Epigenetics and Human Reproduction (Epigenetics and Human Health)
Book file PDF easily for everyone and every device.
You can download and read online Epigenetics and Human Reproduction (Epigenetics and Human Health) file PDF Book only if you are registered here.
And also you can download or read online all Book PDF file that related with Epigenetics and Human Reproduction (Epigenetics and Human Health) book.
Happy reading Epigenetics and Human Reproduction (Epigenetics and Human Health) Bookeveryone.
Download file Free Book PDF Epigenetics and Human Reproduction (Epigenetics and Human Health) at Complete PDF Library.
This Book have some digital formats such us :paperbook, ebook, kindle, epub, fb2 and another formats.
Here is The CompletePDF Book Library.
It's free to register here to get Book file PDF Epigenetics and Human Reproduction (Epigenetics and Human Health) Pocket Guide.
Role of nitric oxide in regulating histone methylation: nitric oxide modifies global histone methylation by inhibiting Jumonji C domain-containing demethylases. Hoffmann, A. DNA memories of early social life. Neuroscience , 64— Horvath, S. DNA methylation age of human tissues and cell types.
Genome Biol. Hou, L. Environmental chemical exposures and human epigenetics. Huang, D. Global DNA hypomethylation, rather than reactive oxygen species ROS , a potential facilitator of cadmium-stimulated K cell proliferation. Hughes, V. Epigenetics: the sins of the father. Nature , 22— Ingrosso, D. Folate treatment and unbalanced methylation and changes of allelic expression induced by hyperhomocysteinaemia in patients with uraemia.
Lancet , — Jennings, B. How folate metabolism affects colorectal cancer development and treatment, a story of heterogeneity and pleiotropy. Jensen, T. Epigenetic remodeling during arsenical-induced malignant transformation. Carcinogenesis 29, — Jones, P. The fundamental role of epigenetic events in cancer. Kala, R. MicroRNAs: an emerging science in cancer epigenetics. Kellner, S. Transcriptional regulation of the Oct4 gene, a master gene for pluripotency. Kikuno, N. Genistein mediated histone acetylation and demethylation activates tumor suppressor genes in prostate cancer cells.
Cancer , — Kim, W. Knopik, V. The epigenetics of maternal cigarette smoking during pregnancy and effects on child development. Kohda, T. Embryo manipulation via assisted reproductive technology and epigenetic asymmetry in mammalian early development. B Biol. Kosa, J. Effect of menopause on gene expression pattern in bone tissue of nonosteoporotic women. Menopause 16, — Kropat, C. Modulation of Nrf2-dependent gene transcription by bilberry anthocyanins in vivo.
Food Res. Kruman, I. Impaired one carbon metabolism and DNA methylation in alcohol toxicity. Kumar, N. Chromatin remodelling is a key mechanism underlying coccaine- induced plasticity in striatum. Neuon 48, Lambrot, R. Low paternal dietary folate alters the mouse sperm epigenome and is associated with negative pregnancy outcomes. Lattal, K. Epigenetics and persistent memory: implications for reconsolidation and silent extinction beyond the zero.
Laviola, G. Risk-taking behavior in adolescent mice: psychobiological determinants and early epigenetic influence. Lee, Y. Carcinogenic nickel silences gene expression by chromatin condensation and DNA methylation: a new model for epigenetic carcinogens. Leonard, S. Metal-induced toxicity, carcinogenesis, mechanisms and cellular responses. Leslie, F. Multigenerational epigenetic effects of nicotine on lung function. BMC Med. Lewis, B. Conserved seed pairing, often flanked by adenosines, indicates that thousands of human genes are microRNA targets.
Cell , 15— Lister, R. Human DNA methylomes at base resolution show widespread epigenomic differences. Liu, B. PIAS1 regulates breast tumorigenesis through selective epigenetic gene silencing. Liu, H. Cigarette smoke induces demethylation of prometastatic oncogene synuclein-gamma in lung cancer cells by downregulation of DNMT3B. Oncogene 26, — Liu, L. Insufficient DNA methylation affects healthy aging and promotes age-related health problems.
Epigenetics 2, — Lomniczi, A.
