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1

McGowan, Patrick O., et Tania L. Roth. « Epigenetic pathways through which experiences become linked with biology ». Development and Psychopathology 27, no 2 (mai 2015) : 637–48. http://dx.doi.org/10.1017/s0954579415000206.

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AbstractThis article highlights the defining principles, progress, and future directions in epigenetics research in relation to this Special Issue. Exciting studies in the fields of neuroscience, psychology, and psychiatry have provided new insights into the epigenetic factors (e.g., DNA methylation) that are responsive to environmental input and serve as biological pathways in behavioral development. Here we highlight the experimental evidence, mainly from animal models, that factors such as psychosocial stress and environmental adversity can become encoded within epigenetic factors with functional consequences for brain plasticity and behavior. We also highlight evidence that epigenetic marking of genes in one generation can have consequences for future generations (i.e., inherited), and work with humans linking epigenetics, cognitive dysfunction, and psychiatric disorder. Though epigenetics has offered more of a beginning than an answer to the centuries-old nature–nurture debate, continued research is certain to yield substantial information regarding biological determinants of central nervous system changes and behavior with relevance for the study of developmental psychopathology.
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Ganesan, A. « Epigenetics : the first 25 centuries ». Philosophical Transactions of the Royal Society B : Biological Sciences 373, no 1748 (23 avril 2018) : 20170067. http://dx.doi.org/10.1098/rstb.2017.0067.

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Epigenetics is a natural progression of genetics as it aims to understand how genes and other heritable elements are regulated in eukaryotic organisms. The history of epigenetics is briefly reviewed, together with the key issues in the field today. This themed issue brings together a diverse collection of interdisciplinary reviews and research articles that showcase the tremendous recent advances in epigenetic chemical biology and translational research into epigenetic drug discovery. This article is part of a discussion meeting issue ‘Frontiers in epigenetic chemical biology’.
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Ivanova, Elitsa, Sandrine Le Guillou, Cathy Hue-Beauvais et Fabienne Le Provost. « Epigenetics : New Insights into Mammary Gland Biology ». Genes 12, no 2 (5 février 2021) : 231. http://dx.doi.org/10.3390/genes12020231.

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The mammary gland undergoes important anatomical and physiological changes from embryogenesis through puberty, pregnancy, lactation and involution. These steps are under the control of a complex network of molecular factors, in which epigenetic mechanisms play a role that is increasingly well described. Recently, studies investigating epigenetic modifications and their impacts on gene expression in the mammary gland have been performed at different physiological stages and in different mammary cell types. This has led to the establishment of a role for epigenetic marks in milk component biosynthesis. This review aims to summarize the available knowledge regarding the involvement of the four main molecular mechanisms in epigenetics: DNA methylation, histone modifications, polycomb protein activity and non-coding RNA functions.
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Linquist, Stefan, et Brady Fullerton. « Transposon dynamics and the epigenetic switch hypothesis ». Theoretical Medicine and Bioethics 42, no 3-4 (août 2021) : 137–54. http://dx.doi.org/10.1007/s11017-021-09548-x.

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AbstractThe recent explosion of interest in epigenetics is often portrayed as the dawning of a scientific revolution that promises to transform biomedical science along with developmental and evolutionary biology. Much of this enthusiasm surrounds what we call the epigenetic switch hypothesis, which regards certain examples of epigenetic inheritance as an adaptive organismal response to environmental change. This interpretation overlooks an alternative explanation in terms of coevolutionary dynamics between parasitic transposons and the host genome. This raises a question about whether epigenetics researchers tend to overlook transposon dynamics more generally. To address this question, we surveyed a large sample of scientific publications on the topics of epigenetics and transposons over the past fifty years. We found that enthusiasm for epigenetics is often inversely related to interest in transposon dynamics across the four disciplines we examined. Most surprising was a declining interest in transposons within biomedical science and cellular and molecular biology over the past two decades. Also notable was a delayed and relatively muted enthusiasm for epigenetics within evolutionary biology. An analysis of scientific abstracts from the past twenty-five years further reveals systematic differences among disciplines in their uses of the term epigenetic, especially with respect to heritability commitments and functional interpretations. Taken together, these results paint a nuanced picture of the rise of epigenetics and the possible neglect of transposon dynamics, especially among biomedical scientists.
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de Lima Camillo, Lucas Paulo, et Robert B. A. Quinlan. « A ride through the epigenetic landscape : aging reversal by reprogramming ». GeroScience 43, no 2 (avril 2021) : 463–85. http://dx.doi.org/10.1007/s11357-021-00358-6.

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AbstractAging has become one of the fastest-growing research topics in biology. However, exactly how the aging process occurs remains unknown. Epigenetics plays a significant role, and several epigenetic interventions can modulate lifespan. This review will explore the interplay between epigenetics and aging, and how epigenetic reprogramming can be harnessed for age reversal. In vivo partial reprogramming holds great promise as a possible therapy, but several limitations remain. Rejuvenation by reprogramming is a young but rapidly expanding subfield in the biology of aging.
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Riddiough, G. « MOLECULAR BIOLOGY : Epigenetic Origins ». Science 305, no 5682 (16 juillet 2004) : 311b. http://dx.doi.org/10.1126/science.305.5682.311b.

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Mir, Snober Shabnam, Uzma Afaq, Adria Hasan, Suroor Fatima Rizvi et Sana Parveen. « Novel Insights into Epigenetic Control of Autophagy in Cancer ». OBM Genetics 06, no 04 (8 novembre 2022) : 1–45. http://dx.doi.org/10.21926/obm.genet.2204170.

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The autophagy mechanism recycles the damaged and long-standing macromolecular substrates and thus maintains cellular homeostatic and proteostatic conditions. Autophagy can be an unavoidable target in cancer therapy because its deregulation leads to cancer formation and progression. Cancer can be controlled by regulating autophagy at different genetic, epigenetic, and post-translational levels. Epigenetics refers to the heritable phenotypic changes that affect gene activity without changing the sequence. Modern biology employs epigenetic alterations as molecular tools to detect and treat a wide range of disorders, including cancer. However, modulating autophagy at the epigenetic level may inhibit cancer growth and progression. Epigenetics-targeting drugs involved in preclinical and clinical trials may trigger antitumor immunity. Here, we have reviewed some experimental evidence in which epigenetics have been used to control deregulated autophagy in cancerous diseases. Furthermore, we also reviewed some current clinical trials of epigenetic therapy against cancer. We hope that this information can be utilized in the near future to treat and overcome cancer.
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Sen, Rwik, et Christopher Barnes. « Do Transgenerational Epigenetic Inheritance and Immune System Development Share Common Epigenetic Processes ? » Journal of Developmental Biology 9, no 2 (12 mai 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 response to stimuli, can escape remodeling and transmit to subsequent generations who are not exposed to those stimuli. This phenomenon is called transgenerational epigenetic inheritance if the epigenetic phenotype persists beyond the third generation in female germlines and second generation in male germlines. Although its primary function is likely immune response for survival, its role in the development and functioning of the immune system is not extensively explored, despite studies reporting transgenerational inheritance of stress-induced epigenetic modifications resulting in immune disorders. Hence, this review draws from studies on transgenerational epigenetic inheritance, immune system development and function, high-throughput epigenetics tools to study those phenomena, and relevant clinical trials, to focus on their significance and deeper understanding for future research, therapeutic developments, and various applications.
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Peixoto, Paul, Pierre-François Cartron, Aurélien A. Serandour et Eric Hervouet. « From 1957 to Nowadays : A Brief History of Epigenetics ». International Journal of Molecular Sciences 21, no 20 (14 octobre 2020) : 7571. http://dx.doi.org/10.3390/ijms21207571.

