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  • 1
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    Drug-based modulation of endogenous stem cells promotes functional remyelination in vivo (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-04-22
    Description: Multiple sclerosis involves an aberrant autoimmune response and progressive failure of remyelination in the central nervous system. Prevention of neural degeneration and subsequent disability requires remyelination through the generation of new oligodendrocytes, but current treatments exclusively target the immune system. Oligodendrocyte progenitor cells are stem cells in the central nervous system and the principal source of myelinating oligodendrocytes. These cells are abundant in demyelinated regions of patients with multiple sclerosis, yet fail to differentiate, thereby representing a cellular target for pharmacological intervention. To discover therapeutic compounds for enhancing myelination from endogenous oligodendrocyte progenitor cells, we screened a library of bioactive small molecules on mouse pluripotent epiblast stem-cell-derived oligodendrocyte progenitor cells. Here we show seven drugs function at nanomolar doses selectively to enhance the generation of mature oligodendrocytes from progenitor cells in vitro. Two drugs, miconazole and clobetasol, are effective in promoting precocious myelination in organotypic cerebellar slice cultures, and in vivo in early postnatal mouse pups. Systemic delivery of each of the two drugs significantly increases the number of new oligodendrocytes and enhances remyelination in a lysolecithin-induced mouse model of focal demyelination. Administering each of the two drugs at the peak of disease in an experimental autoimmune encephalomyelitis mouse model of chronic progressive multiple sclerosis results in striking reversal of disease severity. Immune response assays show that miconazole functions directly as a remyelinating drug with no effect on the immune system, whereas clobetasol is a potent immunosuppressant as well as a remyelinating agent. Mechanistic studies show that miconazole and clobetasol function in oligodendrocyte progenitor cells through mitogen-activated protein kinase and glucocorticoid receptor signalling, respectively. Furthermore, both drugs enhance the generation of human oligodendrocytes from human oligodendrocyte progenitor cells in vitro. Collectively, our results provide a rationale for testing miconazole and clobetasol, or structurally modified derivatives, to enhance remyelination in patients.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4528969/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4528969/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Najm, Fadi J -- Madhavan, Mayur -- Zaremba, Anita -- Shick, Elizabeth -- Karl, Robert T -- Factor, Daniel C -- Miller, Tyler E -- Nevin, Zachary S -- Kantor, Christopher -- Sargent, Alex -- Quick, Kevin L -- Schlatzer, Daniela M -- Tang, Hong -- Papoian, Ruben -- Brimacombe, Kyle R -- Shen, Min -- Boxer, Matthew B -- Jadhav, Ajit -- Robinson, Andrew P -- Podojil, Joseph R -- Miller, Stephen D -- Miller, Robert H -- Tesar, Paul J -- F30 CA183510/CA/NCI NIH HHS/ -- F30CA183510/CA/NCI NIH HHS/ -- NS026543/NS/NINDS NIH HHS/ -- NS030800/NS/NINDS NIH HHS/ -- NS085246/NS/NINDS NIH HHS/ -- P30 CA043703/CA/NCI NIH HHS/ -- P30CA043703/CA/NCI NIH HHS/ -- R01 NS026543/NS/NINDS NIH HHS/ -- R01 NS030800/NS/NINDS NIH HHS/ -- R21 NS085246/NS/NINDS NIH HHS/ -- T32 GM007250/GM/NIGMS NIH HHS/ -- T32 GM008056/GM/NIGMS NIH HHS/ -- T32GM008056/GM/NIGMS NIH HHS/ -- UL1 TR000439/TR/NCATS NIH HHS/ -- England -- Nature. 2015 Jun 11;522(7555):216-20. doi: 10.1038/nature14335. Epub 2015 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA. ; Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA. ; 1] Department of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA [2] Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA [3] Department of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA. ; PerkinElmer, 940 Winter Street, Waltham, Massachusetts 02451, USA. ; Center for Proteomics and Bioinformatics, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA. ; Drug Discovery Center, University of Cincinnati College of Medicine, Cincinnati, Ohio 45237, USA. ; National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, Maryland 20850, USA. ; Department of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Avenue, Chicago, Illinois 60611, USA. ; 1] Department of Genetics and Genome Sciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA [2] Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25896324" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cerebellum/drug effects/metabolism/pathology ; Clobetasol/*pharmacology ; Demyelinating Diseases/drug therapy/metabolism/pathology ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/drug therapy/metabolism/pathology ; Female ; Germ Layers/drug effects/metabolism/pathology ; Humans ; Lysophosphatidylcholines ; MAP Kinase Signaling System ; Male ; Mice ; Miconazole/*pharmacology ; Mitogen-Activated Protein Kinases/metabolism ; Multiple Sclerosis/*drug therapy/*metabolism/pathology ; Myelin Sheath/*drug effects/*metabolism ; Oligodendroglia/cytology/drug effects/metabolism ; Phenotype ; Pluripotent Stem Cells/cytology/*drug effects/metabolism ; Receptors, Glucocorticoid/metabolism ; Regeneration/drug effects ; Tissue Culture Techniques
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Adult-onset primary open-angle glaucoma caused by mutations in optineurin (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-02-09
    Description: Primary open-angle glaucoma (POAG) affects 33 million individuals worldwide and is a leading cause of blindness. In a study of 54 families with autosomal dominantly inherited adult-onset POAG, we identified the causative gene on chromosome 10p14 and designated it OPTN (for "optineurin"). Sequence alterations in OPTN were found in 16.7% of families with hereditary POAG, including individuals with normal intraocular pressure. The OPTN gene codes for a conserved 66-kilodalton protein of unknown function that has been implicated in the tumor necrosis factor-alpha signaling pathway and that interacts with diverse proteins including Huntingtin, Ras-associated protein RAB8, and transcription factor IIIA. Optineurin is expressed in trabecular meshwork, nonpigmented ciliary epithelium, retina, and brain, and we speculate that it plays a neuroprotective role.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rezaie, Tayebeh -- Child, Anne -- Hitchings, Roger -- Brice, Glen -- Miller, Lauri -- Coca-Prados, Miguel -- Heon, Elise -- Krupin, Theodore -- Ritch, Robert -- Kreutzer, Donald -- Crick, R Pitts -- Sarfarazi, Mansoor -- EY-09947/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2002 Feb 8;295(5557):1077-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Ophthalmic Genetics Laboratory, Surgical Research Center, Department of Surgery, University of Connecticut Health Center, Farmington, CT 06030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11834836" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alternative Splicing ; Amino Acid Sequence ; Brain/metabolism ; Chromosome Mapping ; Chromosomes, Human, Pair 10/genetics ; Ciliary Body/metabolism ; Exons ; Eye Proteins/analysis/chemistry/*genetics/physiology ; Female ; Glaucoma, Open-Angle/*genetics ; Golgi Apparatus/chemistry ; Heterozygote ; Humans ; Intraocular Pressure ; Male ; Middle Aged ; *Mutation ; *Mutation, Missense ; Nerve Tissue Proteins/analysis/chemistry/*genetics/physiology ; Ocular Hypertension/genetics ; Pedigree ; Polymorphism, Single-Stranded Conformational ; Retina/metabolism ; Trabecular Meshwork/metabolism ; *Transcription Factor TFIIIA ; Zinc Fingers
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Sperm-female coevolution in Drosophila (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-09
    Description: Rapid evolution of reproductive traits has been attributed to sexual selection arising from interaction between the sexes. However, little is known about the nature of selection driving the evolution of interacting sex-specific phenotypes. Using populations of Drosophila melanogaster selected for divergent sperm length or female sperm-storage organ length, we experimentally show that male fertilization success is determined by an interaction between sperm and female morphology. In addition, sperm length evolution occurred as a correlated response to selection on the female reproductive tract. Giant sperm tails are the cellular equivalent of the peacock's tail, having evolved because females evolved reproductive tracts that selectively bias paternity in favor of males with longer sperm.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Gary T -- Pitnick, Scott -- New York, N.Y. -- Science. 2002 Nov 8;298(5596):1230-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Syracuse University, 108 College Place, Syracuse, NY 13244, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12424377" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Copulation ; Drosophila melanogaster/*anatomy & histology/genetics/*physiology ; Female ; Fertilization ; Genitalia, Female/anatomy & histology/physiology ; Linkage Disequilibrium ; Male ; Selection, Genetic ; Sexual Behavior, Animal ; Sperm Tail/ultrastructure ; Spermatozoa/*cytology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Sexual transmission and propagation of SIV and HIV in resting and activated CD4+ T cells (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-13
