Relevant bibliographies by topics / Quantitative chemical methylation

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Academic literature on the topic 'Quantitative chemical methylation'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Quantitative chemical methylation"

1

Li, Guiping, Qingsong Ba, Gaisheng Zhang, Lanlan Zhang, Chu Chen, and Zhaolin Fu. "DNA methylation of the TAA1 gene regulates formation of the pollen wall in chemically induced male sterility in wheat (Triticum aestivum)." Crop and Pasture Science 68, no. 9 (2017): 817. http://dx.doi.org/10.1071/cp17255.

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DNA methylation is an important epigenetic modification that may contribute to environmentally induced phenotypic variations by regulating gene expression. Chemically induced male sterility (CIMS) lines in wheat (Triticum aestivum L.) can transform from sterile to fertile, induced by a chemical hybridising agent during anther development. So far, little is known about the DNA methylation variation of CIMS in wheat. TAA1 regulates pollen wall development, probably through converting fatty acids to fatty alcohol in wheat. We investigated the DNA methylation pattern of the TAA1 gene in the core promoter region by using the bisulfite genomic sequencing method, and higher methylation was observed in CIMS. The expression levels of the TAA1 gene were also evaluated by real time quantitative reverse transcriptase PCR analysis, which revealed that the expression levels of the TAA1 gene were downregulated in CIMS. The aliphatic composition of the anther underwent accumulation in line 1376-CIMS, revealed by gas chromatography–mass spectrometry, including increments of tetradecanoic acid, hexadecanoic acid and octadecanoic acid. Scanning electron microscopy revealed that anther and pollen wall formation was significantly altered in 1376-CIMS.These results suggested that DNA methylation of the TAA1 gene may be involved in the sterility–fertility transition of CIMS.
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Liu, Shenglin, Xuejun Zhang, and Kebin Zhao. "Methylation-specific electrochemical biosensing strategy for highly sensitive and quantitative analysis of promoter methylation of tumor-suppressor gene in real sample." Journal of Electroanalytical Chemistry 773 (July 2016): 63–68. http://dx.doi.org/10.1016/j.jelechem.2016.03.001.

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Yang, Lin, Lei Bi, Qingwei Liu, et al. "Hiwi Promotes the Proliferation of Colorectal Cancer Cells via Upregulating Global DNA Methylation." Disease Markers 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/383056.

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Hiwi is well known for its role in stem cell renewal, maintaining the resting stage, and downregulating cell cycle of stem cells via RNA silencing. And Hiwi overexpression has been recognized in several types of cancers. In the present study, we examined the Hiwi expression in colorectal cancer (CRC) specimens in both mRNA and protein levels via real-time quantitative PCR, western blot assay, and immunohistochemical staining. Then we explored the role of Hiwi in the cancer cell proliferation and in the DNA methylation in human CRC Caro-2 and HT-29 cell lines. Results demonstrated that both mRNA and protein levels of Hiwi were significantly higher in 38 CRC tissues than in 38 peritumor tissues. Moreover, the Hiwi overexpression with an adenovirus vector significantly promoted the proliferation of Caro-2 and HT-29 cells, associated with significant increase in the global DNA methylation levels. And the chemical inhibition of DNA methylation significantly restrained such proliferation promotion. In summary, we confirmed that Hiwi was overexpressed in CRC tissues and that the forced Hiwi overexpression promoted the proliferation and global DNA methylation of CRC cell lines. Our results imply for the first time that Hiwi promotes the proliferation of CRC cells via promoting global DNA methylation.
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Gilun, Przemysław, Krzysztof Flisikowski, Tatiana Flisikowska, Joanna Kwiatkowska, Barbara Wąsowska, and Magdalena Koziorowska-Gilun. "Role of Methylation in Period2 (PER2) Transcription in the Context of the Presence or Absence of Light Signals: Natural and Chemical—Studies on the Pig Model." International Journal of Molecular Sciences 22, no. 15 (2021): 7796. http://dx.doi.org/10.3390/ijms22157796.