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Due to the spectacular number of studies focusing on epigenetics in the last few decades, and particularly for the last few years, the availability of a chronology of epigenetics appears essential. Indeed, our review places epigenetic events and the identification of the main epigenetic writers, readers and erasers on a historic scale. This review helps to understand the increasing knowledge in molecular and cellular biology, the development of new biochemical techniques and advances in epigenetics and, more importantly, the roles played by epigenetics in many physiological and pathological situations.
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Pacini, Clare, et Magdalena J. Koziol. « Bioinformatics challenges and perspectives when studying the effect of epigenetic modifications on alternative splicing ». Philosophical Transactions of the Royal Society B : Biological Sciences 373, no 1748 (23 avril 2018) : 20170073. http://dx.doi.org/10.1098/rstb.2017.0073.

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It is widely known that epigenetic modifications are important in regulating transcription, but several have also been reported in alternative splicing. The regulation of pre-mRNA splicing is important to explain proteomic diversity and the misregulation of splicing has been implicated in many diseases. Here, we give a brief overview of the role of epigenetics in alternative splicing and disease. We then discuss the bioinformatics methods that can be used to model interactions between epigenetic marks and regulators of splicing. These models can be used to identify alternative splicing and epigenetic changes across different phenotypes. This article is part of a discussion meeting issue ‘Frontiers in epigenetic chemical biology’.
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Nilsson, Eric, Millissia Ben Maamar et Michael K. Skinner. « Environmental impacts on sperm and oocyte epigenetics affect embryo cell epigenetics and transcription to promote the epigenetic inheritance of pathology and phenotypic variation ». Reproduction, Fertility and Development 33, no 2 (2021) : 102. http://dx.doi.org/10.1071/rd20255.

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Previous studies have demonstrated that exposure to environmental factors can cause epigenetic modifications to germ cells, particularly sperm, to promote epigenetic and transcriptome changes in the embryo. These germ cell and embryo cell epigenetic alterations are associated with phenotypic changes in offspring. Epigenetic inheritance requires epigenetic changes (i.e. epimutations) in germ cells that promote epigenetic and gene expression changes in embryos. The objective of this perspective is to examine the evidence that germ cell epigenome modifications are associated with embryo cell epigenetic and transcriptome changes that affect the subsequent development of all developing somatic cells to promote phenotype change. Various epigenetic changes in sperm, including changes to histone methylation, histone retention, non-coding RNA expression and DNA methylation, have been associated with alterations in embryo cell epigenetics and gene expression. Few studies have investigated this link for oocytes. The studies reviewed herein support the idea that environmentally induced epigenetic changes in germ cells affect alterations in embryo cell epigenetics and transcriptomes that have an important role in the epigenetic inheritance of pathology and phenotypic change.
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Nilsson, Eric, Millissia Ben Maamar et Michael K. Skinner. « Environmental impacts on sperm and oocyte epigenetics affect embryo cell epigenetics and transcription to promote the epigenetic inheritance of pathology and phenotypic variation ». Reproduction, Fertility and Development 33, no 2 (2021) : 102. http://dx.doi.org/10.1071/rd20255.

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Previous studies have demonstrated that exposure to environmental factors can cause epigenetic modifications to germ cells, particularly sperm, to promote epigenetic and transcriptome changes in the embryo. These germ cell and embryo cell epigenetic alterations are associated with phenotypic changes in offspring. Epigenetic inheritance requires epigenetic changes (i.e. epimutations) in germ cells that promote epigenetic and gene expression changes in embryos. The objective of this perspective is to examine the evidence that germ cell epigenome modifications are associated with embryo cell epigenetic and transcriptome changes that affect the subsequent development of all developing somatic cells to promote phenotype change. Various epigenetic changes in sperm, including changes to histone methylation, histone retention, non-coding RNA expression and DNA methylation, have been associated with alterations in embryo cell epigenetics and gene expression. Few studies have investigated this link for oocytes. The studies reviewed herein support the idea that environmentally induced epigenetic changes in germ cells affect alterations in embryo cell epigenetics and transcriptomes that have an important role in the epigenetic inheritance of pathology and phenotypic change.
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Karpenko, D. V., N. A. Petinati, N. J. Drize et A. E. Bigildeev. « The Role of epigenetic modifications of DNA and histones in the treatment of oncohematological diseases ». Russian journal of hematology and transfusiology 66, no 2 (2 septembre 2021) : 263–79. http://dx.doi.org/10.35754/0234-5730-2021-66-2-263-279.

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Introduction. Current knowledge of tumour biology attests a dual genetic and epigenetic nature of cancer cell abnormalities. Tumour epigenetics research provided insights into the key pathways mediating oncogenesis and facilitated novel epigenetic therapies.Aim — an overview of intricate involvement of epigenetic change in haematological morbidity and current therapeutic approaches to target the related mechanisms.Main findings. We review the best known epigenetic marks in tumour cells, e.g. DNA cytosine methylation, methylation and acetylation of histone proteins, the underlying enzymatic machinery and its role in oncogenesis. The epigenetic profile-changing drugs are described, including DNA hypomethylating agents, histone deacetylase and methylase inhibitors. A particular focus is made on substances currently approved in haematological therapy or undergoing clinical trial phases for future clinical availability.
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Minow, Mark A. A., et Joseph Colasanti. « Does variable epigenetic inheritance fuel plant evolution ? » Genome 63, no 5 (mai 2020) : 253–62. http://dx.doi.org/10.1139/gen-2019-0190.

