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Journal articles on the topic 'Epigenetic enzymes'

Author: Grafiati

Published: 7 December 2024

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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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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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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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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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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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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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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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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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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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Meiliana, Anna, Nurrani Mustika Dewi, and Andi Wijaya. "Nutritional Influences on Epigenetics, Aging and Disease." Indonesian Biomedical Journal 11, no. 1 (2019): 16–29. http://dx.doi.org/10.18585/inabj.v11i1.780.

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BACKGROUND: Altered epigenetics is regarded to play quite a role in many chronic diseases including cancer, diabetes, obesity, dyslipidemia, hypertension and neurodegeneration, hence nutrition suggested to contribute in epigenetics and disease.CONTENT: Histone modifications, as a part of epigenetics mechanisms, depend on metabolites which acts as cofactors or substrates. Fluctuating levels of specific metabolites become the direct and rapid mechanisms to influence gene activity. Therefore, these metabolites may have a role as gatekeepers of chromatin, in chromatin landscape modulation as a res

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Yesayan, Alexander, Massimiliano Chetta, Bella Babayan, Tigran A. Yesayan Yesayan, Syuzanna Esoyan, and Garegin Sevoyan. "The epigenetic impact of daily diet food choices on human health and chronic diseases." Functional Foods in Health and Disease 14, no. 10 (2024): 739–50. http://dx.doi.org/10.31989/ffhd.v14i10.1464.

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Nutrition, certain lifestyle behaviors (smoking, drug, alcohol addictions, etc.) and environment all contribute to cancer and other lines development. Similarly, epigenetic pathways are known to occur at the intersection between the generally reversible effects of lifestyle or ecological factors and the irreversible alterations that explain numerous diseases. Chemoprevention is the process of intervening in the epigenome to mitigate the detrimental effects of environmental factors or certain lifestyles before they lead to significant consequences. DNA is permanently exposed to various substanc

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Sen, Rwik, and Christopher Barnes. "Do Transgenerational Epigenetic Inheritance and Immune System Development Share Common Epigenetic Processes?" Journal of Developmental Biology 9, no. 2 (2021): 20. http://dx.doi.org/10.3390/jdb9020020.

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Epigenetic modifications regulate gene expression for development, immune response, disease, and other processes. A major role of epigenetics is to control the dynamics of chromatin structure, i.e., the condensed packaging of DNA around histone proteins in eukaryotic nuclei. Key epigenetic factors include enzymes for histone modifications and DNA methylation, non-coding RNAs, and prions. Epigenetic modifications are heritable but during embryonic development, most parental epigenetic marks are erased and reset. Interestingly, some epigenetic modifications, that may be resulting from immune res

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Qureshi, Muhammad Zahid, Uteuliyev Yerzhan Sabitaliyevich, Marat Rabandiyarov, and Arystanbekov Talant Arystanbekuly. "Role of DNA Methyltransferases (DNMTs) in metastasis." Cellular and Molecular Biology 68, no. 1 (2022): 226–36. http://dx.doi.org/10.14715/cmb/2022.68.1.27.

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The DNA methyltransferase (DNMT) family constitutes a conserved set of DNA-modifying enzymes which have essential functions in the modulation of epigenetics. The fundamental role of epigenetic changes in carcinogenesis and metastasis is increasingly being appreciated. DNMTs (DNMT1, DNMT3A and DNMT3B) have been shown to drive metastasis. Epigenetic machinery is installed at the target sites for the regulation of a wide variety of genes. Moreover, microRNAs, long non-coding RNAs and circular RNAs also shape the epigenetic landscape during metastasis. In this review, we have provided a snapshot o

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Bontempo, Paola, Lucia Capasso, Luigi De Masi, Angela Nebbioso, and Daniela Rigano. "Therapeutic Potential of Natural Compounds Acting through Epigenetic Mechanisms in Cardiovascular Diseases: Current Findings and Future Directions." Nutrients 16, no. 15 (2024): 2399. http://dx.doi.org/10.3390/nu16152399.

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Cardiovascular diseases (CVDs) remain a leading global cause of morbidity and mortality. These diseases have a multifaceted nature being influenced by a multitude of biochemical, genetic, environmental, and behavioral factors. Epigenetic modifications have a crucial role in the onset and progression of CVD. Epigenetics, which regulates gene activity without altering the DNA’s primary structure, can modulate cardiovascular homeostasis through DNA methylation, histone modification, and non-coding RNA regulation. The effects of environmental stimuli on CVD are mediated by epigenetic changes, whic

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Zucconi, Beth E., and Philip A. Cole. "Allosteric regulation of epigenetic modifying enzymes." Current Opinion in Chemical Biology 39 (August 2017): 109–15. http://dx.doi.org/10.1016/j.cbpa.2017.05.015.