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It has been proposed that carbon monoxide (CO) is a chemical light carrier that is transferred by the humoral pathway from the retina to the brain. Here, we aimed to study how deeply CO is involved in regulating the expression of Period2 gene (PER2), one of the genes maintaining the intrinsic biological clock. In our in vivo experiment, we studied whether CO may be a chemical signal and is also equivalent to natural light in three groups of pigs: Normal: housed in natural conditions without any procedures, Control: adapted and kept in constant darkness, infused with blank plasma, and CO treated: adapted and kept in constant darkness infused with CO-enriched plasma. After the experiment, the animals were slaughtered at two times of day: 12 p.m. and 12 a.m. Next, hypothalamus samples were collected. Quantitative PCR, the DNA methylation of the promoter sequence containing enhancers (E-box) and a functional analysis of the PER2 promoter was performed. qPCR showed a differential pattern of PER2 mRNA expression at daytime oscillation in the examined groups. Pyrosequencing revealed daytime changes in the methylation level of regulatory sites of the examined sequence. Luciferase reporter assay confirmed that E-boxes (CANNTG) drive the expression of the porcine PER2 in vitro. In conclusion, changes in methylation over 24 h may regulate the oscillatory manner of PER2 expression.
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Wang, Jin, Bing Liang Alvin Chew, Yong Lai, et al. "Quantifying the RNA cap epitranscriptome reveals novel caps in cellular and viral RNA." Nucleic Acids Research 47, no. 20 (2019): e130-e130. http://dx.doi.org/10.1093/nar/gkz751.

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Abstract Chemical modification of transcripts with 5′ caps occurs in all organisms. Here, we report a systems-level mass spectrometry-based technique, CapQuant, for quantitative analysis of an organism's cap epitranscriptome. The method was piloted with 21 canonical caps—m7GpppN, m7GpppNm, GpppN, GpppNm, and m2,2,7GpppG—and 5 ‘metabolite’ caps—NAD, FAD, UDP-Glc, UDP-GlcNAc, and dpCoA. Applying CapQuant to RNA from purified dengue virus, Escherichia coli, yeast, mouse tissues, and human cells, we discovered new cap structures in humans and mice (FAD, UDP-Glc, UDP-GlcNAc, and m7Gpppm6A), cell- and tissue-specific variations in cap methylation, and high proportions of caps lacking 2′-O-methylation (m7Gpppm6A in mammals, m7GpppA in dengue virus). While substantial Dimroth-induced loss of m1A and m1Am arose with specific RNA processing conditions, human lymphoblast cells showed no detectable m1A or m1Am in caps. CapQuant accurately captured the preference for purine nucleotides at eukaryotic transcription start sites and the correlation between metabolite levels and metabolite caps.
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Qin, Wei, Pinou Lv, Xinqi Fan, et al. "Quantitative time-resolved chemoproteomics reveals that stable O-GlcNAc regulates box C/D snoRNP biogenesis." Proceedings of the National Academy of Sciences 114, no. 33 (2017): E6749—E6758. http://dx.doi.org/10.1073/pnas.1702688114.

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O-linked GlcNAcylation (O-GlcNAcylation), a ubiquitous posttranslational modification on intracellular proteins, is dynamically regulated in cells. To analyze the turnover dynamics of O-GlcNAcylated proteins, we developed a quantitative time-resolved O-linked GlcNAc proteomics (qTOP) strategy based on metabolic pulse-chase labeling with an O-GlcNAc chemical reporter and stable isotope labeling with amino acids in cell culture (SILAC). Applying qTOP, we quantified the turnover rates of 533 O-GlcNAcylated proteins in NIH 3T3 cells and discovered that about 14% exhibited minimal removal of O-GlcNAc or degradation of protein backbones. The stability of those hyperstable O-GlcNAcylated proteins was more sensitive to O-GlcNAcylation inhibition compared with the more dynamic populations. Among the hyperstable population were three core proteins of box C/D small nucleolar ribonucleoprotein complexes (snoRNPs): fibrillarin (FBL), nucleolar protein 5A (NOP56), and nucleolar protein 5 (NOP58). We showed that O-GlcNAcylation stabilized these proteins and was essential for snoRNP assembly. Blocking O-GlcNAcylation on FBL altered the 2′-O-methylation of rRNAs and impaired cancer cell proliferation and tumor formation in vivo.
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7

