Relevant bibliographies by topics / Genomic imprinting

Academic literature on the topic 'Genomic imprinting'

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Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Genomic imprinting"

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Bajrami, Emirjeta, and Mirko Spiroski. "Genomic Imprinting." Open Access Macedonian Journal of Medical Sciences 4, no. 1 (February 4, 2016): 181–84. http://dx.doi.org/10.3889/oamjms.2016.028.

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BACKGROUND: Genomic imprinting is the inheritance out of Mendelian borders. Many of inherited diseases and human development violates Mendelian law of inheritance, this way of inheriting is studied by epigenetics.AIM: The aim of this review is to analyze current opinions and options regarding to this way of inheriting.RESULTS: Epigenetics shows that gene expression undergoes changes more complex than modifications in the DNA sequence; it includes the environmental influence on the gametes before conception. Humans inherit two alleles from mother and father, both are functional for the majority of the genes, but sometimes one is turned off or “stamped” and doesn’t show in offspring, that gene is imprinted. Imprinting means that that gene is silenced, and gene from other parent is expressed. The mechanisms for imprinting are still incompletely defined, but they involve epigenetic modifications that are erased and then reset during the creation of eggs and sperm. Genomic imprinting is a process of silencing genes through DNA methylation. The repressed allele is methylated, while the active allele is unmethylated. The most well-known conditions include Prader-Willi syndrome, and Angelman syndrome. Both of these syndromes can be caused by imprinting or other errors involving genes on the long arm of chromosome 15.CONCLUSIONS: Genomic imprinting and other epigenetic mechanisms such as environment is shown that plays role in offspring neurodevelopment and autism spectrum disorder.
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Monk, M. "Genomic imprinting." Genes & Development 2, no. 8 (August 1, 1988): 921–25. http://dx.doi.org/10.1101/gad.2.8.921.

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Maher, E. R. "Genomic Imprinting." Journal of Medical Genetics 28, no. 9 (September 1, 1991): 647. http://dx.doi.org/10.1136/jmg.28.9.647.

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Hall, J. G. "Genomic imprinting." Archives of Disease in Childhood 65, no. 10 Spec No (October 1, 1990): 1013–15. http://dx.doi.org/10.1136/adc.65.10_spec_no.1013.

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Jones, Peter A. "Genomic Imprinting." American Journal of Human Genetics 63, no. 3 (September 1998): 927. http://dx.doi.org/10.1086/302003.

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Pedersen, C. "Genomic imprinting." Reproductive Toxicology 11, no. 2-3 (June 1997): 309–16. http://dx.doi.org/10.1016/s0890-6238(96)00213-4.

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da Rocha, Simao Teixeira, and Anne C. Ferguson-Smith. "Genomic imprinting." Current Biology 14, no. 16 (August 2004): R646—R649. http://dx.doi.org/10.1016/j.cub.2004.08.007.

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Hultén, M., A. Kerr, and WilliamH James. "Genomic imprinting." Lancet 338, no. 8760 (July 1991): 188–89. http://dx.doi.org/10.1016/0140-6736(91)90180-w.

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Lambertini, Luca. "Genomic imprinting." Current Opinion in Pediatrics 26, no. 2 (April 2014): 237–42. http://dx.doi.org/10.1097/mop.0000000000000072.

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Hodgson, Shirley. "Genomic Imprinting." Developmental Medicine & Child Neurology 33, no. 6 (November 12, 2008): 552–56. http://dx.doi.org/10.1111/j.1469-8749.1991.tb14920.x.

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Dissertations / Theses on the topic "Genomic imprinting"

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Santure, Anna Wensley, and n/a. "Quantitative genetic models for genomic imprinting." University of Otago. Department of Zoology, 2006. http://adt.otago.ac.nz./public/adt-NZDU20060811.134008.

