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  • 1
    Publication Date: 2007-09-18
    Description: Antibodies play a central role in immunity by forming an interface with the innate immune system and, typically, mediate proinflammatory activity. We describe a novel posttranslational modification that leads to anti-inflammatory activity of antibodies of immunoglobulin G, isotype 4 (IgG4). IgG4 antibodies are dynamic molecules that exchange Fab arms by swapping a heavy chain and attached light chain (half-molecule) with a heavy-light chain pair from another molecule, which results in bispecific antibodies. Mutagenesis studies revealed that the third constant domain is critical for this activity. The impact of IgG4 Fab arm exchange was confirmed in vivo in a rhesus monkey model with experimental autoimmune myasthenia gravis. IgG4 Fab arm exchange is suggested to be an important biological mechanism that provides the basis for the anti-inflammatory activity attributed to IgG4 antibodies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van der Neut Kolfschoten, Marijn -- Schuurman, Janine -- Losen, Mario -- Bleeker, Wim K -- Martinez-Martinez, Pilar -- Vermeulen, Ellen -- den Bleker, Tamara H -- Wiegman, Luus -- Vink, Tom -- Aarden, Lucien A -- De Baets, Marc H -- van de Winkel, Jan G J -- Aalberse, Rob C -- Parren, Paul W H I -- New York, N.Y. -- Science. 2007 Sep 14;317(5844):1554-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sanquin Research-AMC Landsteiner Laboratory, Department of Immunopathology, Plesmanlaan 125, 1066 CX Amsterdam, the Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872445" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/immunology ; Animals ; Antibodies, Bispecific/immunology ; Antibodies, Monoclonal/immunology ; Antigens, CD20/immunology ; Antigens, Plant ; Autoantibodies/immunology ; Glycoproteins/immunology ; Humans ; Immunoglobulin Constant Regions/chemistry ; Immunoglobulin Fab Fragments/*chemistry/*immunology/metabolism ; Immunoglobulin G/*chemistry/*immunology/metabolism ; Immunoglobulin Heavy Chains ; Macaca mulatta ; Mice ; Mutation ; Myasthenia Gravis, Autoimmune, Experimental/immunology/prevention & control ; Protein Processing, Post-Translational ; Receptor, Epidermal Growth Factor/immunology ; Receptors, Cholinergic/immunology
    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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  • 2
    ISSN: 0196-9781
    Keywords: Angiotensin-converting enzyme ; Captopril ; Dipeptidyl carboxypeptidases ; Enzymatic hydrolysis ; HPLC ; Met-enkephalin ; Mice ; Novelty ; Opioid peptides ; Phosphoramidon
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2016-04-21
    Description: Defects in clearance of dying cells have been proposed to underlie the pathogenesis of systemic lupus erythematosus (SLE). Mice lacking molecules associated with dying cell clearance develop SLE-like disease, and phagocytes from patients with SLE often display defective clearance and increased inflammatory cytokine production when exposed to dying cells in vitro. Previously, we and others described a form of noncanonical autophagy known as LC3-associated phagocytosis (LAP), in which phagosomes containing engulfed particles, including dying cells, recruit elements of the autophagy pathway to facilitate maturation of phagosomes and digestion of their contents. Genome-wide association studies have identified polymorphisms in the Atg5 (ref. 8) and possibly Atg7 (ref. 9) genes, involved in both canonical autophagy and LAP, as markers of a predisposition for SLE. Here we describe the consequences of defective LAP in vivo. Mice lacking any of several components of the LAP pathway show increased serum levels of inflammatory cytokines and autoantibodies, glomerular immune complex deposition, and evidence of kidney damage. When dying cells are injected into LAP-deficient mice, they are engulfed but not efficiently degraded and trigger acute elevation of pro-inflammatory cytokines but not anti-inflammatory interleukin (IL)-10. Repeated injection of dying cells into LAP-deficient, but not LAP-sufficient, mice accelerated the development of SLE-like disease, including increased serum levels of autoantibodies. By contrast, mice deficient in genes required for canonical autophagy but not LAP do not display defective dying cell clearance, inflammatory cytokine production, or SLE-like disease, and, like wild-type mice, produce IL-10 in response to dying cells. Therefore, defects in LAP, rather than canonical autophagy, can cause SLE-like phenomena, and may contribute to the pathogenesis of SLE.