Epigenetic control of female puberty. Lotito, S. Consumption of flavonoid-rich foods and increased plasma antioxidant capacity in humans: cause, consequence, or epiphenomenon? Luger, K. Crystal structure of the nucleosome core particle at 2. Lund, G. Atherosclerosis: an epigenetic balancing act that goes wrong. Makar, K. DNA methylation is non-redundant repressor of the effector program. Malvaez, M. HDAC3 selective inhibitor enhances exinction of coccaine-seeking behaviour in persistent manner. Manning, K. A naturally occurring epigenetic mutation in a gene encoding an SBP-box transcription factor inhibits tomato fruit ripening.
MicroRNA responses to cellular stress. Mastroeni, D. Epigenetic changes in Alzheimer's disease: decrements in DNA methylation. Aging 31, Maze, I. Essential role of the histone methyltransferase G9a in cocaine-induced plasticity. The epigenetic landscape of addiction. McGowan, P. Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Meaney, M. Maternal care, gene expression, and the transmission of individual differences in stress reactivity across generations. Miller, G. Mental health. Predicting the psychological risks of war.
Milroy, C. Differential methylation of pluripotency gene promoters in in vitro matured and vitrified, in vivo -matured mouse oocytes. Monks, T. ROS- induced histone modification and their role in cell survival and cell death. Drug Metab. Montgomery, R. MicroRNA regulation as a therapeutic stratergy for cardiovascular disease. Drug Targets 11, — Morgan, H. Epigenetic inheritance at the agouti locus in the mouse. Morimoto, T. The dietary compound curcumin inhibits p histone acetyltransferase activity and prevents heart failure in rats.
Morrison, K. Epigenetic mechanisms in pubertal brain maturation. Neuroscience , 17— Munro, S. Epigenetic regulation of endometrium during the menstrual cycle. Narita, M. Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence. Natarajan, A. Mutagenesis 7, 83— Nitert, M. Impact of an exercise intervention on DNA methylation in skeletal muscle from first-degree relatives of patients with type 2 diabetes.
Diabetes 61, — Ntanasis-Stathopoulos, J. Epigenetic regulation on gene expression induced by physical exercise. Neuronal Interact. Oberlander, T.
Epigenetics and Reproductive Medicine
Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene NR3C1 and infant cortisol stress responses. Epigenetics 3, 97— Ojeda, S. Gene networks and the neuroendocrine regulation of puberty. Oki, E. Mutated gene-specific phenotypes of dinucleotide repeat instability in human colorectal carcinoma cell lines deficient in DNA mismatch repair.
Oncogene 18, — Olaharski, A. The flavoring agent dihydrocoumarin reverses epigenetic silencing and inhibits sirtuin deacetylases. PLoS Genet. Ordovas, J. Epigenetics and cardiovascular disease. Orozco-Solis, R. Epigenetic control and the circadian clock: linking metabolism to neuronal responses.
Neuroscience , 76— Ouko, L. Effect of alcohol consumption on CpG methylation in the differentially methylated regions of H19 and IG-DMR in male gametes: implications for fetal alcohol spectrum disorders. Paneni, F. Epigenetic signatures and vascular risk in type 2 diabetes: a clinical perspective. Atherosclerosis , — Park, J. Development of type 2 diabetes following intrauterine growth retardation in rats is associated with progressive epigenetic silencing of Pdx1. Phillips, T. The role of methylation in gene expression.
Plotsky, P. Brain Res. Provost, P. Interpretation and applicability of microRNA data to the context of Alzheimer's and age-related diseases. Aging Albany NY 2, — Radom-Aizik, S. Evidence for microRNA involvement in exercise-associated neutrophil gene expression changes. Radtke, K. Transgenerational impact of intimate partner violence on methylation in the promoter of the glucocorticoid receptor. Psychiatry 1:e Reddy, U.
Infertility, assisted reproductive technology, and adverse pregnancy outcomes: executive summary of a National Institute of Child Health and Human Development workshop. Rehan, V. Perinatal nicotine exposure induces asthma in second generation offspring. Reichard, J. Long term low-dose arsenic exposure induces loss of DNA methylation. Reik, W. Stability and flexibility of epigenetic gene regulation in mammalian development. Renthal, W. Epigenetic mechanisms in drug addiction. Trends Mol. Report, W. Geneva: World Health Organisation.