    Description: In sexual transmission of simian immunodeficiency virus, and early and later stages of human immunodeficiency virus-type 1 (HIV-1) infection, both viruses were found to replicate predominantly in CD4(+) T cells at the portal of entry and in lymphoid tissues. Infection was propagated not only in activated and proliferating T cells but also, surprisingly, in resting T cells. The infected proliferating cells correspond to the short-lived population that produces the bulk of HIV-1. Most of the HIV-1-infected resting T cells persisted after antiretroviral therapy. Latently and chronically infected cells that may be derived from this population pose challenges to eradicating infection and developing an effective vaccine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Z -- Schuler, T -- Zupancic, M -- Wietgrefe, S -- Staskus, K A -- Reimann, K A -- Reinhart, T A -- Rogan, M -- Cavert, W -- Miller, C J -- Veazey, R S -- Notermans, D -- Little, S -- Danner, S A -- Richman, D D -- Havlir, D -- Wong, J -- Jordan, H L -- Schacker, T W -- Racz, P -- Tenner-Racz, K -- Letvin, N L -- Wolinsky, S -- Haase, A T -- AI 28246/AI/NIAID NIH HHS/ -- AI 38565/AI/NIAID NIH HHS/ -- RR 00168/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 12;286(5443):1353-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10558989" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-HIV Agents/therapeutic use ; CD4-Positive T-Lymphocytes/cytology/immunology/*virology ; Cell Cycle ; Cervix Uteri/virology ; Epithelial Cells/virology ; Female ; HIV Infections/drug therapy/*transmission/virology ; HIV-1/*physiology ; Lymph Nodes/virology ; *Lymphocyte Activation ; Macaca mulatta ; RNA, Viral/analysis ; Simian Acquired Immunodeficiency Syndrome/*transmission/virology ; Simian Immunodeficiency Virus/*physiology ; Time Factors ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    A sperm cytoskeletal protein that signals oocyte meiotic maturation and ovulation (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-17
    Description: Caenorhabditis elegans oocytes, like those of most animals, arrest during meiotic prophase. Sperm promote the resumption of meiosis (maturation) and contraction of smooth muscle-like gonadal sheath cells, which are required for ovulation. We show that the major sperm cytoskeletal protein (MSP) is a bipartite signal for oocyte maturation and sheath contraction. MSP also functions in sperm locomotion, playing a role analogous to actin. Thus, during evolution, MSP has acquired extracellular signaling and intracellular cytoskeletal functions for reproduction. Proteins with MSP-like domains are found in plants, fungi, and other animals, suggesting that related signaling functions may exist in other phyla.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, M A -- Nguyen, V Q -- Lee, M H -- Kosinski, M -- Schedl, T -- Caprioli, R M -- Greenstein, D -- CA09592/CA/NCI NIH HHS/ -- GM57173/GM/NIGMS NIH HHS/ -- GM58008/GM/NIGMS NIH HHS/ -- HD07043/HD/NICHD NIH HHS/ -- HD25614/HD/NICHD NIH HHS/ -- R01 GM057173/GM/NIGMS NIH HHS/ -- R01 HD025614/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2001 Mar 16;291(5511):2144-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Mass Spectrometry Research Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11251118" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Caenorhabditis elegans/*physiology ; Carrier Proteins/chemistry/physiology ; Cytoskeleton/chemistry/physiology ; Disorders of Sex Development ; Enzyme Activation ; Evolution, Molecular ; Female ; Gonads/cytology/physiology ; Helminth Proteins/chemistry/immunology/pharmacology/*physiology ; MAP Kinase Signaling System ; Male ; *Meiosis ; Membrane Proteins/chemistry/physiology ; Microinjections ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Sequence Data ; Oocytes/*physiology ; Ovulation ; Phylogeny ; Protein Folding ; Protein Structure, Tertiary ; Pseudopodia/physiology ; Recombinant Proteins/pharmacology ; Signal Transduction ; Sperm Motility ; Spermatozoa/chemistry/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Endocrinology. Divorcing estrogen's bright and dark sides (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2002 