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Epigenetic changes influence gene expression and contribute to the modulation of biological processes in response to the environment. Transgenerational epigenetic changes in gene expression have been described in many eukaryotes. However, plants appear to have a stronger propensity for inheriting novel epialleles. This mini-review discusses how plant traits, such as meristematic growth, totipotency, and incomplete epigenetic erasure in gametes promote epiallele inheritance. Additionally, we highlight how plant biology may be inherently tailored to reap the benefits of epigenetic metastability. Importantly, environmentally triggered small RNA expression and subsequent epigenetic changes may allow immobile plants to adapt themselves, and possibly their progeny, to thrive in local environments. The change of epigenetic states through the passage of generations has ramifications for evolution in the natural and agricultural world. In populations containing little genetic diversity, such as elite crop germplasm or habitually self-reproducing species, epigenetics may provide an important source of heritable phenotypic variation. Basic understanding of the processes that direct epigenetic shifts in the genome may allow for breeding or bioengineering for improved plant traits that do not require changes to DNA sequence.
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Venkatesh, Ishwariya, et Khadijah Makky. « Teaching Epigenetic Regulation of Gene Expression Is Critical in 21st-Century Science Education : Key Concepts & ; Teaching Strategies ». American Biology Teacher 82, no 6 (1 août 2020) : 372–80. http://dx.doi.org/10.1525/abt.2020.82.6.372.

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The field of epigenetics is progressing rapidly and becoming indispensable to the study of fundamental gene regulation. Recent advances are redefining our understanding of core components that regulate gene expression during development and in human diseases. Scientific knowledge on the importance of epigenetic regulation is now well known and accepted, and it is not surprising to see epigenetics being introduced into many biology curricula at the high school and college levels. Yet the core concepts of epigenetic regulation are differently perceived by the academic communities. Therefore, it is critical that fundamental concepts of epigenetic regulation are taught to the next generation in a simple yet precise manner to avoid any misconceptions. To that end, this article starts by distilling the extensive scientific literature on epigenetic control of gene regulation into a simple primer on the core fundamental concepts. Next and more importantly, it provides suggestions for student-friendly classroom practices and activities that are centered on these core concepts to ensure that students both recognize and retain knowledge on the importance of epigenetic control in eukaryotic gene regulation.
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GRANT-DOWNTON, R. T., et H. G. DICKINSON. « Epigenetics and its Implications for Plant Biology 2. The ‘Epigenetic Epiphany’ : Epigenetics, Evolution and Beyond ». Annals of Botany 97, no 1 (31 octobre 2005) : 11–27. http://dx.doi.org/10.1093/aob/mcj001.

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Teschendorff, Andrew E. « Epigenetic aging : insights from network biology ». Aging 5, no 10 (20 octobre 2013) : 719–20. http://dx.doi.org/10.18632/aging.100610.

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Choi, J. K. « Systems biology and epigenetic gene regulation ». IET Systems Biology 4, no 5 (1 septembre 2010) : 289–95. http://dx.doi.org/10.1049/iet-syb.2010.0008.

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Markoš, Anton, Eduard Gajdoš, László Hajnal et Fatima Cvrčková. « An epigenetic machine ». Sign Systems Studies 31, no 2 (31 décembre 2003) : 605–16. http://dx.doi.org/10.12697/sss.2003.31.2.16.

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Zaidi, Sayyed K., Daniel W. Young, Martin Montecino, Jane B. Lian, Janet L. Stein, Andre J. van Wijnen et Gary S. Stein. « Architectural Epigenetics : Mitotic Retention of Mammalian Transcriptional Regulatory Information ». Molecular and Cellular Biology 30, no 20 (9 août 2010) : 4758–66. http://dx.doi.org/10.1128/mcb.00646-10.

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ABSTRACT Epigenetic regulatory information must be retained during mammalian cell division to sustain phenotype-specific and physiologically responsive gene expression in the progeny cells. Histone modifications, DNA methylation, and RNA-mediated silencing are well-defined epigenetic mechanisms that control the cellular phenotype by regulating gene expression. Recent results suggest that the mitotic retention of nuclease hypersensitivity, selective histone marks, as well as the lineage-specific transcription factor occupancy of promoter elements contribute to the epigenetic control of sustained cellular identity in progeny cells. We propose that these mitotic epigenetic signatures collectively constitute architectural epigenetics, a novel and essential mechanism that conveys regulatory information to sustain the control of phenotype and proliferation in progeny cells by bookmarking genes for activation or suppression.
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Zhang, Xiaolin, Zhen Dong et Hongjuan Cui. « Interplay between Epigenetics and Cellular Metabolism in Colorectal Cancer ». Biomolecules 11, no 10 (25 septembre 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, epigenetics can regulate major transcriptional factors and signaling pathways that control the transcription of genes encoding metabolic enzymes or transporters, or affecting the translation, activation, stabilization, or translocation of metabolic enzymes or transporters. Interestingly, epigenetics can also be controlled by cellular metabolism. Metabolites not only directly influence epigenetic processes, but also affect the activity of epigenetic enzymes. Actually, both cellular metabolism pathways and epigenetic processes are controlled by enzymes. They are highly intertwined and are essential for oncogenesis and tumor development of CRCs. Therefore, they are potential therapeutic targets for the treatment of CRCs. In recent years, both epigenetic and metabolism inhibitors are studied for clinical use to treat CRCs. In this review, we depict the interplay between epigenetics and cellular metabolism in CRCs and summarize the underlying molecular mechanisms and their potential applications for clinical therapy.
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Lempiäinen, Joanna K., et Benjamin A. Garcia. « Characterizing crosstalk in epigenetic signaling to understand disease physiology ». Biochemical Journal 480, no 1 (11 janvier 2023) : 57–85. http://dx.doi.org/10.1042/bcj20220550.

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Epigenetics, the inheritance of genomic information independent of DNA sequence, controls the interpretation of extracellular and intracellular signals in cell homeostasis, proliferation and differentiation. On the chromatin level, signal transduction leads to changes in epigenetic marks, such as histone post-translational modifications (PTMs), DNA methylation and chromatin accessibility to regulate gene expression. Crosstalk between different epigenetic mechanisms, such as that between histone PTMs and DNA methylation, leads to an intricate network of chromatin-binding proteins where pre-existing epigenetic marks promote or inhibit the writing of new marks. The recent technical advances in mass spectrometry (MS) -based proteomic methods and in genome-wide DNA sequencing approaches have broadened our understanding of epigenetic networks greatly. However, further development and wider application of these methods is vital in developing treatments for disorders and pathologies that are driven by epigenetic dysregulation.
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Olmedo-Suárez, Miguel Ángel, Ivonne Ramírez-Díaz, Andrea Pérez-González, Alejandro Molina-Herrera, Miguel Ángel Coral-García, Sagrario Lobato, Pouya Sarvari, Guillermo Barreto et Karla Rubio. « Epigenetic Regulation in Exposome-Induced Tumorigenesis : Emerging Roles of ncRNAs ». Biomolecules 12, no 4 (28 mars 2022) : 513. http://dx.doi.org/10.3390/biom12040513.