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Copeland, Robert A., Edward J. Olhava, and Margaret Porter Scott. "Targeting epigenetic enzymes for drug discovery." Current Opinion in Chemical Biology 14, no. 4 (2010): 505–10. http://dx.doi.org/10.1016/j.cbpa.2010.06.174.

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18

Sapozhnikov, Daniel M., and Moshe Szyf. "Increasing Specificity of Targeted DNA Methylation Editing by Non-Enzymatic CRISPR/dCas9-Based Steric Hindrance." Biomedicines 11, no. 5 (2023): 1238. http://dx.doi.org/10.3390/biomedicines11051238.

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As advances in genome engineering inch the technology towards wider clinical use—slowed by technical and ethical hurdles—a newer offshoot, termed “epigenome engineering”, offers the ability to correct disease-causing changes in the DNA without changing its sequence and, thus, without some of the unfavorable correlates of doing so. In this review, we note some of the shortcomings of epigenetic editing technology—specifically the risks involved in the introduction of epigenetic enzymes—and highlight an alternative epigenetic editing strategy using physical occlusion to modify epigenetic marks at

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Li, Yinglu, Zhiming Li, and Wei-Guo Zhu. "Molecular Mechanisms of Epigenetic Regulators as Activatable Targets in Cancer Theranostics." Current Medicinal Chemistry 26, no. 8 (2019): 1328–50. http://dx.doi.org/10.2174/0929867324666170921101947.

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Epigenetics is defined as somatically inheritable changes that are not accompanied by alterations in DNA sequence. Epigenetics encompasses DNA methylation, covalent histone modifications, non-coding RNA as well as nucleosome remodeling. Notably, abnormal epigenetic changes play a critical role in cancer development including malignant transformation, metastasis, prognosis, drug resistance and tumor recurrence, which can provide effective targets for cancer prognosis, diagnosis and therapy. Understanding these changes provide effective means for cancer diagnosis and druggable targets for better

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Lachat, Camille, Diane Bruyère, Amandine Etcheverry, et al. "EZH2 and KDM6B Expressions Are Associated with Specific Epigenetic Signatures during EMT in Non Small Cell Lung Carcinomas." Cancers 12, no. 12 (2020): 3649. http://dx.doi.org/10.3390/cancers12123649.

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The role of Epigenetics in Epithelial Mesenchymal Transition (EMT) has recently emerged. Two epigenetic enzymes with paradoxical roles have previously been associated to EMT, EZH2 (Enhancer of Zeste 2 Polycomb Repressive Complex 2 (PRC2) Subunit), a lysine methyltranserase able to add the H3K27me3 mark, and the histone demethylase KDM6B (Lysine Demethylase 6B), which can remove the H3K27me3 mark. Nevertheless, it still remains unclear how these enzymes, with apparent opposite activities, could both promote EMT. In this study, we evaluated the function of these two enzymes using an EMT-inducibl

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Neff, Tobias, and Scott A. Armstrong. "Recent progress toward epigenetic therapies: the example of mixed lineage leukemia." Blood 121, no. 24 (2013): 4847–53. http://dx.doi.org/10.1182/blood-2013-02-474833.

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Abstract The importance of epigenetic gene regulatory mechanisms in normal and cancer development is increasingly evident. Genome-wide analyses have revealed the mutation, deletion, and dysregulated expression of chromatin-modifying enzymes in a number of cancers, including hematologic malignancies. Genome-wide studies of DNA methylation and histone modifications are beginning to reveal the landscape of cancer-specific chromatin patterns. In parallel, recent genetic loss-of-function studies in murine models are demonstrating functional involvement of chromatin-modifying enzymes in malignant ce

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Balch, Curt, Fang Fang, Daniela E. Matei, Tim H. M. Huang, and Kenneth P. Nephew. "Minireview: Epigenetic Changes in Ovarian Cancer." Journal of Clinical Endocrinology & Metabolism 94, no. 8 (2009): 3098. http://dx.doi.org/10.1210/jcem.94.8.9998.