Rideout, W. Progressive increases in the methylation status and heterochromatinization of the myoD CpG island during oncogenic transformation. Rivera, C. Mapping human epigenomes. Cell , 39— Romieu, P. The inhibition of histone deacetylases reduces the reinstatement of cocaine-seeking behavior in rats. Ronn, T. A six months exercise intervention influences the genome-wide DNA methylation pattern in human adipose tissue.
Ronti, T. The endocrine function of adipose tissue: an update. Roth, T. Epigenetics of neurobiology and behavior during development and adulthood. Rudenko, A. Epigenetic regulation in memory and cognitive disorders. Neuroscience , 51— Sahar, S. Circadian rhythms and memory formation: regulation by chromatin remodeling. Sanchis-Gomar, F. Physical exercise as an epigenetic modulator: eustress, the postive stress, as an effector of gene expression. Strength Cond. Santos, F. Schlinzig, T. Epigenetic modulation at birth - altered DNA-methylation in white blood cells after Caesarean section.
Acta Paediatr. Schuz, L. The Dutch hunger winter and the developmental origins of health and disease. Sedivy, J. Aging by epigenetics—a consequence of chromatin damage? Cell Res. Seminara, S. The GPR54 gene as a regulator of puberty. Sharma, P. Genome wide DNA methylation profiling for epigenetic alteration in coronary artery disease patients.
Gene , 31— Shenderov, B. Epigenomic programing: a future way to health? Health Dis. Shim, S. Food Chem. Shukla, S. Epigenetic effects of ethanol on the liver and gastrointestinal system. Alcohol Res. Emerging role of epigenetics in the actions of alcohol.
Epigenetics—new frontier for alcohol research. Silva, P. Alzheimers Dis. Singh, S. Micro-RNA- micro in size but macro in function. FEBS J. Epigenetic effects of environmental chemicals bisphenol a and phthalates. Soubry, A. Starkman, B. Epigenetics-beyond the genome in alcoholism. Stevenson, T. Reversible DNA methylation regulates seasonal photoperiodic time measurement.
Stolk, L. Meta-analyses identify 13 loci associated with age at menopause and highlight DNA repair and immune pathways. Stouder, C. Transgenerational effects of the endocrine disruptor vinclozolin on the methylation pattern of imprinted genes in the mouse sperm. Reproduction , — Sun, H. Modulation of histone methylation and MLH1 gene silencing by hexavalent chromium. Surani, M. Reprogramming of genome function through epigenetic inheritance. Takahashi, Y.
Microsatellite instability and protein expression of the DNA mismatch repair gene, hMLH1, of lung cancer in chromate-exposed workers. Tammen, S. Aging and alcohol interact to alter hepatic DNA hydroxymethylation. Tollefsbol, T. Dietary epigenetics in cancer and aging. Cancer Treat. Ubeda, F. Ecology drives intragenomic conflict over menopause. Urdinguio, R. Epigenetic mechanisms in neurological diseases: genes, syndromes, and therapies. Lancet Neurol. Vassoler, F. Epigenetic inheritance of a cocaine-resistance phenotype. Vogel-Ciernia, A. The neuron-specific chromatin regulatory subunit BAF53b is necessary for synaptic plasticity and memory.
Waris, G. Reactive oxygen species: role in development of cancer and various chronic conditions. Waterland, R. Transposable elements: targets for early nutritional effects on epigenetic gene regulation. Weaver, I. Epigenetic programming by maternal behavior. Webster, A. Whitelaw, N. Epigenetic status in the offspring of spontaneous and assisted conception. Widschwendter, M. HOXA methylation in normal endometrium from premenopausal women is associated with the presence of ovarian cancer: a proof of principle study.
Williams, R. Flavonoids: antioxidants or signalling molecules? Witcher, M. Cell 34, — Epigenetic influence over gene expression possibly originated as a defence against Transposons, parasitic DNA that jumps around in the genome and can disrupt genes by inserting into the middle of them Slotkin and Martienssen, A possible mechanism of defence can be achieved via methylation of DNA, as illustrated in Fig.