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Environmental factors, including pollutants and lifestyle, constitute a significant role in severe, chronic pathologies with an essential societal, economic burden. The measurement of all environmental exposures and assessing their correlation with effects on individual health is defined as the exposome, which interacts with our unique characteristics such as genetics, physiology, and epigenetics. Epigenetics investigates modifications in the expression of genes that do not depend on the underlying DNA sequence. Some studies have confirmed that environmental factors may promote disease in individuals or subsequent progeny through epigenetic alterations. Variations in the epigenetic machinery cause a spectrum of different disorders since these mechanisms are more sensitive to the environment than the genome, due to the inherent reversible nature of the epigenetic landscape. Several epigenetic mechanisms, including modifications in DNA (e.g., methylation), histones, and noncoding RNAs can change genome expression under the exogenous influence. Notably, the role of long noncoding RNAs in epigenetic processes has not been well explored in the context of exposome-induced tumorigenesis. In the present review, our scope is to provide relevant evidence indicating that epigenetic alterations mediate those detrimental effects caused by exposure to environmental toxicants, focusing mainly on a multi-step regulation by diverse noncoding RNAs subtypes.
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Sharma, Abhay. « Transgenerational epigenetic inheritance : resolving uncertainty and evolving biology ». Biomolecular Concepts 6, no 2 (1 avril 2015) : 87–103. http://dx.doi.org/10.1515/bmc-2015-0005.

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AbstractTransgenerational epigenetic inheritance in animals has increasingly been reported in recent years. Controversies, however, surround this unconventional mode of heredity, especially in mammals, for several reasons. First, its existence itself has been questioned due to perceived insufficiency of available evidence. Second, it potentially implies transfer of hereditary information from soma to germline, against the established principle in biology. Third, it inherently requires survival of epigenetic memory across reprogramming, posing another fundamental challenge in biology. Fourth, evolutionary significance of epigenetic inheritance has also been under debate. This article pointwise addresses all these concerns on the basis of recent empirical, theoretical and conceptual advances. 1) Described here in detail are the key experimental findings demonstrating the occurrence of germline epigenetic inheritance in mammals. 2) Newly emerging evidence supporting soma to germline communication in transgenerational inheritance in mammals, and a role of exosome and extracellular microRNA in this transmission, is thoroughly discussed. 3) The plausibility of epigenetic information propagation across reprogramming is highlighted. 4) Analyses supporting evolutionary significance of epigenetic inheritance are briefly mentioned. Finally, an integrative model of ‘evolutionary transgenerational systems biology’ is proposed to provide a framework to guide future advancements in epigenetic inheritance.
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Moore-Morris, Thomas, Patrick Piet van Vliet, Gregor Andelfinger et Michel Puceat. « Role of Epigenetics in Cardiac Development and Congenital Diseases ». Physiological Reviews 98, no 4 (1 octobre 2018) : 2453–75. http://dx.doi.org/10.1152/physrev.00048.2017.

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The heart is the first organ to be functional in the fetus. Heart formation is a complex morphogenetic process regulated by both genetic and epigenetic mechanisms. Congenital heart diseases (CHD) are the most prominent congenital diseases. Genetics is not sufficient to explain these diseases or the impact of them on patients. Epigenetics is more and more emerging as a basis for cardiac malformations. This review brings the essential knowledge on cardiac biology of development. It further provides a broad background on epigenetics with a focus on three-dimensional conformation of chromatin. Then, we summarize the current knowledge of the impact of epigenetics on cardiac cell fate decision. We further provide an update on the epigenetic anomalies in the genesis of CHD.
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Heinbockel, Thomas, et Antonei Csoka. « Epigenetic Effects of Drugs of Abuse ». International Journal of Environmental Research and Public Health 15, no 10 (25 septembre 2018) : 2098. http://dx.doi.org/10.3390/ijerph15102098.

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Drug addiction affects a large extent of young people and disadvantaged populations. Drugs of abuse impede brain circuits or affect the functionality of brain circuits and interfere with bodily functions. Cannabinoids (Δ9-tetrahydrocannabinol) form key constituents of marijuana derived from the cannabis plant. Marijuana is a frequently used illegal drug in the USA. Here, we review the effects of cannabinoids at the epigenetic level and the potential role of these epigenetic effects in health and disease. Epigenetics is the study of alterations in gene expression that are transmitted across generations and take place without an alteration in DNA sequence, but are due to modulation of chromatin associated factors by environmental effects. Epigenetics is now known to offer an extra mechanism of control over transcription and how genes are expressed. Insights from research at the genetic and epigenetic level potentially provide venues that allow the translation of the biology of abused drugs to new means of how to treat marijuana substance use disorder or other addictions using pharmacotherapeutic tools.
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Wasti, Binaya, Shao-kun Liu et Xu-Dong Xiang. « Role of Epigenetics in the Pathogenesis, Treatment, Prediction, and Cellular Transformation of Asthma ». Mediators of Inflammation 2021 (15 septembre 2021) : 1–18. http://dx.doi.org/10.1155/2021/9412929.

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Asthma is a mysterious disease with heterogeneity in etiology, pathogenesis, and clinical phenotypes. Although ongoing studies have provided a better understanding of asthma, its natural history, progression, pathogenesis, diversified phenotypes, and even the exact epigenetic linkage between childhood asthma and adult-onset/old age asthma remain elusive in many aspects. Asthma heritability has been established through genetic studies, but genetics is not the only influencing factor in asthma. The increasing incidence and some unsolved queries suggest that there may be other elements related to asthma heredity. Epigenetic mechanisms link genetic and environmental factors with developmental trajectories in asthma. This review provides an overview of asthma epigenetics and its components, including several epigenetic studies on asthma, and discusses the epigenetic linkage between childhood asthma and adult-onset/old age asthma. Studies involving asthma epigenetics present valuable novel approaches to solve issues related to asthma. Asthma epigenetic research guides us towards gene therapy and personalized T cell therapy, directs the discovery of new therapeutic agents, predicts long-term outcomes in severe cases, and is also involved in the cellular transformation of childhood asthma to adult-onset/old age asthma.
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Gopinathan, Gokul, et Thomas G. H. Diekwisch. « Epigenetics and Early Development ». Journal of Developmental Biology 10, no 2 (16 juin 2022) : 26. http://dx.doi.org/10.3390/jdb10020026.