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A gene is imprinted when its expression is dependent on the sex of the parent from which it was inherited. An increasing number of studies are suggesting that imprinted genes have a major influence on medically, agriculturally and evolutionarily important traits, such as disease severity and livestock production traits. While some genes have a large effect on the traits of an individual, quantitative characters such as height are influenced by many genes and by the environment, including maternal effects. The interaction between these genes and the environment produces variation in the characteristics of individuals. Many quantitative characters are likely to be influenced by a small number of imprinted genes, but at present there is no general theoretical model of the quantitative genetics of imprinting incorporating multiple loci, environmental effects and maternal effects. This research develops models for the quantitative genetics of imprinting incorporating these effects, including deriving expressions for genetic variation and resemblances between relatives. Imprinting introduces both parent-of-origin and generation dependent differences in the derivation of standard quantitative genetic models that are generally equivalent under Mendelian expression. Further, factors such as epistasis, maternal effects and interactions between genotype and environment may mask the effect of imprinting in a quantitative trait. Maternal effects may also mimic a number of signatures in variance and covariance components that are expected in a population with genomic imprinting. This research allows a more comprehensive understanding of the processes influencing an individual�s characteristics.
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Whitehead, Joanne. "Genomic Imprinting in Development and Evolution." Doctoral thesis, Uppsala universitet, Zoologisk utvecklingsbiologi, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4491.

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Genetic information is encoded by the linear sequence of the DNA double helix, while epigenetic information is overlayed as the packaging of DNA and associated proteins into the chromatin structure. Variations in chromatin structure play a vital role in establishing and maintaining patterns of gene expression during differentiation and development of higher eukaryotes, and disruption of this epigenetic gene regulation can lead to cancer. Mammals display an epigenetic phenomenon known as genomic imprinting, which provides an ideal model system for the study of epigenetics. Genes subject to genomic imprinting are differentially expressed within a single cell depending on the parental origin of the chromosome. Imprinting of the maternally expressed H19 gene and the adjacent paternally expressed Igf2 gene is regulated by the chromatin insulator protein CTCF. The studies presented in this thesis aim to investigate the functional mechanisms of CTCF-dependent gene regulation at the H19/Igf2 locus and at numerous other target sites throughout the genome. We have investigated the role of CTCF and a related protein BORIS in establishing the maternal to paternal imprint transition in chromatin structure at the H19/Igf2 locus in the male germline. We have developed novel microarray based methods to identify and characterize numerous new CTCF target sites throughout the mouse genome. We have shown that CTCF acts as part of the RNA polymerase II complex. We have identified the post-translational modification by addition of ADP-ribose polymers to CTCF, and demonstrated that this modification regulates its insulating ability. The results of these studies of CTCF-dependent epigenetic gene regulation are discussed in light of the evolution of genomic imprinting and chromatin insulators, and a novel role for poly ADP-ribosylation of CTCF in the progression of cancer is proposed.
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McCann, Jennifer. "Variability of genomic imprinting in human disease." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84294.

