Additional file 11 of Modulation of macrophage inflammatory function through selective inhibition of the epigenetic reader protein SP140
Mohammed GhiboubJan KösterPeter D. CraggsAndrew Y. F. Li YimAnthony ShillingsSue HutchinsonRyan P. BinghamKelly GatfieldIshtu HagemanGang YaoHeather P. O’KeefeAaron CoffinAmish J. PatelLisa A. SloanDarren J. MitchellThomas G. HayhowLaurent LunvenRobert J. WatsonChristopher E. BluntLee A. HarrisonGordon BrutonUmesh KumarNatalie HamerJohn R. SpaullDanny A. ZwijnenburgOlaf WeltingTheodorus B. M. HakvoortAnje A. te VeldeJohan Van LimbergenPeter HennemanRab K. PrinjhaMenno P.J. de WintherNicola HarkerDavid F. ToughWouter J. de Jonge
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Additional file 11: Table 11. The normalized read count for ChIP-seq (GSK761-pretreated “M1” macrophages).Keywords:
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Substantial progress has been made in identifying genetic loci associated with multifactorial disorders, including variants that seem to impact outcomes following solid organ transplantation. Despite these advances, much of the heritability and susceptibility to chronic disease processes remains unexplained. Epigenetic modifications may exert their effect independently or complementary to genetic variants. Epigenetic modifications can change gene expression without altering the DNA sequence. These modifications are dynamic, potentially heritable, and can be induced by environmental stimuli or drugs. The impact of epigenetic phenomena on the outcomes of organ transplantation is currently poorly understood. Epigenetic modifications can occur during periods of illness; these may persist and potentially influence allograft outcomes. Epigenetic mechanisms influence the activation, proliferation, and differentiation of the immune cells involved in allograft rejection. The donor's epigenome may also impact transplant survival, and initial research has demonstrated that peritransplant conditions induce rapid epigenetic modification within the allograft. Further research will help to define the importance of epigenetic modifications in transplantation. This will potentially lead to the identification of useful biomarkers and the development of novel pharmacotherapies. This review explores the nature of epigenetic modification in disease and the emerging evidence for epigenetic influences on allograft survival.
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Epigenetic mechanisms affect cellular gene expression levels independently from DNA sequence. Epigenetic modifications can cause heritable phenotypic changes by the influence of environmental factors such as toxicants, nutrition and stress. Specific epigenetic marks that escape embryonic epigenetic reprogramming may have a role in obesity, cancer and cardiovascular disease susceptibility through subsequent generations. Recent studies point out that epigenetic may be related with complex diseases with unknown etiopathology. In this review, we summarized the effects of environmental factors on epigenome, epigenetic inheritance mechanisms across generations and related pathologies.
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Epigenetic alterations during aging are manifested with altered gene expression linking it to lifespan regulation, genetic instability, and diseases. Diet and epigenetic modifiers exert a profound effect on the lifespan of an organism by modulating the epigenetic marks. However, our understanding of the multifactorial nature of the epigenetic process during aging and the onset of disease conditions as well as its reversal by epidrugs, diet, or environmental factors is still mystifying. This review covers the key findings in epigenetics related to aging and age-related diseases. Furthermore, it holds a discussion about the epigenetic clocks and their implications in various age-related disease conditions, including cancer. Although, epigenetics is a reversible process, how fast the epigenetic alterations can revert to normal is an intriguing question. Therefore, this article touches on the possibility of utilizing nutrition and mesenchymal stem cell secretome to accelerate the epigenetic reversal and emphasizes the identification of new therapeutic epigenetic modifiers to counter epigenetic alteration during aging.
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Epigenetics refers to a steady change in the level of gene expression caused by non-DNA sequence changes. Microbes can modulate host inflammation through epigenetic pathways to evade or expend immune responses. As an important part of human microbes, oral bacteria also have various epigenetic regulation mechanisms to affect host inflammatory responses. This article reviews the common pathways of epigenetic regulation in microbe infection and the regulation of host epigenetics by using oral microbes to provide a reference for the study of epigenetic-related mechanisms in oral diseases.表观遗传是指非基因序列改变所导致的基因表达水平的稳定改变,微生物能通过表观遗传途径调节宿主炎症,从而逃避或者扩大免疫反应。口腔细菌作为人体微生物的重要组成部分,目前已发现多种表观遗传调控机制可影响宿主对口腔细菌的反应。本文就细菌调控表观遗传的常见途径以及不同疾病中口腔细菌对宿主表观遗传的调控进行综述,以期为口腔疾病中表观遗传相关机制研究提供参考。.
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The number of children with mild neurodevelopmental disorders, such as autism, has been recently increasing in advanced countries. This increase is probably caused by environmental factors rather than genetic factors, because it is unlikely that genetic mutation rates suddenly increased within a short period. Epigenetics is a mechanism that regulates gene expression, depending not on the underlying DNA sequence but on the chemical modifications of DNA and histone proteins. Because mental stress can alter the epigenetic status in neuronal cells, environmental factors may alter brain function through epigenetic changes. However, one advantage of epigenetic changes is their reversibility. Therefore, diseases due to abnormal epigenetic regulation are theoretically treatable. In fact, several drugs for treating mental diseases are known to have restoring effects on aberrant epigenetic statuses, and a novel therapeutic strategy targeting gene has been developed. In this review, we discuss epigenetic mechanisms of congenital and acquired neurodevelopmental disorders, drugs with epigenetic effects, novel therapeutic strategies for epigenetic diseases, and future perspectives in epigenetic medicine.
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