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The epigenome controls all aspect of eukaryotic development as the packaging of DNA greatly affects gene expression. Epigenetic changes are reversible and do not affect the DNA sequence itself but rather control levels of gene expression. As a result, the science of epigenetics focuses on the physical configuration of chromatin in the proximity of gene promoters rather than on the mechanistic effects of gene sequences on transcription and translation. In the present review we discuss three prominent epigenetic modifications, DNA methylation, histone methylation/acetylation, and the effects of chromatin remodeling complexes. Specifically, we introduce changes to the methylated state of DNA through DNA methyltransferases and DNA demethylases, discuss the effects of histone tail modifications such as histone acetylation and methylation on gene expression and present the functions of major ATPase subunit containing chromatin remodeling complexes. We also introduce examples of how changes in these epigenetic factors affect early development in humans and mice. In summary, this review provides an overview over the most important epigenetic mechanisms and provides examples of the dramatic effects of epigenetic changes in early mammalian development.
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Ben Maamar, Millissia, Eric E. Nilsson et Michael K. Skinner. « Epigenetic transgenerational inheritance, gametogenesis and germline development† ». Biology of Reproduction 105, no 3 (30 avril 2021) : 570–92. http://dx.doi.org/10.1093/biolre/ioab085.

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Abstract One of the most important developing cell types in any biological system is the gamete (sperm and egg). The transmission of phenotypes and optimally adapted physiology to subsequent generations is in large part controlled by gametogenesis. In contrast to genetics, the environment actively regulates epigenetics to impact the physiology and phenotype of cellular and biological systems. The integration of epigenetics and genetics is critical for all developmental biology systems at the cellular and organism level. The current review is focused on the role of epigenetics during gametogenesis for both the spermatogenesis system in the male and oogenesis system in the female. The developmental stages from the initial primordial germ cell through gametogenesis to the mature sperm and egg are presented. How environmental factors can influence the epigenetics of gametogenesis to impact the epigenetic transgenerational inheritance of phenotypic and physiological change in subsequent generations is reviewed.
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GRANT-DOWNTON, R. T., et H. G. DICKINSON. « Epigenetics and its Implications for Plant Biology. 1. The Epigenetic Network in Plants ». Annals of Botany 96, no 7 (27 octobre 2005) : 1143–64. http://dx.doi.org/10.1093/aob/mci273.

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Abdullah, Omeima, et Mahmoud Alhosin. « HAUSP Is a Key Epigenetic Regulator of the Chromatin Effector Proteins ». Genes 13, no 1 (24 décembre 2021) : 42. http://dx.doi.org/10.3390/genes13010042.

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HAUSP (herpes virus-associated ubiquitin-specific protease), also known as Ubiquitin Specific Protease 7, plays critical roles in cellular processes, such as chromatin biology and epigenetics, through the regulation of different signaling pathways. HAUSP is a main partner of the “Epigenetic Code Replication Machinery,” ECREM, a large protein complex that includes several epigenetic players, such as the ubiquitin-like containing plant homeodomain (PHD) and an interesting new gene (RING), finger domains 1 (UHRF1), as well as DNA methyltransferase 1 (DNMT1), histone deacetylase 1 (HDAC1), histone methyltransferase G9a, and histone acetyltransferase TIP60. Due to its deubiquitinase activity and its ability to team up through direct interactions with several epigenetic regulators, mainly UHRF1, DNMT1, TIP60, the histone lysine methyltransferase EZH2, and the lysine-specific histone demethylase LSD1, HAUSP positions itself at the top of the regulatory hierarchies involved in epigenetic silencing of tumor suppressor genes in cancer. This review highlights the increasing role of HAUSP as an epigenetic master regulator that governs a set of epigenetic players involved in both the maintenance of DNA methylation and histone post-translational modifications.
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Stanzione, Rosita, Maria Cotugno, Franca Bianchi, Simona Marchitti, Maurizio Forte, Massimo Volpe et Speranza Rubattu. « Pathogenesis of Ischemic Stroke : Role of Epigenetic Mechanisms ». Genes 11, no 1 (13 janvier 2020) : 89. http://dx.doi.org/10.3390/genes11010089.

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Epigenetics is the branch of molecular biology that studies modifications able to change gene expression without altering the DNA sequence. Epigenetic modulations include DNA methylation, histone modifications, and noncoding RNAs. These gene modifications are heritable and modifiable and can be triggered by lifestyle and nutritional factors. In recent years, epigenetic changes have been associated with the pathogenesis of several diseases such as diabetes, obesity, renal pathology, and different types of cancer. They have also been related with the pathogenesis of cardiovascular diseases including ischemic stroke. Importantly, since epigenetic modifications are reversible processes they could assist with the development of new therapeutic approaches for the treatment of human diseases. In the present review article, we aim to collect the most recent evidence concerning the impact of epigenetic modifications on the pathogenesis of ischemic stroke in both animal models and humans.
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Peedicayil, Jacob. « The role of epigenetics in social psychiatry ». International Journal of Social Psychiatry 63, no 1 (18 novembre 2016) : 14–20. http://dx.doi.org/10.1177/0020764016677556.

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Background: Epigenetics refers to the study of heritable changes in gene expression not involving changes in DNA sequence and is presently an active area of research in biology and medicine. There is increasing evidence that epigenetics is involved in the pathogenesis of psychiatric disorders. Aims and Methods: Several studies conducted to date have suggested that psychosocial factors act by modifying epigenetic mechanisms of gene expression in the brain in the pathogenesis of psychiatric disorders. Such studies have been conducted both on brain tissues and also using peripheral tissues as substitutes for brain tissues. This article reviews such studies. Results and Conclusion: Epigenetic mechanisms of gene expression in the brain appear to link one individual with another in the context of social psychiatry. Epigenetics appears to be of major importance to the field of social psychiatry.
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Waghmare, Sagar S., O. G. Bhusnure, M. R. Mali et S. T. Mule. « Epigenetics : Pharmacology and Modification Mechanisms Involved in Cardiac, Hepatic and Renal Disease ». Journal of Drug Delivery and Therapeutics 10, no 4 (15 juillet 2020) : 260–66. http://dx.doi.org/10.22270/jddt.v10i4.4148.

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For a long time scientists have tried to describe disorders are due to genetic as well as environmental factors. In the past few years, revolution in technology that has made it possible to decipher the human genome. Epigenetics explains the capability gene expression regulation without modifying the genetic sequence. Epigenetic mechanisms are rooted changes in molecules, or nuclear characteristics that can alter gene expression without altering the sequences of DNA, i.e. DNA methylation, histone modification, and non-coding RNAs. Learning of the fundamental epigenetic modification allowing gene expression as well as cellular phenotype are advanced that novel insights into the epigenetic control of cardiovascular disease, hepatic disease, as well as chronic kidney disease are now emerging. From a half of century ago, in human disease the role of epigenetics has been considered. This subject has attracted many interests in the past decade, especially in complicated diseases like cardiovascular disease, hepatic disease as well as chronic kidney disease. This review first illustrates the history and classification of epigenetic modifications and the factors (i.e. genetic, environment, dietary, thought process and lifestyle) affecting to the epigenetics mechanisms. Likewise, the epigenetics role in human diseases is think out by targeting on some diseases and at the end, we have given the future perspective of this field. This review article provides concepts with some examples to describe a broad view of distinct aspects of epigenetics in biology and human diseases. Keywords: - Epigenetics, DNA methylation, Histone modifications, microRNAs and Gene expression and Disease.
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Youngson, Neil A., et Margaret J. Morris. « What obesity research tells us about epigenetic mechanisms ». Philosophical Transactions of the Royal Society B : Biological Sciences 368, no 1609 (5 janvier 2013) : 20110337. http://dx.doi.org/10.1098/rstb.2011.0337.