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Epigenetic aberrations, including DNA methylation, histone modifications, and micro-RNA dysregulation, are now well established in the development and progression of ovarian cancer, and their gradual accumulation is associated with advancing disease stage and grade. Epigenetic aberrations are relatively stable, associated with distinct disease subtypes, and present in circulating serum, representing promising diagnostic, prognostic, and pharmacodynamic biomarkers. In contrast to DNA mutations and deletions, aberrant gene-repressive epigenetic modifications are potentially reversible by epigene

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Balch, Curt, Fang Fang, Daniela E. Matei, Tim H. M. Huang, and Kenneth P. Nephew. "Minireview: Epigenetic Changes in Ovarian Cancer." Journal of Clinical Endocrinology & Metabolism 94, no. 9 (2009): 3617. http://dx.doi.org/10.1210/jcem.94.9.9997.

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Epigenetic aberrations, including DNA methylation, histone modifications, and micro-RNA dysregulation, are now well established in the development and progression of ovarian cancer, and their gradual accumulation is associated with advancing disease stage and grade. Epigenetic aberrations are relatively stable, associated with distinct disease subtypes, and present in circulating serum, representing promising diagnostic, prognostic, and pharmacodynamic biomarkers. In contrast to DNA mutations and deletions, aberrant gene-repressive epigenetic modifications are potentially reversible by epigene

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Balch, Curt, Fang Fang, Daniela E. Matei, Tim H. M. Huang, and Kenneth P. Nephew. "Minireview: Epigenetic Changes in Ovarian Cancer." Endocrinology 150, no. 9 (2009): 4003–11. http://dx.doi.org/10.1210/en.2009-0404.

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Abstract Epigenetic aberrations, including DNA methylation, histone modifications, and micro-RNA dysregulation, are now well established in the development and progression of ovarian cancer, and their gradual accumulation is associated with advancing disease stage and grade. Epigenetic aberrations are relatively stable, associated with distinct disease subtypes, and present in circulating serum, representing promising diagnostic, prognostic, and pharmacodynamic biomarkers. In contrast to DNA mutations and deletions, aberrant gene-repressive epigenetic modifications are potentially reversible b

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Coker, Sharna J., Carlos C. Smith-Díaz, Rebecca M. Dyson, Margreet C. M. Vissers, and Mary J. Berry. "The Epigenetic Role of Vitamin C in Neurodevelopment." International Journal of Molecular Sciences 23, no. 3 (2022): 1208. http://dx.doi.org/10.3390/ijms23031208.

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The maternal diet during pregnancy is a key determinant of offspring health. Early studies have linked poor maternal nutrition during gestation with a propensity for the development of chronic conditions in offspring. These conditions include cardiovascular disease, type 2 diabetes and even compromised mental health. While multiple factors may contribute to these outcomes, disturbed epigenetic programming during early development is one potential biological mechanism. The epigenome is programmed primarily in utero, and during this time, the developing fetus is highly susceptible to environment

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Clark, Daniel F., Rachael Schmelz, Nicole Rogers, Nuri E. Smith, and Kimberly R. Shorter. "Acute high folic acid treatment in SH-SY5Y cells with and without MTHFR function leads to gene expression changes in epigenetic modifying enzymes, changes in epigenetic marks, and changes in dendritic spine densities." PLOS ONE 16, no. 1 (2021): e0245005. http://dx.doi.org/10.1371/journal.pone.0245005.

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Epigenetics are known to be involved in various disorders, including neurobiological disorders like autism. Dietary factors such as folic acid can affect epigenetic marks using methylenetetrahydrofolate reductase (MTHFR) to metabolize folic acid to a one-carbon methyl group. As MTHFR mutations are frequent, it is curious as to whether excess folic acid, with or without functioning MTHFR, could affect gene expression, epigenetics, and neuromorphology. Here, we investigated gene expression and activity of epigenetic modifying enzymes, genome-wide DNA methylation, histone 3 modifications, and den

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Skalnik, David G. "The epigenetic regulator Cfp1." BioMolecular Concepts 1, no. 5-6 (2010): 325–34. http://dx.doi.org/10.1515/bmc.2010.031.