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Genomic imprinting is the differential expression of genetic material depending on the parent from which it is transmitted. It is involved in the pathogenesis of many diseases, especially those involved in development, growth abnormalities and cancer. We examined the extent of and the variability of genomic imprinting amongst individuals in three human diseases, Wilms' tumour, Type 1 diabetes and Silver-Russell syndrome.
Wilms' tumour (WT) is a renal embryonal cancer associated with overexpression of the insulin-like growth factor 2 (IGF2). IGF2 is directed to the lysosomes for degradation by the mannose-6-phosphate/insulin-like growth factor two receptor (M6P/IGF2R) encoded by the IGF2R gene, a known tumour suppressor gene on 6826. IGF2R is imprinted in the mouse, with exclusive maternal expression. In humans, however, IGF2R imprinting is a polymorphic phenomenon only being found in a small subset of people. We present results suggesting that IGF2R imprinting provides the first "hit" in IGF2R inactivation in WT, and show the presence of a second "hit" in the form of deletions detectable as loss of heterozygosity.
Another disease investigated in this report is Type 1 diabetes (TID), an autoimmune, polygenic disease. Of the several T1D loci, IDDM8 on 6q, has been found to be subject to parent-of-origin effects and encompasses IGF2R. M6P/IGF2R is involved in immune system regulation. In this study we show an association between TID and IGF2R that is confined to maternally inherited alleles. Our results strongly suggest that IGF2R is a TID susceptibility gene and may be universally imprinted at some tissue or developmental stage not yet studied.
A third disease displaying both tissue-specific and isoform-specific imprinting is Silver-Russell syndrome (SRS), a growth disorder associated with double dose of a maternally expressed gene within 7p11.2--p13, a region in which the imprinted GRB10 gene was a prime candidate. We studied the complex tissue and isoform-dependence of GRB10 imprinting and demonstrated absence of imprinting in growth plate cartilage, the tissue most directly involved in linear growth thus eliminating GRB10 as the gene responsible for SRS.
It is evident that genomic imprinting plays a prominent role in various diseases. Imprinted genes can be expressed in a tissue-specific, isoform-specific or a temporally regulated manner. In addition, there is a wide variability of imprinting between individuals.
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Sun, Bowen. "Genomic imprinting in mouse pluripotent stem cells." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609478.

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Zhou, Jiyuan. "Single-marker and haplotype analyses for detecting parent-of-origin effects using family and pedigree data." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B4308543X.

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Lucifero, Diana. "Developmental regulation of genomic imprinting by DNA methylation." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85573.

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Maintaining appropriate patterns of gene expression in the gametes and during early embryogenesis is essential for normal development. DNA methylation is an epigenetic means of regulating gene expression and is an important molecular mark regulating the sex-specific expression of genes subject to genomic imprinting. Imprinted genes are expressed from only one of two inherited chromosomes and are differentially marked during gametogenesis to allow for their parental allele specific expression. These genes affect embryo growth, placental function, behavior after birth and are implicated in the etiology of a number of human diseases. The primary objective of this thesis was to gain a better understanding of the developmental dynamics and origins of DNA methylation profiles regulating maternally methylated imprinted genes during mouse oocyte development. Studies revealed that maternally methylated imprinted genes acquire methylation within their DMRs during postnatal oocyte growth and that this acquisition occurs in a gene and allele specific manner. It was also observed that maternal methylation imprint acquisition is related to oocyte diameter and that a repetitive parasitic element also acquires methylation during this period. DNA methylation is catalyzed by DNMTs and investigations into the developmental expression profiles of Dnmt3a, Dnmt3b and Dnmt3L indicated that transcript accumulation of these enzymes during oocyte development coincided with the timing of maternal methylation imprint establishment. Moreover, expression analysis in DNMT-depleted oocytes suggested these enzymes to be coordinately regulated. Additional studies aimed at developing another model of oocyte imprinting lead to the identification and characterization of a putative bovine Snrpn DMR. Its DNA methylation profile was found to be conserved with that of mouse and human. Snrpn DNA methylation analysis in bovine IVF and SCNT embryos revealed slight loss of methylatio
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Rancourt, Rebecca Catherine. "Functional genomic analysis of an imprinting control region." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608514.

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Adams, Sally. "Genomic imprinting in the endosperm of Arabidopsis thaliana." Thesis, University of Bath, 2002. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.760803.

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Coan, Philip Michael. "Placental development and genomic imprinting in the mouse." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613928.

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Hore, Timothy Alexander, and timothy hore@anu edu au. "THE EVOLUTION OF GENOMIC IMPRINTING AND X CHROMOSOME INACTIVATION IN MAMMALS." The Australian National University. Research School of Biological Sciences, 2008. http://thesis.anu.edu.au./public/adt-ANU20081216.152553.