Oct 25;298(5594):723-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12399556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Density/*drug effects ; Breast Neoplasms/pathology ; Cell Division/drug effects ; Cell Nucleus/metabolism ; Cells, Cultured ; Estrenes/*pharmacology ; Estrogens/metabolism/pharmacology ; Female ; Gene Expression Regulation/drug effects ; Humans ; Mice ; Osteoblasts/*drug effects/physiology ; Osteoclasts/*drug effects/physiology ; Ovariectomy ; Receptors, Estrogen/metabolism ; Signal Transduction ; Uterus/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Neuroscience. Researchers thrilled with seminal discovery (2002)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2002-08-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2002 Aug 30;297(5586):1460-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12202793" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ejaculation/*physiology ; Humans ; Lumbosacral Region ; Male ; Neurons/*physiology ; Rats ; Spinal Cord/cytology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    RANK ligand mediates progestin-induced mammary epithelial proliferation and carcinogenesis (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-01
    Description: RANK ligand (RANKL), a TNF-related molecule, is essential for osteoclast formation, function and survival through interaction with its receptor RANK. Mammary glands of RANK- and RANKL-deficient mice develop normally during sexual maturation, but fail to form lobuloalveolar structures during pregnancy because of defective proliferation and increased apoptosis of mammary epithelium. It has been shown that RANKL is responsible for the major proliferative response of mouse mammary epithelium to progesterone during mammary lactational morphogenesis, and in mouse models, manipulated to induce activation of the RANK/RANKL pathway in the absence of strict hormonal control, inappropriate mammary proliferation is observed. However, there is no evidence so far of a functional contribution of RANKL to tumorigenesis. Here we show that RANK and RANKL are expressed within normal, pre-malignant and neoplastic mammary epithelium, and using complementary gain-of-function (mouse mammary tumour virus (MMTV)-RANK transgenic mice) and loss-of function (pharmacological inhibition of RANKL) approaches, define a direct contribution of this pathway in mammary tumorigenesis. Accelerated pre-neoplasias and increased mammary tumour formation were observed in MMTV-RANK transgenic mice after multiparity or treatment with carcinogen and hormone (progesterone). Reciprocally, selective pharmacological inhibition of RANKL attenuated mammary tumour development not only in hormone- and carcinogen-treated MMTV-RANK and wild-type mice, but also in the MMTV-neu transgenic spontaneous tumour model. The reduction in tumorigenesis upon RANKL inhibition was preceded by a reduction in pre-neoplasias as well as rapid and sustained reductions in hormone- and carcinogen-induced mammary epithelial proliferation and cyclin D1 levels. Collectively, our results indicate that RANKL inhibition is acting directly on hormone-induced mammary epithelium at early stages in tumorigenesis, and the permissive contribution of progesterone to increased mammary cancer incidence is due to RANKL-dependent proliferative changes in the mammary epithelium. The current study highlights a potential role for RANKL inhibition in the management of proliferative breast disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gonzalez-Suarez, Eva -- Jacob, Allison P -- Jones, Jon -- Miller, Robert -- Roudier-Meyer, Martine P -- Erwert, Ryan -- Pinkas, Jan -- Branstetter, Dan -- Dougall, William C -- England -- Nature. 2010 Nov 4;468(7320):103-7. doi: 10.1038/nature09495. Epub 2010 Sep 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Hematology/Oncology Research, Amgen Inc, Seattle, Washington 98119, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20881963" target="_blank"〉PubMed〈/a〉
    Keywords: 9,10-Dimethyl-1,2-benzanthracene/administration & dosage/adverse effects ; Animals ; Breast Neoplasms/metabolism/pathology ; Cell Proliferation/drug effects ; Cell Transformation, Neoplastic/*chemically induced/*drug effects/pathology ; Disease Models, Animal ; Epithelial Cells/drug effects/metabolism/pathology ; Female ; Humans ; Lung Neoplasms/secondary ; Mammary Neoplasms, Experimental/*chemically ; induced/genetics/metabolism/*pathology ; Mammary Tumor Virus, Mouse/genetics/physiology ; Medroxyprogesterone Acetate/administration & dosage/adverse effects ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neoplasm Invasiveness ; Precancerous Conditions/pathology/prevention & control ; Progesterone/administration & dosage/adverse effects ; Progestins/administration & dosage/*adverse effects ; RANK Ligand/antagonists & inhibitors/genetics/*metabolism ; Receptor Activator of Nuclear Factor-kappa B/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Genome, epigenome and RNA sequences of monozygotic twins discordant for multiple sclerosis (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-30
