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Relevant bibliographies by topics / Epigenetic enzymes

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Journal articles

Academic literature on the topic 'Epigenetic enzymes'

Author: Grafiati

Published: 7 December 2024

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Journal articles on the topic "Epigenetic enzymes"

1

Zhang, Xiaolin, Zhen Dong, and Hongjuan Cui. "Interplay between Epigenetics and Cellular Metabolism in Colorectal Cancer." Biomolecules 11, no. 10 (2021): 1406. http://dx.doi.org/10.3390/biom11101406.

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Cellular metabolism alterations have been recognized as one of the most predominant hallmarks of colorectal cancers (CRCs). It is precisely regulated by many oncogenic signaling pathways in all kinds of regulatory levels, including transcriptional, post-transcriptional, translational and post-translational levels. Among these regulatory factors, epigenetics play an essential role in the modulation of cellular metabolism. On the one hand, epigenetics can regulate cellular metabolism via directly controlling the transcription of genes encoding metabolic enzymes of transporters. On the other hand

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2

Kringel, Dario, Sebastian Malkusch, and Jörn Lötsch. "Drugs and Epigenetic Molecular Functions. A Pharmacological Data Scientometric Analysis." International Journal of Molecular Sciences 22, no. 14 (2021): 7250. http://dx.doi.org/10.3390/ijms22147250.

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Interactions of drugs with the classical epigenetic mechanism of DNA methylation or histone modification are increasingly being elucidated mechanistically and used to develop novel classes of epigenetic therapeutics. A data science approach is used to synthesize current knowledge on the pharmacological implications of epigenetic regulation of gene expression. Computer-aided knowledge discovery for epigenetic implications of current approved or investigational drugs was performed by querying information from multiple publicly available gold-standard sources to (i) identify enzymes involved in c

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3

Ramarao-Milne, Priya, Olga Kondrashova, Sinead Barry, John D. Hooper, Jason S. Lee, and Nicola Waddell. "Histone Modifying Enzymes in Gynaecological Cancers." Cancers 13, no. 4 (2021): 816. http://dx.doi.org/10.3390/cancers13040816.

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Genetic and epigenetic factors contribute to the development of cancer. Epigenetic dysregulation is common in gynaecological cancers and includes altered methylation at CpG islands in gene promoter regions, global demethylation that leads to genome instability and histone modifications. Histones are a major determinant of chromosomal conformation and stability, and unlike DNA methylation, which is generally associated with gene silencing, are amenable to post-translational modifications that induce facultative chromatin regions, or condensed transcriptionally silent regions that decondense res

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4

Ruoß, Marc, Georg Damm, Massoud Vosough, et al. "Epigenetic Modifications of the Liver Tumor Cell Line HepG2 Increase Their Drug Metabolic Capacity." International Journal of Molecular Sciences 20, no. 2 (2019): 347. http://dx.doi.org/10.3390/ijms20020347.

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Although human liver tumor cells have reduced metabolic functions as compared to primary human hepatocytes (PHH) they are widely used for pre-screening tests of drug metabolism and toxicity. The aim of the present study was to modify liver cancer cell lines in order to improve their drug-metabolizing activities towards PHH. It is well-known that epigenetics is strongly modified in tumor cells and that epigenetic regulators influence the expression and function of Cytochrome P450 (CYP) enzymes through altering crucial transcription factors responsible for drug-metabolizing enzymes. Therefore, w

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5

Maleszewska, Marta, Bartosz Wojtas, Bartlomiej Gielniewski, et al. "ECOA-6. Genomic and transcriptomic analyses reveal diverse mechanisms responsible for deregulation of epigenetic enzyme/modifier expression in glioblastoma." Neuro-Oncology Advances 3, Supplement_2 (2021): ii2. http://dx.doi.org/10.1093/noajnl/vdab070.006.