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Genomic imprinting is responsible for monoallelic gene expression that depends on the sex of the parent from which the alleles (one active, one silent) were inherited. X-chromosome inactivation is also a form of monoallelic gene expression. One of the two X chromosomes is transcriptionally silenced in the somatic cells of females, effectively equalising gene dosage with males who have only one X chromosome that is not complemented by a gene poor Y chromosome. X chromosome inactivation is random in eutherian mammals, but imprinted in marsupials, and in the extraembryonic membranes of some placentals. Imprinting and X inactivation have been studied in great detail in placental mammals (particularly humans and mice), and appear to occur also in marsupial mammals. However, both phenomena appear to have evolved specifically in mammals, since there is no evidence of imprinting or X inactivation in non-mammalian vertebrates, which do not show parent of origin effects and possess different sex chromosomes and dosage compensation mechanisms to mammals.¶ In order to understand how imprinting and X inactivation evolved, I have focused on the mammals most distantly related to human and mouse. I compared the sequence, location and expression of genes from major imprinted domains, and genes that regulate genomic imprinting and X-chromosome inactivation in the three extant mammalian groups and other vertebrates. Specifically, I studied the evolution of an autosomal region that is imprinted in humans and mouse, the evolution of the X-linked region thought to control X inactivation, and the evolution of the genes thought to establish and control differential expression of various imprinted loci. This thesis is presented as a collection of research papers that examines each of these topics, and a review and discussion that synthesizes my findings.¶ The first paper reports a study of the imprinted locus responsible for the human Prader-Willi and Angelman syndromes (PWS and AS). A search for kangaroo and platypus orthologues of PWS-AS genes identified only the putative AS gene UBE3A, and showed it was in a completely different genomic context to that of humans and mice. The only PWS gene found in marsupials (SNRPN) was located in tandem with its ancient paralogue SNRPB, on a different chromosome to UBE3A. Monotremes apparently have no orthologue of SNRPN. The several intronless genes of the PWS-AS domain also have no orthologues in marsupials or monotremes or non-mammal vertebrates, but all have close paralogues scattered about the genome from which they evidently retrotransposed. UBE3A in marsupials and monotremes, and SNRPN in marsupials were found to be expressed from both alleles, so are not imprinted. Thus, the PWA-AS imprinted domain was assembled from many non-imprinted components relatively recently, demonstrating that the evolution of imprinting has been an ongoing process during mammalian radiation.¶ In the second paper, I examine the evolution of the X-inactivation centre, the key regulatory region responsible for X-chromosome inactivation in humans and mice, which is imprinted in mouse extraembryonic membranes. By sequencing and aligning flanking regions across the three mammal groups and non-mammal vertebrates, I discovered that the region homologous to the X-inactivation centre, though intact in birds and frogs, was disrupted independently in marsupial and monotreme mammals. I showed that the key regulatory RNA of this locus (X-inactive specific transcript or XIST) is absent, explaining why a decade-long search for marsupial XIST was unsuccessful. Thus, XIST is eutherian-specific and is therefore not a basic requirement for X-chromosome inactivation in all mammals.¶ The broader significance of the findings reported in these two papers is explored with respect to other current work regarding the evolution and construction of imprinted loci in mammals in the form of a review. This comparison enabled me to conclude that like the PWS-AS domain and the X-inactivation centre, many domains show unexpected construction from disparate genomic elements that correlate with their acquisition of imprinting.¶ The fourth and last paper examines the evolution of CCCTC-binding Factor (CTCF) and its parologue Brother Of Regulator of Imprinted Sites (BORIS) which contribute to the establishment and interpretation of genomic imprinting at the Insulin-Like Growth Factor 2/H19 locus. In this paper I show that the duplication of CTCF giving rise to BORIS occurred much earlier than previously recognised, and demonstrate that a major change in BORIS expression (restriction to the germline) occurred in concert with the evolution of genomic imprinting. The papers that form the bulk of this thesis show that the evolution of epigenetic traits such as genomic imprinting and X-chromosome inactivation is labile and has apparently responded rapidly to different selective pressures during the independent evolution of the three mammal groups. I have introduced these papers, and discussed them generally in terms of current theories of how and why these forms of monoallelic expression have evolved in mammals.
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Books on the topic "Genomic imprinting"

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Ward, Andrew, ed. Genomic Imprinting. Totowa, NJ: Humana Press, 2002. http://dx.doi.org/10.1385/1592592112.