MacDonald, Ian A., Kyle V. Butler, Laura E. Herring, et al. "Pathway-Based High-Throughput Chemical Screen Identifies Compounds That Decouple Heterochromatin Transformations." SLAS DISCOVERY: Advancing the Science of Drug Discovery 24, no. 8 (2019): 802–16. http://dx.doi.org/10.1177/2472555219849838.

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Heterochromatin protein 1 (HP1) facilitates the formation of repressive heterochromatin domains by recruiting histone lysine methyltransferase enzymes to chromatin, resulting in increased levels of histone H3K9me3. To identify chemical inhibitors of the HP1-heterochromatin gene repression pathway, we combined a cell-based assay that utilized chemical-mediated recruitment of HP1 to an endogenous active gene with high-throughput flow cytometry. Here we characterized small molecule inhibitors that block HP1-mediated heterochromatin formation. Our lead compounds demonstrated dose-dependent inhibition of HP1-stimulated gene repression and were validated in an orthogonal cell-based system. One lead inhibitor was improved by a change in stereochemistry, resulting in compound 2, which was further used to decouple the inverse relationship between H3K9 and H3K4 methylation states. We identified molecular components that bound compound 2, either directly or indirectly, by chemical affinity purification with a biotin-tagged derivative, followed by quantitative proteomic techniques. In summary, our pathway-based chemical screening approach resulted in the discovery of new inhibitors of HP1-mediated heterochromatin formation while identifying exciting new molecular interactions in the pathway to explore in the future. This modular platform can be expanded to test a wide range of chromatin modification pathways yielding inhibitors that are cell permeable and function in a physiologically relevant setting.
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8

Tsymbal, O., D. Isubakova, E. Bronikovskaya, et al. "The Role of Bak1 Methylation in the Induction of Chromosomal Aberrations under Chronic Low-Intensity External Radiation." Medical Radiology and radiation safety 65, no. 5 (2021): 29–34. http://dx.doi.org/10.12737/1024-6177-2020-65-5-29-34.

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Purpose: To study the relationship between the methylation status of the Bаk1 promoter and the frequency of chromosomal aberrations in human blood lymphocytes under chronic low-intensity external ionizing radiation.
 Material and methods: The study was performed on 41 people (31 men and 10 women, aged from 36 to 83 years) who are former or current employees of the Siberian Group of Chemical Enterprises, who have been exposed or haven't been exposed to chronic low-intensity external radiation in the course of their professional activities. The workers included in the study were divided into two groups: the first – 15 people who did not have exposure, the second – 26 people who had external exposure (gamma radiation, total dose 89–716 mSv). Whole blood was used to isolate DNA and evaluate chromosomal aberrations in lymphocytes. The methylation status of the Bаk1 promoter was determined using methylsensitive PCR, which was performed after pretreatment of the isolated DNA with methylsensitive AoxI restrictase. The obtained quantitative data were analyzed using the Statistica 10. The differences were considered statistically significant at p ≤ 0.05.
 Results: The methylation status of the Bаk1 promoter in the study groups does not differ (p = 0.18). The study of the effect of external radiation dose on the methylation status of the Bak1 promoter showed that the unmethylated promoter prevails in workers with an average radiation dose of 273.37 ± 43.82 mSv, while the methylated promoter – in workers with an average radiation dose of 183.63 ± 20.58 mSv (p = 0.03). The unmethylated promoter Bаk1 is associated with an increased frequency of chromatid fragments in the blood lymphocytes of group 2 workers (p = 0.03).
 Conclusion: The status of methylation of the Bаk1 promoter in human blood lymphocytes under chronic low-intensity ionizing radiation does not change, but it is observed to depend on the radiation dose and is associated with an increased frequency of chromosomal aberrations (chromatid fragments). Thus, the unmethylated Bаk1 promoter prevails when the external radiation dose is increased. An increase in the frequency of chromatid fragments is associated with an unmethylated Bаk1 promoter. In addition, exposure to chronic low-intensity external radiation is accompanied by a decrease in the frequency of chromosomal fragments in the blood lymphocytes of workers of the Siberian Group of Chemical Enterprises.
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9