    Description: Monozygotic or 'identical' twins have been widely studied to dissect the relative contributions of genetics and environment in human diseases. In multiple sclerosis (MS), an autoimmune demyelinating disease and common cause of neurodegeneration and disability in young adults, disease discordance in monozygotic twins has been interpreted to indicate environmental importance in its pathogenesis. However, genetic and epigenetic differences between monozygotic twins have been described, challenging the accepted experimental model in disambiguating the effects of nature and nurture. Here we report the genome sequences of one MS-discordant monozygotic twin pair, and messenger RNA transcriptome and epigenome sequences of CD4(+) lymphocytes from three MS-discordant, monozygotic twin pairs. No reproducible differences were detected between co-twins among approximately 3.6 million single nucleotide polymorphisms (SNPs) or approximately 0.2 million insertion-deletion polymorphisms. Nor were any reproducible differences observed between siblings of the three twin pairs in HLA haplotypes, confirmed MS-susceptibility SNPs, copy number variations, mRNA and genomic SNP and insertion-deletion genotypes, or the expression of approximately 19,000 genes in CD4(+) T cells. Only 2 to 176 differences in the methylation of approximately 2 million CpG dinucleotides were detected between siblings of the three twin pairs, in contrast to approximately 800 methylation differences between T cells of unrelated individuals and several thousand differences between tissues or between normal and cancerous tissues. In the first systematic effort to estimate sequence variation among monozygotic co-twins, we did not find evidence for genetic, epigenetic or transcriptome differences that explained disease discordance. These are the first, to our knowledge, female, twin and autoimmune disease individual genome sequences reported.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862593/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862593/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baranzini, Sergio E -- Mudge, Joann -- van Velkinburgh, Jennifer C -- Khankhanian, Pouya -- Khrebtukova, Irina -- Miller, Neil A -- Zhang, Lu -- Farmer, Andrew D -- Bell, Callum J -- Kim, Ryan W -- May, Gregory D -- Woodward, Jimmy E -- Caillier, Stacy J -- McElroy, Joseph P -- Gomez, Refujia -- Pando, Marcelo J -- Clendenen, Leonda E -- Ganusova, Elena E -- Schilkey, Faye D -- Ramaraj, Thiruvarangan -- Khan, Omar A -- Huntley, Jim J -- Luo, Shujun -- Kwok, Pui-Yan -- Wu, Thomas D -- Schroth, Gary P -- Oksenberg, Jorge R -- Hauser, Stephen L -- Kingsmore, Stephen F -- P20 RR016480/RR/NCRR NIH HHS/ -- P20 RR016480-09/RR/NCRR NIH HHS/ -- R01 NS026799/NS/NINDS NIH HHS/ -- R01 NS026799-20A1/NS/NINDS NIH HHS/ -- R01 NS046297/NS/NINDS NIH HHS/ -- R01 NS046297-06/NS/NINDS NIH HHS/ -- R01NS26799/NS/NINDS NIH HHS/ -- R01NS46297/NS/NINDS NIH HHS/ -- RR016480/RR/NCRR NIH HHS/ -- U01 AI066569/AI/NIAID NIH HHS/ -- U01 AI066569-05/AI/NIAID NIH HHS/ -- U19 HD077693/HD/NICHD NIH HHS/ -- England -- Nature. 2010 Apr 29;464(7293):1351-6. doi: 10.1038/nature08990.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California at San Francisco, San Francisco, California 94143, USA. sebaran@cgl.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20428171" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Allelic Imbalance/genetics ; Breast/metabolism ; Breast Neoplasms/genetics ; CD4-Positive T-Lymphocytes/metabolism ; Case-Control Studies ; CpG Islands/genetics ; DNA Copy Number Variations/genetics ; DNA Methylation/genetics ; Epigenesis, Genetic/*genetics ; Female ; Genetic Predisposition to Disease/genetics ; Genome, Human/*genetics ; Haplotypes/genetics ; Heterozygote ; Humans ; INDEL Mutation/genetics ; Lung/metabolism ; Lung Neoplasms/genetics ; Male ; Multiple Sclerosis/*genetics ; Polymorphism, Genetic/genetics ; Quantitative Trait Loci/genetics ; RNA, Messenger/analysis/*genetics/metabolism ; Twins, Monozygotic/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Genome analysis of the platypus reveals unique signatures of evolution (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-05-10