Eventually this process evolved into a method of promoting and repressing host genes Feinberg, that could not only be acquired throughout the lifetime of an individual, but also passed onto its offspring Jones, This mechanism of gene silencing may have also allowed for the development of multicellular organisms by allowing a single genome to tailor its expressed genes in each individual cell within the larger organism Badyaev, Methylation as a defence against Transposons.
The figure illustrates how methylation can help an organism defend itself from Transposons. While epigenetics is a relatively new understanding of the systems involved in gene control and expression it also represents something very important, a fundamental revaluation of the theory of evolution. Acquired traits, while not alterations of the genome, can be inherited Jones, This review will examine the implications this has for the concept of human evolution and highlight interesting examples and case studies in which these effects are notable. The study of epigenetics has revealed an interesting facet of this method of gene expression control.
The methylation of DNA and other epigenetic marks do not alter the genes that they influence at a sequence level but nonetheless alter the expression of these genes. Furthermore these marks can be acquired throughout the lifetime of the individual and, if carried in their gametes, these marks are inheritable. In this section, the focus will be on the ways in which these marks can be inherited. The semi-conserved nature of mitosis results in two sets of daughter chromatids, one in each set carrying the Epigenetic marks from the original chromosome Feinberg, , as illustrated in Fig.
This allows the transfer of epigenetic marks from mother cells to daughter cells in somatic tissue. This explains how these marks can be maintained in an individual, but not how they are spread to the next generation of offspring.
Phenotypic plasticity and the epigenetics of human disease. | Learn Science at Scitable
As can be seen in A the original chromosome contains epigenetic marks on both chromatids, and in B both daughter chromosomes contain some of the epigenetic marks of the mother chromosome due to the semi-conserved nature of mitosis. These marks can also be conserved in their daughter chromatid during meiosis, resulting in all gametes carrying the epigenetic marks of the individual of origin. However, many of these marks are removed during the process of gamete formation. Methylation marks can be inherited from either the maternal Giuliani et al.
Through the father, the offspring can inherit a wide array of methylation marks, with the majority of these marks in some way affecting the digestive systems of the child Soubry, For an example of this deleterious nature of hypomethylation one can look at the Dutch Winter of Hunger, a well-documented example of famine in the modern world that occurred from to due to a blockage preventing the movement of fuel and food in the Netherlands.
This starvation resulted in the hypomethylation of the IGF-2 gene, the gene responsible for the formation of insulin-like growth factor 2. The ability of parental malnutrition to affect the epigenome of the offspring in an overtly negative and harmful way will be examined more closely later in the review. This was very useful and advantageous for nomadic peoples and a case study of this can be seen in the comparison of the Oromo peoples and the Amhara peoples of Ethiopia Alkorta-Aranburu et al.
In this case it appears that epigenetic marks actual favour immunological variation within the newly arrived population.
This will be examined in more depth as part of the Case studies section later in the review. This will eventually result in a population that is genetically similar to the original settlers but will be more adapted to their surrounding environment. To understand the impact epigenetics has had on our development into modern humans we have to compare the areas of gene methylation seen in our species and our closest living relatives. Many of the regions in the human genome that are methylated are not genes that are unique to humans, with the biggest differences in methylation occurring in regions of DNA involved with Transcription Factors or TFs and gene control Hernando-Herraez et al.
This is because TFs have a wide-reaching influence on the expressed phenotype of an individual due to these factors functioning as a form of gene expression regulation, therefore promoting or suppressing other genes in the genome. Even small differences in the epigenome surrounding TFs can result in widely varying phenotypes between individuals of the same species due to their wide-reaching influences Heyn et al. So it can only be assumed just how important these phenotypic changes are in the variation that separates us from our ancestor species.
HARs are regions of DNA that have undergone rapid changes since the emergence of the human species far and above the normal rate of mutation. These regions stand out due to the extremely accelerated rate of mutations they have undergone and are widely understood to be responsible for the speedy divergence of humans from other species Hubisz and Pollard, The exact nature of the role played by epigenetic changes in HARs is not clear but the importance of their role is undoubtable, with epigenetic changes possibly predating sequential changes in DNA Badyaev, A suggested theory is that these marks actually promoted the occurrence of mutations in the genes that are responsible for our species existence.