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Abstract Malignant gliomas represent over 70% of primary brain tumors and the most deadly is glioblastoma (GBM, WHO grade IV), due to frequent dysfunctions of tumor suppressors or/and oncogenes. Recent whole genome studies of gliomas demonstrated that besides genetic alterations, epigenetic dysfunctions contribute to tumor development and progression. Alterations in genes encoding epigenetic enzyme/protein or aberrations in epigenetic modification pattern have been found in gliomas of lower grade, yet no epigenetic driver was identified in GBM. We sought to identify different mechanisms drivin

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6

Amsalem, Zohar, Tasleem Arif, Anna Shteinfer-Kuzmine, Vered Chalifa-Caspi, and Varda Shoshan-Barmatz. "The Mitochondrial Protein VDAC1 at the Crossroads of Cancer Cell Metabolism: The Epigenetic Link." Cancers 12, no. 4 (2020): 1031. http://dx.doi.org/10.3390/cancers12041031.

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Carcinogenesis is a complicated process that involves the deregulation of epigenetics, resulting in cellular transformational events, such as proliferation, differentiation, and metastasis. Most chromatin-modifying enzymes utilize metabolites as co-factors or substrates and thus are directly dependent on such metabolites as acetyl-coenzyme A, S-adenosylmethionine, and NAD+. Here, we show that using specific siRNA to deplete a tumor of VDAC1 not only led to reprograming of the cancer cell metabolism but also altered several epigenetic-related enzymes and factors. VDAC1, in the outer mitochondri

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7

Jelinek, Mary Anne. "Biochemical Assays for Epigenetic Enzymes." Genetic Engineering & Biotechnology News 36, no. 15 (2016): 16–17. http://dx.doi.org/10.1089/gen.36.15.08.

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8

Jasim, Dr Hiba Sabah. "The Role of Epigenetic Drugs in Cancer Therapy." South Asian Research Journal of Medical Sciences 4, no. 4 (2022): 54–62. http://dx.doi.org/10.36346/sarjms.2022.v04i04.001.

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Epigenetics refers to heritable and dynamic alterations in the whole genes which present in the sequence of nucleic acids. It consider as concurrent reaction with enzymes and several molecular ingredients. Epigenetic changes can cause the incorrect start of coding genes, allowing tumor development. Epigenetic modifiers are becoming potential targets in numerous malignant tumor therapies since they are sensitive to foreign drugs. Different epigenetic medicines that were lately refined and implicated in clinical experiences using of epigenetic medicines solitary or together with immunotherapy an

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9

Alghamdi, Bandar Ali, Intisar Mahmoud Aljohani, Bandar Ghazi Alotaibi, et al. "Studying Epigenetics of Cardiovascular Diseases on Chip Guide." Cardiogenetics 12, no. 3 (2022): 218–34. http://dx.doi.org/10.3390/cardiogenetics12030021.

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Epigenetics is defined as the study of inheritable changes in the gene expressions and phenotypes that occurs without altering the normal DNA sequence. These changes are mainly due to an alteration in chromatin or its packaging, which changes the DNA accessibility. DNA methylation, histone modification, and noncoding or microRNAs can best explain the mechanism of epigenetics. There are various DNA methylated enzymes, histone-modifying enzymes, and microRNAs involved in the cause of various CVDs (cardiovascular diseases) such as cardiac hypertrophy, heart failure, and hypertension. Moreover, va

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10

Bunsick, David A., Jenna Matsukubo, and Myron R. Szewczuk. "Cannabinoids Transmogrify Cancer Metabolic Phenotype via Epigenetic Reprogramming and a Novel CBD Biased G Protein-Coupled Receptor Signaling Platform." Cancers 15, no. 4 (2023): 1030. http://dx.doi.org/10.3390/cancers15041030.

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The concept of epigenetic reprogramming predicts long-term functional health effects. This reprogramming can be activated by exogenous or endogenous insults, leading to altered healthy and different disease states. The exogenous or endogenous changes that involve developing a roadmap of epigenetic networking, such as drug components on epigenetic imprinting and restoring epigenome patterns laid down during embryonic development, are paramount to establishing youthful cell type and health. This epigenetic landscape is considered one of the hallmarks of cancer. The initiation and progression of

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