution of environmental factors, and convincing evidence suggests that socio-economic status, early life stressors, and childhood trauma impact significantly on the risk of psychiatric disorders via lifelong epigenetic modifications. This chapter will discuss in detail the different epigenetic mechanisms underlying the pathogenesis of psychiatric diseases and their interaction with genetic factors, providing an overall picture about the recent advances in psychiatric epigenomics.
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Тези доповідей конференцій з теми "Tissue specific methylation"

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Kinoshita, R., and Y. H. Taguchi. "Tissue specific methylation and genotype." In 2011 IEEE International Conference on Bioinformatics and Biomedicine Workshops (BIBMW). IEEE, 2011. http://dx.doi.org/10.1109/bibmw.2011.6112517.

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Castle, James R., Nan Lin, Jingpeng Liu, Chi Wang, Yunlong Liu, and Chunyan He. "Abstract 827: Estimating breast tissue-specific epigenetic age using next-generation methylation sequencing data." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-827.

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Castle, James R., Nan Lin, Jingpeng Liu, Chi Wang, Yunlong Liu, and Chunyan He. "Abstract 827: Estimating breast tissue-specific epigenetic age using next-generation methylation sequencing data." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-827.

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Hon, Gary C., Yin Shen, David F. McCleary, Lee Edsall, Samantha Kuan, and Bing Ren. "Abstract 1111: Whole genome bisulfite sequencing reveals tissue-specific DNA methylation in a normal mouse." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1111.

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Meyer, Karolin F. M., Susanne Krauss-Etschmann, Rikst Nynke Verkaik-Schakel, Wim Timens, Lester Kobzik, Torsten Plösch, and Machteld Hylkema. "Pregnancy smoking: Tissue- and sex-specific drift of Igf1r and Igf1 methylation in mouse fetuses and neonates." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa2947.

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He, Chunyan, James Castle, Nan Lin, Jinpeng Liu, Chi Wang, and Yunlong Liu. "Abstract 2087: Breast tissue-specific DNA methylation levels predicted by genetic variants in association with breast cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2087.

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Ali, I., and H. Seker. "A comparative study for characterisation and prediction of tissue-specific DNA methylation of CpG islands in chromosomes 6, 20 and 22." In 2010 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC 2010). IEEE, 2010. http://dx.doi.org/10.1109/iembs.2010.5626437.

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Bae, Jeong Mo, Kwangsoo Kim, Hee Jun Chae, Xianyu Wen, Kang Yeol Kim, Hwang Kwan Gwon, Nam-Yun Cho, and Gyeong Hoon Kang. "Abstract 3312: Identification of tissue-of-origin in cancer of unknown primary site (CUPS) using methylation-specific targeted resequencing: A pilot study." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3312.

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Звіти організацій з теми "Tissue specific methylation"

1

Eshed-Williams, Leor, and Daniel Zilberman. Genetic and cellular networks regulating cell fate at the shoot apical meristem. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699862.bard.

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The shoot apical meristem establishes plant architecture by continuously producing new lateral organs such as leaves, axillary meristems and flowers throughout the plant life cycle. This unique capacity is achieved by a group of self-renewing pluripotent stem cells that give rise to founder cells, which can differentiate into multiple cell and tissue types in response to environmental and developmental cues. Cell fate specification at the shoot apical meristem is programmed primarily by transcription factors acting in a complex gene regulatory network. In this project we proposed to provide significant understanding of meristem maintenance and cell fate specification by studying four transcription factors acting at the meristem. Our original aim was to identify the direct target genes of WUS, STM, KNAT6 and CNA transcription factor in a genome wide scale and the manner by which they regulate their targets. Our goal was to integrate this data into a regulatory model of cell fate specification in the SAM and to identify key genes within the model for further study. We have generated transgenic plants carrying the four TF with two different tags and preformed chromatin Immunoprecipitation (ChIP) assay to identify the TF direct target genes. Due to unforeseen obstacles we have been delayed in achieving this aim but hope to accomplish it soon. Using the GR inducible system, genetic approach and transcriptome analysis [mRNA-seq] we provided a new look at meristem activity and its regulation of morphogenesis and phyllotaxy and propose a coherent framework for the role of many factors acting in meristem development and maintenance. We provided evidence for 3 different mechanisms for the regulation of WUS expression, DNA methylation, a second receptor pathway - the ERECTA receptor and the CNA TF that negatively regulates WUS expression in its own domain, the Organizing Center. We found that once the WUS expression level surpasses a certain threshold it alters cell identity at the periphery of the inflorescence meristem from floral meristem to carpel fate [FM]. When WUS expression highly elevated in the FM, the meristem turn into indeterminate. We showed that WUS activate cytokinine, inhibit auxin response and represses the genes required for root identity fate and that gradual increase in WUCHEL activity leads to gradual meristem enlargement that affect phyllotaxis. We also propose a model in which the direction of WUS domain expansion laterally or upward affects meristem structure differently. We preformed mRNA-seq on meristems with different size and structure followed by k-means clustering and identified groups of genes that are expressed in specific domains at the meristem. We will integrate this data with the ChIP-seq of the 4 TF to add another layer to the genetic network regulating meristem activity.
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