Geneimprint : Home
Title: Geneimprint : Home
Description: Geneimprint, the website for information about genomic imprinting and imprinted genes featuring articles, reviews, meeting videos and abstracts, and genetic databases. is ranked 0 in the world (amongst the 40 million domains). A low-numbered rank means that this website gets lots of visitors. This site is relatively popular among users in the united states. It gets 50% of its traffic from the united states .This site is estimated to be worth $0. This site has a low Pagerank(0/10). It has 1 backlinks. has 43% seo score. Information

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Geneimprint : Home Geneimprint Home Features Articles Genes Meetings Randy Jirtle Portal What is Genomic Imprinting? About this Site Announcements Jirtle delivers 2016 NCSU Commencement Address Jirtle receives IFM 2014 Linus Pauling Award - [Presentation] [Lecture] RWJF What's Next Health - Jirtle interview by Nancy Barrand Germline Exposures- Jirtle Interview by Jill Escher World Science Festival - Destiny and DNA: Our Pliable Genome NIH Director's WALS Lecture - Epigenetics: How Genes and Environment Interact (Speaker: Randy Jirtle) DUKE Office Hours - Jirtle Interview on Epigenetics, 2010 [YouTube] [MP4] Jirtle Interview on Epigenetics by Jeffery Bland - [MP3] [Transcript] NOVA scienceNOW PBS - Epigenetics Program Featured Articles Epigenomics meets splicing through the TETs and CTCF Gliomas Genomics and Epigenomics: Arriving at the Start and Knowing It for the First Time Genetic sources of population epigenomic variation Visualizing allele-specific expression in single cells reveals epigenetic mosaicism in an H19 loss-of-imprinting mutant FOXG1-Dependent Dysregulation of GABA/Glutamate Neuron Differentiation in Autism Spectrum Disorders Quantitative and functional interrogation of parent-of-origin allelic expression biases in the brain Lead Exposure during Early Human Development and DNA Methylation of Imprinted Gene Regulatory Elements in Adulthood Maternal-fetal conflict, genomic imprinting and mammalian vulnerabilities to cancer Brain feminization requires active repression of masculinization via DNA methylation Genetic conflict reflected in tissue-specific maps of genomic imprinting in human and mouse Loss of inherited genomic imprints in mice leads to severe disruption in placental lipid metabolism A systems-level approach to parental genomic imprinting: the imprinted gene network includes extracellular matrix genes and regulates cell cycle exit and differentiation Antagonistic roles in fetal development and adult physiology for the oppositely imprinted Grb10 and Dlk1 genes Recurrent epimutation of SDHC in gastrointestinal stromal tumors An integrative analysis reveals coordinated reprogramming of the epigenome and the transcriptome in human skeletal muscle after training Genomic imprinting, action, and interaction of maternal and fetal genomes Early life stress in fathers improves behavioural flexibility in their offspring Genetic Variation in Imprinted Genes is Associated with Risk of Late-Onset Alzheimer's Disease Conferences 2005 — Durham, NC Environmental Epigenomics, Imprinting and Disease Susceptibility 2002 — Washington, DC Epigenetic Mechanisms in Human Disease 2002 — London, England Imprinting and Growth Congress 2001 — Osaka, Japan Genomic Imprinting Workshop 1999 — Dublin, Ireland Genomic Imprinting Conference 1998 — Durham, NC Genomic Imprinting Symposium Hot Off the Press Recent advances in epigenomics in NSCLC: real-time detection and therapeutic implications Teratozoospermia and asthenozoospermia are associated with specific epigenetic signatures Emerging concepts of epigenetic dysregulation in hematological malignancies Complete in vitro generation of fertile oocytes from mouse primordial germ cells Review: DNA G-quadruplexes show strong interaction with DNA methyltransferases in vitro Integrated epigenomics analysis reveals a DNA methylation panel for endometrial cancer detection using cervical scrapings Impulsive choices in mice lacking imprinted Nesp55 A Simplified, Langendorff-Free Method for Concomitant Isolation of Viable Cardiac Myocytes and Non-Myocytes from the Adult Mouse Heart ATP-binding cassette transmembrane transporters and their epigenetic control in cancer: an overview Review: Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis Angelman syndrome-derived neurons display late onset of paternal UBE3A silencing Review: The Many Roles of BAF (mSWI/SNF) and PBAF Complexes in Cancer GenomeRunner web server: regulatory similarity and differences define the functional impact of SNP sets Chromatin and epigenetics in all their states: Meeting report of the first conference on Epigenetic and Chromatin Regulation of Plant Traits - January 14 - 15, 2016 - Strasbourg, France Rapid Evolution of Genomic Imprinting in Two Species of the Brassicaceae Conservation of DNA Methylation Programming Between Mouse and Human Gametes and Preimplantation Embryos Meta-analysis of Telomere Length in Alzheimer's Disease Fine-scale mapping of 8q24 locus identifies multiple independent risk variants for breast cancer Nongenomic regulation of gene expression H19ICR mediated transcriptional silencing does not require target promoter methylation 'Hot off the press' is a daily listing of the most recent articles in epigenetics and imprinting Imprinted Genes