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Engel, Nora, ed. Genomic Imprinting. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-011-3.

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Ohlsson, Rolf, ed. Genomic Imprinting. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-540-69111-2.

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Wilkins, Jon F., ed. Genomic Imprinting. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-77576-0.

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Wolf, Reik, and Surani Azim, eds. Genomic imprinting. Oxford: IRL Press at Oxford University Press, 1997.

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F, Wilkins Jon, ed. Genomic imprinting. New York, N.Y: Springer Science+Business Media, 2008.

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R, Ohlsson, Hall Kerstin, and Ritzén Martin 1937-, eds. Genomic imprinting: Causes and consequences. Cambridge: Cambridge University Press, 1995.

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R, Ohlsson, ed. Genomic imprinting: An interdisciplinary approach. Berlin: Springer, 1999.

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Eric, Engel. Genomic imprinting and uniparental disomy in medicine: Clinical and molecular aspects. New York: Wiley, 2002.

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Flint, Jonathan. How genes influence behavior. New York, NY: Oxford University Press, 2010.

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Book chapters on the topic "Genomic imprinting"

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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro, and Anton Wutz. "Genomic Imprinting." In Introduction to Epigenetics, 91–115. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_5.

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AbstractA typical cell contains two sets of chromosomes: one that was inherited from the mother, the other from the father. Usually, autosomal alleles are expressed at similar levels from the maternally and paternally inherited chromosomes. This chapter is dedicated to an exception of this rule: the expression of genes that are regulated by genomic imprinting depends on the parental origin of the allele, leading to the non-equivalence of maternal and paternal genomes. Genomic imprinting is a paradigm of epigenetic gene regulation as genetically identical alleles can exist in two expression states within the same nucleus. The imprints marking the parental alleles are established in the parental germline, maintained during the development of the offspring, but reset before they are passed on to the next generation. In mammals, the primary imprint is usually a differentially methylated region at the locus but there are also examples where histone modifications mark the parental alleles. Many imprinted genes play important roles for development and are associated with human disease. Interestingly, genomic imprinting evolved independently in mammals and seed plants and similar mechanisms have been recruited to regulate imprinted expression in the two kingdoms. We will discuss evolutionary constraints that could have led to the evolution of genomic imprinting in these seemingly disparate lineages.
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Manji, Husseini K., Jorge Quiroz, R. Andrew Chambers, Anthony Absalom, David Menon, Patrizia Porcu, A. Leslie Morrow, et al. "Genomic Imprinting." In Encyclopedia of Psychopharmacology, 559. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4273.

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Feinberg, Andrew P. "Genomic Imprinting." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2390-2.

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Magenis, R. Ellen. "Genomic imprinting." In The AGT Cytogenetics Laboratory Manual, 481–98. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781119061199.ch10.

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Choufani, Sanaa, and Rosanna Weksberg. "Genomic Imprinting." In The Functional Nucleus, 449–65. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-38882-3_19.

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Khan, Scheherazade, and Angela Hilliker. "Genomic Imprinting." In Molecular Life Sciences, 1–3. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-6436-5_759-1.

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Carlberg, Carsten, and Ferdinand Molnár. "Genomic Imprinting." In Mechanisms of Gene Regulation, 147–58. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-017-7741-4_9.

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Brahmachari, Vani, and Shruti Jain. "Genomic Imprinting." In Encyclopedia of Systems Biology, 838. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_848.

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Feinberg, Andrew P. "Genomic Imprinting." In Encyclopedia of Cancer, 1888–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_2390.

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Feinberg, Andrew P. "Genomic Imprinting." In Encyclopedia of Cancer, 1536–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2390.