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The pathophysiology of obesity is extremely complex and is associated with extensive gene expression changes in tissues throughout the body. This situation, combined with the fact that all gene expression changes are thought to have associated epigenetic changes, means that the links between obesity and epigenetics will undoubtedly be vast. Much progress in identifying epigenetic changes induced by (or inducing) obesity has already been made, with candidate and genome-wide approaches. These discoveries will aid the clinician through increasing our understanding of the inheritance, development and treatment of obesity. However, they are also of great value for epigenetic researchers, as they have revealed mechanisms of environmental interactions with epigenetics that can produce or perpetuate a disease state. Here, we will review the evidence for four mechanisms through which epigenetics contributes to obesity: as downstream effectors of environmental signals; through abnormal global epigenetic state driving obesogenic expression patterns; through facilitating developmental programming and through transgenerational epigenetic inheritance.
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Chen, Zhao-xia, et Arthur D. Riggs. « Maintenance and regulation of DNA methylation patterns in mammals ». Biochemistry and Cell Biology 83, no 4 (1 août 2005) : 438–48. http://dx.doi.org/10.1139/o05-138.

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Proper establishment and faithful maintenance of epigenetic information is crucial for the correct development of complex organisms. For mammals, it is now accepted that DNA methylation is an important mechanism for establishing stable heritable epigenetic marks. The distribution of methylation in the genome is not random, and patterns of methylated and unmethylated DNA are well regulated during normal development. The molecular mechanisms by which methylation patterns are established and maintained are complex and just beginning to be understood. In this review, we summarize recent progress in understanding the regulation of mammalian DNA methylation patterns, with an emphasis on the emerging roles of several protein and possible RNA factors. We also revisit the stochastic model of maintenance methylation and discuss its implications for epigenetic fidelity and gene regulation.Key words: Epigenetics, epigenetic fidelity, DNA methyltransferase, DNA demethylase, gene regulation.
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Holt, William V., et Pierre Comizzoli. « Conservation Biology and Reproduction in a Time of Developmental Plasticity ». Biomolecules 12, no 9 (14 septembre 2022) : 1297. http://dx.doi.org/10.3390/biom12091297.

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The objective of this review is to ask whether, and how, principles in conservation biology may need to be revisited in light of new knowledge about the power of epigenetics to alter developmental pathways. Importantly, conservation breeding programmes, used widely by zoological parks and aquariums, may appear in some cases to reduce fitness by decreasing animals’ abilities to cope when confronted with the ‘wild side’ of their natural habitats. Would less comfortable captive conditions lead to the selection of individuals that, despite being adapted to life in a captive environment, be better able to thrive if relocated to a more natural environment? While threatened populations may benefit from advanced reproductive technologies, these may actually induce undesirable epigenetic changes. Thus, there may be inherent risks to the health and welfare of offspring (as is suspected in humans). Advanced breeding technologies, especially those that aim to regenerate the rarest species using stem cell reprogramming and artificial gametes, may also lead to unwanted epigenetic modifications. Current knowledge is still incomplete, and therefore ethical decisions about novel breeding methods remain controversial and difficult to resolve.
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Berber, Andrea. « Is Lamarckism returning to evolutionary biology ? » Theoria, Beograd 63, no 2 (2020) : 119–34. http://dx.doi.org/10.2298/theo2002119b.

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In this paper, we address the question whether insights on the inheritance of environmentally induced epigenetic marks can be considered as the return to Lamarckism in evolutionary biology, as it is sometimes proclaimed. We analyze and clarify Lamarck?s understanding of the inheritance of acquired traits. After that, we briefly summarize the contemporary insights on the inheritance of acquired epigenetic marks. We differentiate between the two roles that epigenetic inheritance can play in the evolutionary process. For each of these roles, we analyze whether it can be seen as Lamarckism. The conclusion of our analysis is that neither of the two roles listed can be regarded as the return to Lamarckian concept of evolution.
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Verdikt, Roxane, et Patrick Allard. « Metabolo-epigenetics : the interplay of metabolism and epigenetics during early germ cells development† ». Biology of Reproduction 105, no 3 (16 juin 2021) : 616–24. http://dx.doi.org/10.1093/biolre/ioab118.

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Abstract Metabolites control epigenetic mechanisms, and conversly, cell metabolism is regulated at the epigenetic level in response to changes in the cellular environment. In recent years, this metabolo-epigenetic control of gene expression has been implicated in the regulation of multiple stages of embryonic development. The developmental potency of stem cells and their embryonic counterparts is directly determined by metabolic rewiring. Here, we review the current knowledge on the interplay between epigenetics and metabolism in the specific context of early germ cell development. We explore the implications of metabolic rewiring in primordial germ cells in light of their epigenetic remodeling during cell fate determination. Finally, we discuss the relevance of concerted metabolic and epigenetic regulation of primordial germ cells in the context of mammalian transgenerational epigenetic inheritance.
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Iyer, Sucharitha, et Sunita K. Agarwal. « Epigenetic regulation in the tumorigenesis of MEN1-associated endocrine cell types ». Journal of Molecular Endocrinology 61, no 1 (juillet 2018) : R13—R24. http://dx.doi.org/10.1530/jme-18-0050.

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Epigenetic regulation is emerging as a key feature in the molecular characteristics of various human diseases. Epigenetic aberrations can occur from mutations in genes associated with epigenetic regulation, improper deposition, removal or reading of histone modifications, DNA methylation/demethylation and impaired non-coding RNA interactions in chromatin. Menin, the protein product of the gene causative for the multiple endocrine neoplasia type 1 (MEN1) syndrome, interacts with chromatin-associated protein complexes and also regulates some non-coding RNAs, thus participating in epigenetic control mechanisms. Germline inactivating mutations in theMEN1gene that encodes menin predispose patients to develop endocrine tumors of the parathyroids, anterior pituitary and the duodenopancreatic neuroendocrine tissues. Therefore, functional loss of menin in the various MEN1-associated endocrine cell types can result in epigenetic changes that promote tumorigenesis. Because epigenetic changes are reversible, they can be targeted to develop therapeutics for restoring the tumor epigenome to the normal state. Irrespective of whether epigenetic alterations are the cause or consequence of the tumorigenesis process, targeting the endocrine tumor-associated epigenome offers opportunities for exploring therapeutic options. This review presents epigenetic control mechanisms relevant to the interactions and targets of menin, and the contribution of epigenetics in the tumorigenesis of endocrine cell types from menin loss.
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Karpathakis, A., H. Dibra et C. Thirlwell. « Neuroendocrine tumours : cracking the epigenetic code ». Endocrine-Related Cancer 20, no 3 (21 février 2013) : R65—R82. http://dx.doi.org/10.1530/erc-12-0338.