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AbstractNumerous epigenetic modifications have been identified and correlated with transcriptionally active euchromatin or repressed heterochromatin and many enzymes responsible for the addition and removal of these marks have been characterized. However, less is known regarding how these enzymes are regulated and targeted to appropriate genomic locations. Mammalian CXXC finger protein 1 is an epigenetic regulator that was originally identified as a protein that binds specifically to any DNA sequence containing an unmethylated CpG dinucleotide. Mouse embryos lacking CXXC finger protein 1 die p

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Liu, Yu’e, Chao Chen, Xinye Wang, et al. "An Epigenetic Role of Mitochondria in Cancer." Cells 11, no. 16 (2022): 2518. http://dx.doi.org/10.3390/cells11162518.

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Mitochondria are not only the main energy supplier but are also the cell metabolic center regulating multiple key metaborates that play pivotal roles in epigenetics regulation. These metabolites include acetyl-CoA, α-ketoglutarate (α-KG), S-adenosyl methionine (SAM), NAD+, and O-linked beta-N-acetylglucosamine (O-GlcNAc), which are the main substrates for DNA methylation and histone post-translation modifications, essential for gene transcriptional regulation and cell fate determination. Tumorigenesis is attributed to many factors, including gene mutations and tumor microenvironment. Mitochond

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Symeonidis, Argiris, Theodora Chatzilygeroudi, Vasiliki Chondrou, and Argyro Sgourou. "Contingent Synergistic Interactions between Non-Coding RNAs and DNA-Modifying Enzymes in Myelodysplastic Syndromes." International Journal of Molecular Sciences 23, no. 24 (2022): 16069. http://dx.doi.org/10.3390/ijms232416069.

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Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal hematopoietic stem cell disorders with maturation and differentiation defects exhibiting morphological dysplasia in one or more hematopoietic cell lineages. They are associated with peripheral blood cytopenias and by increased risk for progression into acute myelogenous leukemia. Among their multifactorial pathogenesis, age-related epigenetic instability and the error-rate DNA methylation maintenance have been recognized as critical factors for both the initial steps of their pathogenesis and for disease progression. Although

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Consalvi, Silvia, Martina Sandoná, and Valentina Saccone. "Epigenetic Reprogramming of Muscle Progenitors: Inspiration for Clinical Therapies." Stem Cells International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/6093601.

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In the context of regenerative medicine, based on the potential of stem cells to restore diseased tissues, epigenetics is becoming a pivotal area of interest. Therapeutic interventions that promote tissue and organ regeneration have as primary objective the selective control of gene expression in adult stem cells. This requires a deep understanding of the epigenetic mechanisms controlling transcriptional programs in tissue progenitors. This review attempts to elucidate the principle epigenetic regulations responsible of stem cells differentiation. In particular we focus on the current understa

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Crispo, Fabiana, Michele Pietrafesa, Valentina Condelli, et al. "IDH1 Targeting as a New Potential Option for Intrahepatic Cholangiocarcinoma Treatment—Current State and Future Perspectives." Molecules 25, no. 16 (2020): 3754. http://dx.doi.org/10.3390/molecules25163754.

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Cholangiocarcinoma is a primary malignancy of the biliary tract characterized by late and unspecific symptoms, unfavorable prognosis, and few treatment options. The advent of next-generation sequencing has revealed potential targetable or actionable molecular alterations in biliary tumors. Among several identified genetic alterations, the IDH1 mutation is arousing interest due to its role in epigenetic and metabolic remodeling. Indeed, some IDH1 point mutations induce widespread epigenetic alterations by means of a gain-of-function of the enzyme, which becomes able to produce the oncometabolit

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Blanquart, Christophe, Camille Linot, Pierre-François Cartron, Daniela Tomaselli, Antonello Mai, and Philippe Bertrand. "Epigenetic Metalloenzymes." Current Medicinal Chemistry 26, no. 15 (2019): 2748–85. http://dx.doi.org/10.2174/0929867325666180706105903.

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Epigenetics controls the expression of genes and is responsible for cellular phenotypes. The fundamental basis of these mechanisms involves in part the post-translational modifications (PTMs) of DNA and proteins, in particular, the nuclear histones. DNA can be methylated or demethylated on cytosine. Histones are marked by several modifications including acetylation and/or methylation, and of particular importance are the covalent modifications of lysine. There exists a balance between addition and removal of these PTMs, leading to three groups of enzymes involved in these processes: the writer

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Kolarz, Bogdan, and Maria Majdan. "Epigenetic determinants in rheumatoid arthritis: the influence of DNA methylation and histone modifications." Postępy Higieny i Medycyny Doświadczalnej 71 (December 22, 2017): 0. http://dx.doi.org/10.5604/01.3001.0010.7478.