Studying the epigenomes of our related species sheds light on the relatively large divergence that has occurred since our emergence from our distant cousins, a divergence of such stature that it cannot be solely explained by nucleotide changes Hernando-Herraez et al. It has even been speculated that epigenetic changes could be more impactful on the Darwinian evolution of a species than genomic mutations Badyaev, and this area of research only adds more weight to these claims. Modern humans have survived and thrived in a wide array of environments for thousands of years, from the Arctic tundra to Saharan deserts.
The key to this success has always been the uniquely human ability to adapt quickly and epigenetics has played a role in this capacity to adapt. While cultural adaptations to environments, such as changes in clothing or ritualistic behaviour, are the most visual signs of this adaptability, no less important are the more subtle genetic and epigenetic changes that a population undergoes as they live in an area for generations. For example a population that has lived in an arid environment will carry many genetic mutations that make them more suitable to a dry climate.
If a catastrophic climate shift occurs and their ancestral lands suddenly become cold and damp they can adapt to wear thicker clothing Cavalli-Sforza and Feldman, to protect against the cold and may even take on new customs and rituals around hygienic behaviour to protect against new diseases that have taken root in the region Wiesenfeld, This population will however still carry many of the genetic mutations that made them suited to their old environment until selection pressure allows new mutations to compensate for these genetic relics.
An important idea is the way in which to consider each different type of adaptation in comparison to one another. Cultural adaptation is a catch all term that encompasses all artificial adaptations an individual can pick up to become more comfortable in an environment Cavalli-Sforza and Feldman, In comparison genetic changes, such as the prevalence of Sickle Cell Anaemia in regions prone to malaria outbreaks, represent much longer term adaptations.
These changes take longer to gain and cannot as easily be shaken off once their usefulness has run its course, such as an individual simply changing their attire to suit the weather Laland, Odling-Smee, and Myles, What do epigenetic changes represent in this model then? Firstly they exemplify medium-term adaptations, falling between cultural changes and genetic evolution in the time it takes an individual to acquire them Giuliani et al.
In this model of understanding human adaptation epigenetic changes also serve as a time-keeping mechanism, helping to mitigate the negative effects of genetic relics acquired by ancestor populations under different evolutionary pressures Badyaev, By silencing older genes that once served a vital purpose epigenetics also helps to prevent the build-up of complexity in an organism, silencing older, less frequently transcribed genes Badyaev, , much in the same way that DNA methylation combats the damage caused by transposons Slotkin and Martienssen, A good way to examine this model of adaptation is to consider the way each of these changes would affect a hypothetical population that has suddenly become exposed to a harsh, cold climate.
Very quickly, this population will adapt, first by increasing their protection against the elements by wearing thicker clothes. While this is an effective method of staying warm their bodies have not yet adapted to the cold, and so, their genes controlling homoeostasis will still function in the same way as they had in a warmer climate, something that might be considerably wasteful and possibly deleterious.
Where once their perspiration would help keep the heat from damaging their bodies it now wastes water. At this stage, after a considerable number of generations, epigenetic changes will begin to take affect under selective pressure. DNA methylations and histone modifications will accumulate, fine tuning their homoeostatic gene expression to the colder environment.
This results in the silencing of genes that were better suited to the hotter climate and promotes the expression of other genes that confer an advantage in this colder one. Finally, after even more generations new alleles will take hold in the populations that represent novel genes. These novel genes will encode new proteins that in some way will provide a selective advantage that is near permanent in expression, if not in providing an advantage. Another point highlighted by this model is that the longer an adaptation takes to be acquired the less likely it is to ever be lost.
After all, it is much easier to take a jacket off than to spontaneously lose a gene responsible for increasing metabolic activity. Epigenetics comes in yet again at this point as not only does it silence older genes that are no longer required, under the influence of selective pressure, it also introduces more plasticity into the expression of genes Giuliani et al. Through this mechanism epigenetics allows the variability of phenotypes that are required for adaptation and selection Tobi et al. Since genome-wide profiling in some cases does not give a sufficient answer to explain the complex biological processes in autoimmune disorders, epigenetic modifications are retained additional regulators in immune responses Fig.