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The field of epigenetics has evolved rapidly over recent years providing insight into the tumorigenesis of many solid and haematological malignancies. Determination of epigenetic modifications in neuroendocrine tumour (NET) development is imperative if we are to improve our understanding of the biology of this heterogenous group of tumours. Epigenetic marks such as DNA methylation atRASSF1Aare frequent findings in NETs of all origins and may be associated with worse prognosis. MicroRNA signatures and histone modifications have been identified which can differentiate subtypes of NET and distinguish NET from adenocarcinoma in cases of diagnostic uncertainty. Historically, candidate gene-driven approaches have yielded limited insight into the epigenetics of NET. Recent progress has been facilitated by development of high-throughput tools including second-generation sequencing and arrays for analysis of the ‘epigenome’ of tumour and normal tissue, permitting unbiased approaches such as exome sequencing that identified mutations of chromatin-remodelling genesATRX/DAXXin 44% of pancreatic NETs. Epigenetic changes are reversible and therefore represent an attractive therapeutic target; to date, clinical outcomes of epigenetic therapies in solid tumours have been disappointing; however,in vitrostudies on NETs are promising and further clinical trials are required to determine utility of this class of novel agents. In this review, we perform a comprehensive evaluation of epigenetic changes found in NETs to date, including rare NETs such as phaeochromocytoma and adrenocortical tumours. We suggest priorities for future research and discuss potential clinical applications and novel therapies.
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Miller, Alexander, Catherine Malabou, Emily Apter, Peter Szendy, Emanuela Bianchi et Alexander R. Galloway. « On Epigenesis ». October, no 175 (2021) : 109–44. http://dx.doi.org/10.1162/octo_a_00418.

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Abstract “On Epigenesis” consists of a series of interrelated short articles examining the philosophical concept of epigenesis, with a particular focus on Catherine Malabou's development of it in contemporary thought. Alexander Miller introduces the topic of epigenesis and considers its significance as a new paradigm. He also presents the reader with an overview of Malabou's work on the topic: Drawing from recent advances in the life sciences as well as the Western philosophical tradition, he claims, Malabou has proposed “an epigenetic paradigm for rationality” for the 21st century. Catherine Malabou explains that when, in 2001, the scientific journal Nature published virtually the entire sequence of three billion bases that make up the human genome, people were surprised: Only five percent of the sequence turned out to actually be genes. Assembled in bunches and clusters, they are separated by vast expanses of so-called gene deserts made up of DNA characterized as “junk” or “repetitive,” which is to say, non-coding. The sequencing of the genome did not offer the revelations that people had expected, marking the end of the “everything is genetic” creed and announcing the rise of the “epigenetic paradigm.” The present article analyzes the implications of this new paradigm in biology, philosophy, and hermeneutics. Emily Apter situates Catherine Malabou's theory of epigenesis within a broader disciplinary context of Continental philosophy, the cognitive turn, and what a brain does or “is” as an object of aesthetic representation. Peter Szendy argues that even if they are not the central focus of her philosophical work, media and medial metaphors play a key role in Catherine Malabou's understanding of epigenetics. Indeed, her views on the epigenetic paradigm shift could lead to a rethinking of mediality. A medium, according to such an epigenetic approach, would be neither simply a storage space nor a carrier: It would be what happens along with the events (whether they involve works or data) that it hosts or transports. Emanuela Bianchi asks whether the epigenesis of “pure reason” can in any sense be “pure,” since epigenesis necessarily involves empirical processes. Foregrounding the topological involvement of the developing organism in its environment in both biological and psychoanalytic registers, she suggests a way forward can be found in thinking of the genesis of reason as both empirical and rational. Alexander R. Galloway traces an etymological path from “epigenetic” back to the Greek verb “gignomai,” meaning “to be born” or “to become.” But what is becoming? And why is becoming better than (mere) being? One answer is that becoming helps one to escape the confines of identity and rote determination. But what happens when the epigenetic paradigm becomes dominant, when contingency, evolution, and becoming prevail over essence, stasis, and determinism?
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Wong, Thian-Sze, Wei Gao, Zeng-Hong Li, Jimmy Yu-Wai Chan et Wai-Kuen Ho. « Epigenetic Dysregulation in Laryngeal Squamous Cell Carcinoma ». Journal of Oncology 2012 (2012) : 1–10. http://dx.doi.org/10.1155/2012/739461.

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Laryngeal carcinoma is a common head and neck cancer with poor prognosis. Patients with laryngeal carcinoma usually present late leading to the reduced treatment efficacy and high rate of recurrence. Despite the advance in the use of molecular markers for monitoring human cancers in the past decades, there are still no reliable markers for use to screen laryngeal carcinoma and follow the patients after treatment. Epigenetics emerged as an important field in understanding the biology of the human malignancies. Epigenetic alterations refer to the dysregulation of gene, which do not involve the alterations of the DNA sequence. Major epigenetic changes including methylation imbalance, histone modification, and small RNA dysregulation could play a role in the development of human malignancies. Global epigenetic change is now regarded as a molecular signature of cancer. The characteristics and behavior of a cancer could be predicted based on the specific epigenetic pattern. We here provide a review on the understanding of epigenetic dysregulation in laryngeal carcinoma. Further knowledge on the initiation and progression of laryngeal carcinoma at epigenetic level could promote the translation of the knowledge to clinical use.
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Kaushik, Prashant, et James T. Anderson. « Obesity : epigenetic aspects ». Biomolecular Concepts 7, no 3 (1 juin 2016) : 145–55. http://dx.doi.org/10.1515/bmc-2016-0010.