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Epigenetics is a field of science which describes external and environmental modifications to DNA without altering their primary sequences of nucleotides. Contrary to genetic changes, epigenetic modifications are reversible. The epigenetic changes appear as a result of the influence of external factors, such as diet or stress. Epigenetic mechanisms alter the accessibility of DNA by methylation of DNA or post-translational modifications of histones (acetylation, methylation, phosphorylation, ubiquitinqation). The extent of DNA methylation depends on the balance between DNA methyltransferases an

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Huang, Yi, Laurence J. Marton, Patrick M. Woster, and Robert A. Casero. "Polyamine analogues targeting epigenetic gene regulation." Essays in Biochemistry 46 (October 30, 2009): 95–110. http://dx.doi.org/10.1042/bse0460007.

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Over the past three decades the metabolism and functions of the polyamines have been actively pursued as targets for antineoplastic therapy. Interactions between cationic polyamines and negatively charged nucleic acids play a pivotal role in DNA stabilization and RNA processing that may affect gene expression, translation and protein activity. Our growing understanding of the unique roles that the polyamines play in chromatin regulation, and the discovery of novel proteins homologous with specific regulatory enzymes in polyamine metabolism, have led to our interest in exploring chromatin remod

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Wjst, Matthias, Irene Heimbeck, David Kutschke, and Katrin Pukelsheim. "Epigenetic regulation of vitamin D converting enzymes." Journal of Steroid Biochemistry and Molecular Biology 121, no. 1-2 (2010): 80–83. http://dx.doi.org/10.1016/j.jsbmb.2010.03.056.

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Lu, Duo. "Epigenetic modification enzymes: catalytic mechanisms and inhibitors." Acta Pharmaceutica Sinica B 3, no. 3 (2013): 141–49. http://dx.doi.org/10.1016/j.apsb.2013.04.007.

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Sibuh, Belay Zeleke, Sameer Quazi, Hrithika Panday, et al. "The Emerging Role of Epigenetics in Metabolism and Endocrinology." Biology 12, no. 2 (2023): 256. http://dx.doi.org/10.3390/biology12020256.

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Each cell in a multicellular organism has its own phenotype despite sharing the same genome. Epigenetics is a somatic, heritable pattern of gene expression or cellular phenotype mediated by structural changes in chromatin that occur without altering the DNA sequence. Epigenetic modification is an important factor in determining the level and timing of gene expression in response to endogenous and exogenous stimuli. There is also growing evidence concerning the interaction between epigenetics and metabolism. Accordingly, several enzymes that consume vital metabolites as substrates or cofactors

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Bridgeman, Stephanie, Wendy Northrop, Gaewyn Ellison, et al. "Statins Do Not Directly Inhibit the Activity of Major Epigenetic Modifying Enzymes." Cancers 11, no. 4 (2019): 516. http://dx.doi.org/10.3390/cancers11040516.

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The potential anticancer effects of statins—a widely used class of cholesterol lowering drugs—has generated significant interest, as has the use of epigenetic modifying drugs such as HDAC and DNMT inhibitors. We set out to investigate the effect of statin drugs on epigenetic modifications in multiple cell lines, including hepatocellular carcinoma, breast carcinoma, leukemic macrophages, cervical adenocarcinoma, and insulin-secreting cells, as well as liver extracts from statin-treated C57B1/6J mice. Cells or cell extracts were treated with statins and with established epigenetic modulators, an

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Park, Lara K., Simonetta Friso, and Sang-Woon Choi. "Nutritional influences on epigenetics and age-related disease." Proceedings of the Nutrition Society 71, no. 1 (2011): 75–83. http://dx.doi.org/10.1017/s0029665111003302.

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Nutritional epigenetics has emerged as a novel mechanism underlying gene–diet interactions, further elucidating the modulatory role of nutrition in aging and age-related disease development. Epigenetics is defined as a heritable modification to the DNA that regulates chromosome architecture and modulates gene expression without changes in the underlying bp sequence, ultimately determining phenotype from genotype. DNA methylation and post-translational histone modifications are classical levels of epigenetic regulation. Epigenetic phenomena are critical from embryonic development through the ag

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Illam, Soorya P., Sruthi P. Kandiyil, and Achuthan C. Raghavamenon. "Targeting Histone Onco- Modifications Using Plant-Derived Products." Current Drug Targets 22, no. 11 (2021): 1317–31. http://dx.doi.org/10.2174/1389450122666210118150716.