Teng, Jian, Seyedali Hejazi, Lotte Hiddingh, et al. "Recycling drug screen repurposes hydroxyurea as a sensitizer of glioblastomas to temozolomide targeting de novo DNA synthesis, irrespective of molecular subtype." Neuro-Oncology 20, no. 5 (2017): 642–54. http://dx.doi.org/10.1093/neuonc/nox198.

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Abstract Background Glioblastoma (GBM) is the most common and most aggressive primary malignant brain tumor. Standard-of-care treatment involves maximal surgical resection of the tumor followed by radiation and chemotherapy (temozolomide [TMZ]). The 5-year survival rate of patients with GBM is <10%, a colossal failure that has been partially attributed to intrinsic and/or acquired resistance to TMZ through O6-methylguanine DNA methyltransferase (MGMT) promoter methylation status in the tumor. Methods A drug screening aimed at evaluating the potential recycling and repurposing of known drugs was conducted in TMZ-resistant GBM cell lines and primary cultures of newly diagnosed GBM with different MGMT promoter methylation status, phenotypic/genotypic background and subtype, and validated with sphere formation, cell migration assays, and quantitative invasive orthotopic in vivo models. Results We identified hydroxyurea (HU) to synergize with TMZ in GBM cells in culture and in vivo, irrespective of MGMT promoter methylation status, subtype, and/or stemness. HU acts specifically on the S-phase of the cell cycle by inhibiting the M2 unit of enzyme ribonucleotide reductase. Knockdown of this enzyme using RNA interference and other known chemical inhibitors exerted a similar effect to HU in combination with TMZ both in culture and in vivo. Conclusions We demonstrate preclinical efficacy of repurposing hydroxyurea in combination with TMZ for adjuvant GBM therapy. This combination benefit is of direct clinical interest given the extensive use of TMZ and the associated problems with TMZ-related resistance and treatment failure.
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10

Erales, Jenny, Virginie Marchand, Baptiste Panthu, et al. "Evidence for rRNA 2′-O-methylation plasticity: Control of intrinsic translational capabilities of human ribosomes." Proceedings of the National Academy of Sciences 114, no. 49 (2017): 12934–39. http://dx.doi.org/10.1073/pnas.1707674114.

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Ribosomal RNAs (rRNAs) are main effectors of messenger RNA (mRNA) decoding, peptide-bond formation, and ribosome dynamics during translation. Ribose 2′-O-methylation (2′-O-Me) is the most abundant rRNA chemical modification, and displays a complex pattern in rRNA. 2′-O-Me was shown to be essential for accurate and efficient protein synthesis in eukaryotic cells. However, whether rRNA 2′-O-Me is an adjustable feature of the human ribosome and a means of regulating ribosome function remains to be determined. Here we challenged rRNA 2′-O-Me globally by inhibiting the rRNA methyl-transferase fibrillarin in human cells. Using RiboMethSeq, a nonbiased quantitative mapping of 2′-O-Me, we identified a repertoire of 2′-O-Me sites subjected to variation and demonstrate that functional domains of ribosomes are targets of 2′-O-Me plasticity. Using the cricket paralysis virus internal ribosome entry site element, coupled to in vitro translation, we show that the intrinsic capability of ribosomes to translate mRNAs is modulated through a 2′-O-Me pattern and not by nonribosomal actors of the translational machinery. Our data establish rRNA 2′-O-Me plasticity as a mechanism providing functional specificity to human ribosomes.
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Dissertations / Theses on the topic "Quantitative chemical methylation"

1

Berardinelli, Anthony Michael. "Development of a Mass Spectrometry-Based Method for the Quantitation of Lysine Methylation." University of Toledo / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1483710924985294.

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