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AbstractEpigenetics, defined as inheritable and reversible phenomena that affect gene expression without altering the underlying base pair sequence has been shown to play an important role in the etiopathogenesis of obesity. Obesity is associated with extensive gene expression changes in tissues throughout the body. Epigenetics is emerging as perhaps the most important mechanism through which the lifestyle-choices we make can directly influence the genome. Considerable epidemiological, experimental and clinical data have been amassed showing that the risk of developing disease in later life is dependent on early life conditions, mainly operating within the normative range of developmental exposures. In addition to the ‘maternal’ interactions, there has been increasing interest in the epigenetic mechanisms through which ‘paternal’ influences on offspring development can be achieved. Nutrition, among many other environmental factors, is a key player that can induce epigenetic changes not only in the directly exposed organisms but also in subsequent generations through the transgenerational inheritance of epigenetic traits. Overall, significant progress has been made in the field of epigenetics and obesity and the first potential epigenetic markers for obesity that could be detected at birth have been identified. Fortunately, epigenetic phenomena are dynamic and rather quickly reversible with intensive lifestyle changes. This is a very promising and sustainable resolution to the obesity pandemic.
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Shao, Jingrong, Jiao Liu et Shengkai Zuo. « Roles of Epigenetics in Cardiac Fibroblast Activation and Fibrosis ». Cells 11, no 15 (30 juillet 2022) : 2347. http://dx.doi.org/10.3390/cells11152347.

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Cardiac fibrosis is a common pathophysiologic process associated with numerous cardiovascular diseases, resulting in cardiac dysfunction. Cardiac fibroblasts (CFs) play an important role in the production of the extracellular matrix and are the essential cell type in a quiescent state in a healthy heart. In response to diverse pathologic stress and environmental stress, resident CFs convert to activated fibroblasts, referred to as myofibroblasts, which produce more extracellular matrix, contributing to cardiac fibrosis. Although multiple molecular mechanisms are implicated in CFs activation and cardiac fibrosis, there is increasing evidence that epigenetic regulation plays a key role in this process. Epigenetics is a rapidly growing field in biology, and provides a modulated link between pathological stimuli and gene expression profiles, ultimately leading to corresponding pathological changes. Epigenetic modifications are mainly composed of three main categories: DNA methylation, histone modifications, and non-coding RNAs. This review focuses on recent advances regarding epigenetic regulation in cardiac fibrosis and highlights the effects of epigenetic modifications on CFs activation. Finally, we provide some perspectives and prospects for the study of epigenetic modifications and cardiac fibrosis.
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Cipriano, Alessandra, Gianluca Sbardella et Alessio Ciulli. « Targeting epigenetic reader domains by chemical biology ». Current Opinion in Chemical Biology 57 (août 2020) : 82–94. http://dx.doi.org/10.1016/j.cbpa.2020.05.006.

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Socolovsky, Merav. « Systems Biology and Epigenetic Mechanisms in Erythropoiesis ». Blood 122, no 21 (15 novembre 2013) : SCI—11—SCI—11. http://dx.doi.org/10.1182/blood.v122.21.sci-11.sci-11.

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Abstract Irreversible rapid cellular decisions are often controlled by network motifs known as bistable switches. We identified a cell-cycle regulated bistable switch that controls activation of the erythroid transcriptional program during early S phase of the last generation of erythroid colony-forming-unit progenitors (CFUe). This switch drives a rapid, multi-layered commitment event that activates GATA-1 transcription, renders the cells dependent on erythropoietin, and brings about chromatin reconfiguration at erythroid gene loci. In addition, it triggers an unusual process of genome-wide DNA demethylation, the first known example of such a process in somatic cell development. Approximately 25 to 30 percent of all methylation marks are lost from essentially all genomic elements during erythroid terminal differentiation. The bistable switch activating erythroid transcription consists of two linked double-negative feedback interactions of the erythroid transcriptional repressor PU.1, which antagonizes both S phase progression, and the erythroid master transcriptional regulator GATA-1. During operation of the switch, a rapid S phase-dependent decline in PU.1 activates GATA-1 transcription. The dependence of this switch on S phase progression coincides with a dramatic change in the nature of S phase itself, which becomes shorter and 50 percent faster. The accelerated intra-S phase DNA synthesis rate is essential for the loss of genome-wide DNA methylation, which in turn is required for the rapid induction of erythroid genes. Disclosures: No relevant conflicts of interest to declare.
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Horsthemke, Bernhard. « Waddington's epigenetic landscape and post-Darwinian biology ». BioEssays 34, no 8 (10 avril 2012) : 711–12. http://dx.doi.org/10.1002/bies.201200038.

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Yasmin, Rehana, Sami Siraj, Amjad Hassan, Abdul Rehman Khan, Rashda Abbasi et Nafees Ahmad. « Epigenetic Regulation of Inflammatory Cytokines and Associated Genes in Human Malignancies ». Mediators of Inflammation 2015 (2015) : 1–8. http://dx.doi.org/10.1155/2015/201703.

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Inflammation is a multifaceted defense response of immune system against infection. Chronic inflammation has been implicated as an imminent threat for major human malignancies and is directly linked to various steps involved in tumorigenesis. Inflammatory cytokines, interleukins, interferons, transforming growth factors, chemokines, and adhesion molecules have been associated with chronic inflammation. Numerous cytokines are reported to be aberrantly regulated by different epigenetic mechanisms like DNA methylation and histone modifications in tumor tissues, contributing to pathogenesis of tumor in multiple ways. Some of these cytokines also work as epigenetic regulators of other crucial genes in tumor biology, either directly or indirectly. Such regulations are reported in lung, breast, cervical, gastric, colorectal, pancreatic, prostate, and head and neck cancers. Epigenetics of inflammatory mediators in cancer is currently subject of extensive research. These investigations may help in understanding cancer biology and to develop effective therapeutic strategies. The purpose of this paper is to have a brief view of the aberrant regulation of inflammatory cytokines in human malignancies.
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Manev, Hari, et Svetlana Dzitoyeva. « Progress in mitochondrial epigenetics ». BioMolecular Concepts 4, no 4 (1 août 2013) : 381–89. http://dx.doi.org/10.1515/bmc-2013-0005.

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AbstractMitochondria, intracellular organelles with their own genome, have been shown capable of interacting with epigenetic mechanisms in at least four different ways. First, epigenetic mechanisms that regulate the expression of nuclear genome influence mitochondria by modulating the expression of nuclear-encoded mitochondrial genes. Second, a cell-specific mitochondrial DNA content (copy number) and mitochondrial activity determine the methylation pattern of nuclear genes. Third, mitochondrial DNA variants influence the nuclear gene expression patterns and the nuclear DNA (ncDNA) methylation levels. Fourth and most recent line of evidence indicates that mitochondrial DNA similar to ncDNA also is subject to epigenetic modifications, particularly by the 5-methylcytosine and 5-hydroxymethylcytosine marks. The latter interaction of mitochondria with epigenetics has been termed ‘mitochondrial epigenetics’. Here we summarize recent developments in this particular area of epigenetic research. Furthermore, we propose the term ‘mitoepigenetics’ to include all four above-noted types of interactions between mitochondria and epigenetics, and we suggest a more restricted usage of the term ‘mitochondrial epigenetics’ for molecular events dealing solely with the intra-mitochondrial epigenetics and the modifications of mitochondrial genome.
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