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The regulatory mechanisms lying over the genome that determines the differential expression of genes are termed epigenetic mechanisms. DNA methylation, acetylation, and phosphorylation of histone proteins and RNAi are typical examples. These epigenetic modifications are important determinants of normal growth and metabolism; at the same time, aberrant histone modifications play a major role in pathological conditions and are emerging as a new area of research for the last decades. Histone onco-modification is a term introduced by the scientific world to denote histone post-translational modifi

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Mora, Yuselin, María Elena Reyes, Louise Zanella, et al. "Resistance to platinum-based cancer drugs: a special focus on epigenetic mechanisms." Pharmacogenomics 22, no. 12 (2021): 777–90. http://dx.doi.org/10.2217/pgs-2021-0020.

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Chemoresistance is a significant clinical challenge, limiting the drug response in cancer. Several mechanisms associated with drug resistance have been characterized, and the role of epigenetics in generating resistance to platinum-based drugs has been clarified. Epigenetic mechanisms such as DNA methylation, histone modification, long noncoding RNA, and microRNA affect the expression of genes implicated in absorption, distribution, metabolism and excretion (ADME) of drugs, and other non-ADME genes that encode enzymes involved in the processes of cell proliferation, DNA repair, apoptosis and s

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Markouli, Mariam, Dimitrios Strepkos, and Christina Piperi. "Impact of Histone Modifications and Their Therapeutic Targeting in Hematological Malignancies." International Journal of Molecular Sciences 23, no. 21 (2022): 13657. http://dx.doi.org/10.3390/ijms232113657.

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Hematologic malignancies are a large and heterogeneous group of neoplasms characterized by complex pathogenetic mechanisms. The abnormal regulation of epigenetic mechanisms and specifically, histone modifications, has been demonstrated to play a central role in hematological cancer pathogenesis and progression. A variety of epigenetic enzymes that affect the state of histones have been detected as deregulated, being either over- or underexpressed, which induces changes in chromatin compaction and, subsequently, affects gene expression. Recent advances in the field of epigenetics have revealed

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Arif, K. M. Taufiqul, Esther K. Elliott, Larisa M. Haupt, and Lyn R. Griffiths. "Regulatory Mechanisms of Epigenetic miRNA Relationships in Human Cancer and Potential as Therapeutic Targets." Cancers 12, no. 10 (2020): 2922. http://dx.doi.org/10.3390/cancers12102922.

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Initiation and progression of cancer are under both genetic and epigenetic regulation. Epigenetic modifications including alterations in DNA methylation, RNA and histone modifications can lead to microRNA (miRNA) gene dysregulation and malignant cellular transformation and are hereditary and reversible. miRNAs are small non-coding RNAs which regulate the expression of specific target genes through degradation or inhibition of translation of the target mRNA. miRNAs can target epigenetic modifier enzymes involved in epigenetic modulation, establishing a trilateral regulatory “epi–miR–epi” feedba

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Kowluru, Renu A., Julia M. Santos, and Manish Mishra. "Epigenetic Modifications and Diabetic Retinopathy." BioMed Research International 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/635284.

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Diabetic retinopathy remains one of the most debilitating chronic complications, but despite extensive research in the field, the exact mechanism(s) responsible for how retina is damaged in diabetes remains ambiguous. Many metabolic pathways have been implicated in its development, and genes associated with these pathways are altered. Diabetic environment also facilitates epigenetics modifications, which can alter the gene expression without permanent changes in DNA sequence. The role of epigenetics in diabetic retinopathy is now an emerging area, and recent work has shown that genes encoding

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Abdulsalam, Mustapha, Fatima Umar Hamza, Fatima Abubakar Saddeeq, Hafsa Hamisu Ibrahim, Hafsa Ahmad Isa Dutse, and Aisha Mustapha Falaki. "Unveiling the Molecular Symphony: Exploring Mechanisms, Diversity and Applications of Restriction Enzymes in Biology." International Journal of Applied and Scientific Research 2, no. 3 (2024): 325–42. http://dx.doi.org/10.59890/ijasr.v2i3.1554.