Epigenetic dysregulation directly influences the development of autoimmunity by regulating immune cell functions [ 2 ]. The recognition of the complexity of the interaction between epigenetic events and the alteration of the immune system in autoimmune disorders is a prominent challenge for the discovery of novel potential therapeutic strategies. Epigenetic mechanisms, such as DNA methylation, chromatin remodeling, and noncoding RNAs, have been identified as crucial regulators in cellular immunity, owing to their mechanisms in modulating gene expression and transcription in targeted cells and tissues [ 3 ].
Extensive evidences indicate that autoimmune diseases are mainly an interplay of genetic and non-genetic factors, although the role of the latter ones often remains unclear. Over the last decade, the influence of epigenetic modifications on innate and adaptive immunity has been intensively investigated, especially in autoimmune disorders. Histone modifications Histone-modifying enzymes have an essential role in modulating chromatin compaction state, nucleosomal processes, and DNA repair [ 16 — 18 ].
Autoimmune diseases are characterized by an immune response to antigenic components of the host itself autoantigens. Two main types of autoimmune diseases can be distinguished: on the one hand, the systemic ones and on the other, the organ-specific ones. In systemic diseases, the immune system attacks in a generalized manner its own antigens in several organs, while in organ-specific diseases the immune response is directed towards a single organ. Table 1 Most relevant autoimmune diseases with known autoantigen targets. Rheumatoid arthritis Joints, lung, heart, etc.
IgG, filaggrin, fibrin etc. Dermal fibroblast antigens, fibrillarin-1, metalloproteinases, etc. Antibody 0. Autoimmunity is defined by the breakdown of self-tolerance that produces a state of abnormal humoral and cell-mediated responses against self-components. Until now, no effective treatments have been identified for SARDs, even though the use of glucocorticoids has been considered as a first-line therapy.
Nowadays, however, antimalarial and immunosuppressive drugs are most commonly used due to their limited long-term side effects. Such autoimmune disorders are often associated with an autoimmune dysregulation which determines morbidity and, in most cases, premature mortality [ 35 , 36 ]. In particular, most of these conditions happen when the immune system produces autoantibodies ANA directed against intracellular antigens. Understanding the molecular mechanisms of SARDs appears to be extremely important to achieve beneficial outcomes in these chronic conditions.
Characterization of epigenetic modifications that occur across these autoimmune diseases may yield valuable insights into their pathogenesis and treatment. Thus, in an attempt to determine the most important epigenetic changes in SARDs, researchers investigated the role of epigenetic processes in regulating autoimmunity. Up to now, blockers of the immune response produced a greater success in the clinical use than treatments exploiting natural immune regulation.
In fact, blocking the immune response is crucial in autoimmunity, even though immunosuppression leads to various side effects, including the reactivation of latent infections and the reduction of immunosurveillance. Thus, antigen-specific immune therapeutical options, instead of rather unspecific therapies targeting the immune system, are an important goal to reach towards the treatment of autoimmune disorders. Importantly, the discovery of an epigenetic therapy to treat such autoimmune disorders may unearth potential biomarkers for disease diagnosis and prediction. Table 4 Effects of Epi-drugs on autoimmune disorders discussed in this review.
Acknowledgments Not applicable. Availability of data and materials Not applicable. Ethics approval and consent to participate Not applicable. Consent for publication Not applicable. Competing interests The authors declare that they have no competing interests. References Bird A. Perceptions of epigenetics. Role of epigenetics in biology and human diseases.
Iran Biomed J. Epi-drugs in combination with immunotherapy: a new avenue to improve anticancer efficacy. Clin Epigenetics. DNA methylation pathways and their crosstalk with histone methylation. Nat Rev Mol Cell Biol. Functional coupling between writers, erasers and readers of histone and DNA methylation. Curr Opin Struct Biol. Function and information content of DNA methylation. An integrated epigenetic and genetic approach to common human disease. Trends Genet. Epigenetic interplay between histone modifications and DNA methylation in gene silencing.