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Conference papers on the topic "Genomic imprinting"

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Guo, Chenkai, and Yaoxuan Wu. "Genomic imprinting in haemopoietic stem cells and leukemia." In 4TH INTERNATIONAL CONFERENCE ON FRONTIERS OF BIOLOGICAL SCIENCES AND ENGINEERING (FBSE 2021). AIP Publishing, 2022. http://dx.doi.org/10.1063/5.0095078.

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Anisimova, Inga V. "The etiology of intellectual development disorders." In Proceedings of III Research-to-Practice Conference with International Participation “The Value of Everyone. The Life of a Person with Mental Disorder: Support, Life Arrangements, Social Integration”. Terevinf, 2023. http://dx.doi.org/10.61157/978-5-4212-0676-7-2023-73-76.

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the causes of intellectual developmental disorders of various etiologies are described: the impact of external factors, hypoxic-ischemic brain lesions, the influence of genetic factors: chromosomal pathologies, monogenic diseases, genomic imprinting diseases
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Gonzalez-Pons, Maria, Mercedes Y. Lacourt, Sharon Fonseca-Williams, Lorena Marcano, Xiomara Castillo, Ronghua Zhao, Raul Bernabe-Dones, and Marcia Cruz-Correa. "Abstract 5362: Analysis of loss of IGF2 genomic imprinting and colorectal cancer risk in Puertorrican Hispanics." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5362.

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Wang, Xu. "Allele-specific transcriptome and methylome analysis revealscis-regulation of DNA methylation and lack of genomic imprinting inNasonia." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.105137.

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Kenny, D., R. D. Sleator, C. P. Murphy, R. D. Evans, and D. P. Berry. "370. Detecting the presence of genomic imprinting for carcass traits in cattle using imputed high-density genotypes." In World Congress on Genetics Applied to Livestock Production. The Netherlands: Wageningen Academic Publishers, 2022. http://dx.doi.org/10.3920/978-90-8686-940-4_370.

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Reports on the topic "Genomic imprinting"

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Ohad, Nir, and Robert Fischer. Regulation of plant development by polycomb group proteins. United States Department of Agriculture, January 2008. http://dx.doi.org/10.32747/2008.7695858.bard.

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Our genetic and molecular studies have indicated that FIE a WD-repeat Polycomb group (PcG) protein takes part in multi-component protein complexes. We have shown that FIE PcG protein represses inappropriate programs of development during the reproductive and vegetative phases of the Arabidopsis life cycle. Moreover, we have shown that FIE represses the expression of key regulatory genes that promote flowering (AG and LFY), embryogenesis (LEC1), and shoot formation (KNAT1). These results suggest that the FIE PcG protein participates in the formation of distinct PcG complexes that repress inappropriate gene expression at different stages of plant development. PcG complexes modulate chromatin compactness by modifying histones and thereby regulate gene expression and imprinting. The main goals of our original project were to elucidate the biological functions of PcG proteins, and to understand the molecular mechanisms used by FIE PcG complexes to repress the expression of its gene targets. Our results show that the PcG complex acts within the central cell of the female gametophyte to maintain silencing of MEA paternal allele. Further more we uncovered a novel example of self-imprinting mechanism by the PgG complex. Based on results obtained in the cures of our research program we extended our proposed goals and elucidated the role of DME in regulating plant gene imprinting. We discovered that in addition to MEA,DME also imprints two other genes, FWA and FIS2. Activation of FWA and FIS2 coincides with a reduction in 5-methylcytosine in their respective promoters. Since endosperm is a terminally differentiated tissue, the methylation status in the FWA and FIS2 promoters does not need to be reestablished in the following generation. We proposed a “One-Way Control” model to highlight differences between plant and animal genomic imprinting. Thus we conclude that DEMETER is a master regulator of plant gene imprinting. Future studies of DME function will elucidate its role in processes and disease where DNA methylation has a key regulatory role both in plants and animals. Such information will provide valuable insight into developing novel strategies to control and improve agricultural traits and overcome particular human diseases.
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