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This research delves into the multifaceted role of restriction enzymes in molecular biology, examining their historical evolution, intricate mechanisms, and diverse applications. It aims to comprehensively understand their versatility and integration with modern technologies like CRISPR-Cas9, particularly in personalized medicine and gene therapy. Addressing a research gap in the synergism of restriction enzymes with CRISPR-Cas9 and their role in epigenetic modifications, qualitative methods critically assess existing literature and propose future research models. Findings highlight the potent

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Mohammed, Hero I., Sahar Hassannejad, and Hoshyar S. Ali. "Cancer Prevention by Epigenetic Modulation of Phytochemicals." Pharmacy and Applied Health Sciences 1, no. 2 (2022): 27–41. http://dx.doi.org/10.59480/phahs.v1i2.18.

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"Epigenetics," which emphasizes the impact of active dietary agents on the function of epigenetics, has become an exciting new field of study in recent years. Focusing on aberrant epigenetic alterations during earlier carcinogenesis has been considered in cancer chemotherapy research since, unlike genetic mutations, these differences are reversible. Genes that operate as signal transducers, nuclear receptors, cell cycle regulators, and transcription factors, among others, can be silenced by abnormal epigenetic processes such as DNA promoter methylation, histone changes, and post-transcriptiona

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Kadayifci, Fatma Zehra, Shasha Zheng, and Yuan-Xiang Pan. "Molecular Mechanisms Underlying the Link between Diet and DNA Methylation." International Journal of Molecular Sciences 19, no. 12 (2018): 4055. http://dx.doi.org/10.3390/ijms19124055.

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DNA methylation is a vital modification process in the control of genetic information, which contributes to the epigenetics by regulating gene expression without changing the DNA sequence. Abnormal DNA methylation—both hypomethylation and hypermethylation—has been associated with improper gene expression, leading to several disorders. Two types of risk factors can alter the epigenetic regulation of methylation pathways: genetic factors and modifiable factors. Nutrition is one of the strongest modifiable factors, which plays a direct role in DNA methylation pathways. Large numbers of studies ha

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Butler, Jill S., and Sharon Y. R. Dent. "The role of chromatin modifiers in normal and malignant hematopoiesis." Blood 121, no. 16 (2013): 3076–84. http://dx.doi.org/10.1182/blood-2012-10-451237.

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Abstract Complex developmental processes such as hematopoiesis require a series of precise and coordinated changes in cellular identity to ensure blood homeostasis. Epigenetic mechanisms help drive changes in gene expression that accompany the transition from hematopoietic stem cells to terminally differentiated blood cells. Genome-wide profiling technologies now provide valuable glimpses of epigenetic changes that occur during normal hematopoiesis, and genetic mouse models developed to investigate the in vivo functions of chromatin-modifying enzymes clearly demonstrate significant roles for t

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Wulansari, Noviana, Yanuar Alan Sulistio, Wahyu Handoko Wibowo Darsono, Chang-Hoon Kim, and Sang-Hun Lee. "LIF maintains mouse embryonic stem cells pluripotency by modulating TET1 and JMJD2 activity in a JAK2-dependent manner." Stem Cells 39, no. 6 (2021): 750–60. http://dx.doi.org/10.1002/stem.3345.

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Abstract The LIF-JAK2-STAT3 pathway is the central signal transducer that maintains undifferentiated mouse embryonic stem cells (mESCs), which is achieved by the recruitment of activated STAT3 to the master pluripotency genes and activation of the gene transcriptions. It remains unclear, however, how the epigenetic status required for the master gene transcriptions is built into LIF-treated mESC cultures. In this study, Jak2, but not Stat3, in the LIF canonical pathway, establishes an open epigenetic status in the pluripotency gene promoter regions. Upon LIF activation, cytosolic JAK2 was tran

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Pethő, Gábor, Boglárka Kántás, Ádám Horváth, and Erika Pintér. "The Epigenetics of Neuropathic Pain: A Systematic Update." International Journal of Molecular Sciences 24, no. 24 (2023): 17143. http://dx.doi.org/10.3390/ijms242417143.

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Epigenetics deals with alterations to the gene expression that occur without change in the nucleotide sequence in the DNA. Various covalent modifications of the DNA and/or the surrounding histone proteins have been revealed, including DNA methylation, histone acetylation, and methylation, which can either stimulate or inhibit protein expression at the transcriptional level. In the past decade, an exponentially increasing amount of data has been published on the association between epigenetic changes and the pathomechanism of pain, including its most challenging form, neuropathic pain. Epigenet

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