Mutat Res. DNA methyltransferases inhibitors from natural sources. Curr Top Med Chem. On the evolutionary origin of eukaryotic DNA methyltransferases and Dnmt2. PLoS One. Mechanisms and biological roles of DNA methyltransferases and DNA methylation: from past achievements to future challenges. Adv Exp Med Biol. Bromodomain inhibitor review: Bromodomain and extra-terminal family protein inhibitors as a potential new therapy in central nervous system tumors. Increased DNA methylation variability in type 1 diabetes across three immune effector cell types.
Nat Commun. Comprehensive DNA methylation profiling of inflammatory mucosa in ulcerative colitis. Inflamm Bowel Dis. Lateral thinking: how histone modifications regulate gene expression. Histone exchange, chromatin structure and the regulation of transcription. Epigenetic histone code and autoimmunity. Clin Rev Allergy Immunol. Emerging approaches for histone deacetylase inhibitor drug discovery. Expert Opin Drug Discovery. Treatment of cardiovascular pathology with epigenetically active agents: focus on natural and synthetic inhibitors of DNA methylation and histone deacetylation.
Int J Cardiol.
Histone deacetylases and their inhibitors in cancer, neurological diseases and immune disorders. Nat Rev Drug Discov. Future Med Chem. Mol Cell Endocrinol. J Immunol. Genome regulation by long noncoding RNAs. Annu Rev Biochem. Many human large intergenic noncoding RNAs associate with chromatin-modifying complexes and affect gene expression.
Chromatin signature reveals over a thousand highly conserved large non-coding RNAs in mammals. Towards a molecular understanding of microRNA-mediated gene silencing. Nat Rev Genet. Deregulation and therapeutic potential of microRNAs in arthritic diseases. Nat Rev Rheumatol. The role of microRNAs in the pathogenesis of autoimmune diseases.
Autoimmun Rev. Epidemiology and estimated population burden of selected autoimmune diseases in the United States. Clin Immunol Immunopathol. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part I Arthritis Rheum. Autoimmune diseases: a leading cause of death among young and middle-aged women in the United States. Am J Public Health. Polymyositis and dermatomyositis: short term and longterm outcome, and predictive factors of prognosis. J Rheumatol.
- Product details.
- Mauras Dream.
- Those Flannigan Boys.
- Le Dix-huit Brumaire (French Edition).
- Blood Sex & Scooby Snacks.
ANA screening: an old test with new recommendations. Ann Rheum Dis. Guidelines for clinical use of the antinuclear antibody test and tests for specific autoantibodies to nuclear antigens. American College of Pathologists. Arch Pathol Lab Med. Arthritis Res Ther.
Join Kobo & start eReading today
Identification of activated cytokine pathways in the blood of systemic lupus erythematosus, myositis, rheumatoid arthritis, and scleroderma patients. Int J Rheum Dis. Genomics and the multifactorial nature of human autoimmune disease. N Engl J Med. Autoimmune diseases. Pervasive sharing of genetic effects in autoimmune disease. PLoS Genet. Polyautoimmunity and familial autoimmunity in systemic sclerosis. J Autoimmun. Autoimmune disease in the epigenetic era: how has epigenetics changed our understanding of disease and how can we expect the field to evolve? Expert Rev Clin Immunol. Epigenetics in human autoimmunity.
Epigenetics in autoimmunity - DNA methylation in systemic lupus erythematosus and beyond.
Epigenetics and autoimmunity. The epigenetics of autoimmunity. Cell Mol Immunol. Epigenome profiling reveals significant DNA demethylation of interferon signature genes in lupus neutrophils. Primer: epigenetics of autoimmunity. Nat Clin Pract Rheumatol. Mechanism of drug-induced lupus. Cloned Th2 cells modified with DNA methylation inhibitors in vitro cause autoimmunity in vivo.
J Clin Invest. Effect of an inhibitor of DNA methylation on T cells. Hum Immunol. Arthritis Rheum. The 1A4 molecule CD27 is involved in T cell activation. J Biol Chem. Isolation and biochemical and functional characterization of perforin 1 from cytolytic T-cell granules. Stat3 promotes IL expression in lupus T cells through trans-activation and chromatin remodeling. J Biomed Biotechnol.