    Description: We present a draft genome sequence of the platypus, Ornithorhynchus anatinus. This monotreme exhibits a fascinating combination of reptilian and mammalian characters. For example, platypuses have a coat of fur adapted to an aquatic lifestyle; platypus females lactate, yet lay eggs; and males are equipped with venom similar to that of reptiles. Analysis of the first monotreme genome aligned these features with genetic innovations. We find that reptile and platypus venom proteins have been co-opted independently from the same gene families; milk protein genes are conserved despite platypuses laying eggs; and immune gene family expansions are directly related to platypus biology. Expansions of protein, non-protein-coding RNA and microRNA families, as well as repeat elements, are identified. Sequencing of this genome now provides a valuable resource for deep mammalian comparative analyses, as well as for monotreme biology and conservation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803040/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803040/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warren, Wesley C -- Hillier, LaDeana W -- Marshall Graves, Jennifer A -- Birney, Ewan -- Ponting, Chris P -- Grutzner, Frank -- Belov, Katherine -- Miller, Webb -- Clarke, Laura -- Chinwalla, Asif T -- Yang, Shiaw-Pyng -- Heger, Andreas -- Locke, Devin P -- Miethke, Pat -- Waters, Paul D -- Veyrunes, Frederic -- Fulton, Lucinda -- Fulton, Bob -- Graves, Tina -- Wallis, John -- Puente, Xose S -- Lopez-Otin, Carlos -- Ordonez, Gonzalo R -- Eichler, Evan E -- Chen, Lin -- Cheng, Ze -- Deakin, Janine E -- Alsop, Amber -- Thompson, Katherine -- Kirby, Patrick -- Papenfuss, Anthony T -- Wakefield, Matthew J -- Olender, Tsviya -- Lancet, Doron -- Huttley, Gavin A -- Smit, Arian F A -- Pask, Andrew -- Temple-Smith, Peter -- Batzer, Mark A -- Walker, Jerilyn A -- Konkel, Miriam K -- Harris, Robert S -- Whittington, Camilla M -- Wong, Emily S W -- Gemmell, Neil J -- Buschiazzo, Emmanuel -- Vargas Jentzsch, Iris M -- Merkel, Angelika -- Schmitz, Juergen -- Zemann, Anja -- Churakov, Gennady -- Kriegs, Jan Ole -- Brosius, Juergen -- Murchison, Elizabeth P -- Sachidanandam, Ravi -- Smith, Carly -- Hannon, Gregory J -- Tsend-Ayush, Enkhjargal -- McMillan, Daniel -- Attenborough, Rosalind -- Rens, Willem -- Ferguson-Smith, Malcolm -- Lefevre, Christophe M -- Sharp, Julie A -- Nicholas, Kevin R -- Ray, David A -- Kube, Michael -- Reinhardt, Richard -- Pringle, Thomas H -- Taylor, James -- Jones, Russell C -- Nixon, Brett -- Dacheux, Jean-Louis -- Niwa, Hitoshi -- Sekita, Yoko -- Huang, Xiaoqiu -- Stark, Alexander -- Kheradpour, Pouya -- Kellis, Manolis -- Flicek, Paul -- Chen, Yuan -- Webber, Caleb -- Hardison, Ross -- Nelson, Joanne -- Hallsworth-Pepin, Kym -- Delehaunty, Kim -- Markovic, Chris -- Minx, Pat -- Feng, Yucheng -- Kremitzki, Colin -- Mitreva, Makedonka -- Glasscock, Jarret -- Wylie, Todd -- Wohldmann, Patricia -- Thiru, Prathapan -- Nhan, Michael N -- Pohl, Craig S -- Smith, Scott M -- Hou, Shunfeng -- Nefedov, Mikhail -- de Jong, Pieter J -- Renfree, Marilyn B -- Mardis, Elaine R -- Wilson, Richard K -- 062023/Wellcome Trust/United Kingdom -- HG002238/HG/NHGRI NIH HHS/ -- MC_U137761446/Medical Research Council/United Kingdom -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-37/CA/NCI NIH HHS/ -- R01 GM59290/GM/NIGMS NIH HHS/ -- R01 HG002939/HG/NHGRI NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG004037-02/HG/NHGRI NIH HHS/ -- R01HG02385/HG/NHGRI NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2008 May 8;453(7192):175-83. doi: 10.1038/nature06936.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genome Sequencing Center, Washington University School of Medicine, Campus Box 8501, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA. wwarren@wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18464734" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; Dentition ; *Evolution, Molecular ; Female ; Genome/*genetics ; Genomic Imprinting/genetics ; Humans ; Immunity/genetics ; Male ; Mammals/genetics ; MicroRNAs/genetics ; Milk Proteins/genetics ; Phylogeny ; Platypus/*genetics/immunology/physiology ; Receptors, Odorant/genetics ; Repetitive Sequences, Nucleic Acid/genetics ; Reptiles/genetics ; Sequence Analysis, DNA ; Spermatozoa/metabolism ; Venoms/genetics ; Zona Pellucida/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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