Implicated in the Puzzle of Autism Mariani, et. al. Cell 162:375-90 (2015) Press Reports: The Scientist Magazine 28 July 2015: FOXG1 is potentially involved in the development of autism spectrum disorder (ASD). In a recent study, Dr. Vaccarino and her colleagues at Yale University used a novel 3D organoid culture of human neural cells that were derived from induced pluripotent stem cells (iPSCs) obtained from the skin cells of people with and without severe idiopathic ASD. This study provides evidence that FOXG1 overexpression, rather than gene mutation, induces a GABAergic neuron fate that functions as a developmental precursor to ASD. DLGAP2, the other gene listed in the accompanying graphic, has also been implicated in the development of autism in a copy number variation (CNV) analysis of people with ASD. Interestingly, there is strong evidence that both of these genes are imprinted and expressed from the paternal allele (Luedi et al. 2007), as predicted by Christopher Badcock and Bernard Crespi in their imprinted brain theory. Imprinted genes are monoallelically expressed in a parent-of-origin dependent manner. Since the nonfunctional copy is silenced epigenetically, environmental factors that alter the epigenome can result in what is called loss of imprinting (LOI). This results in imprinted genes being either hypo or hyper expressed because of alterations in the epigenome (e.g. DNA methylation) rather than mutations in the genome. To determine the overall role of imprinting in the puzzle of ASD requires the identification of the complete repertoire of human imprinted genes and their regulatory elements - The Imprintome. Although this information is presently not available, it is crucial to determine now if the expression of FOXG1 and/or DLGAP2 are epigenetically dysregulated in ASD. Environmental Lead Exposure in Early Childhood Alters Imprinted Gene Regulation Although lead (Pb) is a neurotoxin, the mechanism by which it effects neurodevelopment, and the acceptable threshold of exposure to the developing child are still unclear. Imprinted genes have one parental allele silenced epigenetically, and they play critical roles in human development (Jirtle and Weidman 2007). In a recent study published in Environmental Health Perspectives, Cathrine Hoyo and her colleagues at North Carolina State University demonstrated, with the use of participants in the Cincinnati Lead Study, that children exposed early in development to high levels of Pb have altered DNA methylation in the regulatory elements of imprinted genes - PEG3, H19/IGF2 and PLAGL1/HYMAI - over three decades after exposure. Read more... p16 Epimutation Causes Cancer Hypermethylation of the promoter region of p16 causes cancer and reduces survival in mice according to a recent report by Lanlan Shen and her colleagues in The Journal of Clinical Investigation. The history of p16 as a human tumor suppressor gene is complex. Only months after gene deletion evidence from a variety of tumor cell lines indicated the involvement of p16 in the genesis of cancer (Nobori et al. 1994; Kamb et al. 1994), its tumor suppressor function was brought into question (Spruck et al. 1994; Cairns et al. 1994). According to the two-hit theory of carcinogenesis by Read more... Antagonistic Growth Promoting Effects of Imprinted Genes Imprinted genes are monoallelic expressed in a parent-of-origin dependent manner (Jirtle and Weidman 2007).The conflict theory of genomic imprinting predicts that maternally expressed genes are antigrowth while paternally expressed genes are progrowth (Haig and Graham 1991). The first two genes experimentally identified to be imprinted, the maternally expressed Igf2r (Barlow et al. 1991) and the paternally expressed Igf2 (DeChiara et al. 1991), were shown over two decades ago to adhere to this prediction. A second set of oppositely imprinted, fetal growth antagonistic genes has now been identified, the maternally expressed [Grb10]( Read more... Autism and Schizophrenia: The Antithesis of Each Other? Genomic imprinting is a phenomenon where one parental allele is silenced epigenetically, resulting in monoallelic parent-of-origin gene expression (Jirtle and Weidman 2007). It evolved about 150 million years ago with the advent of viviparity and placentation in a common ancestor to Therian mammals (i.e. Marsupials and Eutherians) (Killian et al. 2000). Badcock and Crespi postulated in their imprinted brain theory that autism spectrum disorders (AS) and schizophrenia spectrum (SS) disorders are the antithesis of each other, and result from the skewing of paternally and maternally imprinted gene expression in the brain during development. Paternally expressed imprinted genes tend to be progrowth, and those that are maternally expressed antigrowth. Read more... Environmental Epigenomics in Health and Disease Springer has recently published two books on environmental epigenomics that are edited by Randy L. Jirtle and Frederick L. Tyson -- Epigenetics and Disease Origins and Epigenetics and Complex Diseases. The overall purpose of these books is to give readers an overview of how environmental exposures can influence the risk of disease in adulthood by disrupting epigenetic processes and reprogramming during early development. Read more... Copyright ? 2012, Randy L. Jirtle, PhD. All rights reserved. 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