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860026/" 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/PMC4860026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, Jennifer -- Cunha, Larissa D -- Park, Sunmin -- Yang, Mao -- Lu, Qun -- Orchard, Robert -- Li, Quan-Zhen -- Yan, Mei -- Janke, Laura -- Guy, Cliff -- Linkermann, Andreas -- Virgin, Herbert W -- Green, Douglas R -- 1ZIAES10328601/PHS HHS/ -- R01 AI040646/AI/NIAID NIH HHS/ -- R01 AI40646/AI/NIAID NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- ZIA ES103286-01/Intramural NIH HHS/ -- England -- Nature. 2016 May 5;533(7601):115-9. doi: 10.1038/nature17950. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, North Carolina 27709, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Division of Nephrology and Hypertension, Christian-Albrechts-University, Kiel 24105, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096368" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/metabolism ; Autoantibodies/blood ; *Autophagy/genetics ; Cytokines/biosynthesis/blood ; Inflammation/blood/genetics/*pathology ; Interleukin-10/biosynthesis ; Kidney/metabolism/pathology ; Lupus Erythematosus, Systemic/blood/genetics/*immunology/*pathology ; Male ; Mice ; Microtubule-Associated Proteins/metabolism ; Phagocytes/cytology/physiology ; Phagosomes/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2008-08-02
    Description: Peripheral pain pathways are activated by a range of stimuli. We used diphtheria toxin to kill all mouse postmitotic sensory neurons expressing the sodium channel Nav1.8. Mice showed normal motor activity and low-threshold mechanical and acute noxious heat responses but did not respond to noxious mechanical pressure or cold. They also showed a loss of enhanced pain responses and spontaneous pain behavior upon treatment with inflammatory insults. In contrast, nerve injury led to heightened pain sensitivity to thermal and mechanical stimuli indistinguishable from that seen with normal littermates. Pain behavior correlates well with central input from sensory neurons measured electrophysiologically in vivo. These data demonstrate that Na(v)1.8-expressing neurons are essential for mechanical, cold, and inflammatory pain but not for neuropathic pain or heat sensing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abrahamsen, Bjarke -- Zhao, Jing -- Asante, Curtis O -- Cendan, Cruz Miguel -- Marsh, Steve -- Martinez-Barbera, Juan Pedro -- Nassar, Mohammed A -- Dickenson, Anthony H -- Wood, John N -- BB/F000227/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G9717869/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):702-5. doi: 10.1126/science.1156916.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Nociception Group, University College London (UCL), Gower Street, London, WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cold Temperature ; Electrophysiology ; Freund's Adjuvant ; Hot Temperature ; Inflammation/*physiopathology ; Mice ; Mice, Knockout ; NAV1.8 Voltage-Gated Sodium Channel ; Neurons, Afferent/*physiology ; Nociceptors/physiology ; Pain/*physiopathology ; Pain Measurement ; Pain Threshold ; Pressure ; Sodium Channels/genetics/*metabolism ; TRPV Cation Channels/genetics/metabolism
    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
    Publication Date: 2012-08-11
    Description: During development of the mammalian cerebral cortex, radial glial cells (RGCs) generate layer-specific subtypes of excitatory neurons in a defined temporal sequence, in which lower-layer neurons are formed before upper-layer neurons. It has been proposed that neuronal subtype fate is determined by birthdate through progressive restriction of the neurogenic potential of a common RGC progenitor. Here, we demonstrate that the murine cerebral cortex contains RGC sublineages with distinct fate potentials. Using in vivo genetic fate mapping and in vitro clonal analysis, we identified an RGC lineage that is intrinsically specified to generate only upper-layer neurons, independently of niche and birthdate. Because upper cortical layers were expanded during primate evolution, amplification of this RGC pool may have facilitated human brain evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4287277/" 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/PMC4287277/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Franco, Santos J -- Gil-Sanz, Cristina -- Martinez-Garay, Isabel -- Espinosa, Ana -- Harkins-Perry, Sarah R -- Ramos, Cynthia -- Muller, Ulrich -- MH078833/MH/NIMH NIH HHS/ -- NS046456/NS/NINDS NIH HHS/ -- NS060355/NS/NINDS NIH HHS/ -- R01 NS046456/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 10;337(6095):746-9. doi: 10.1126/science.1223616.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dorris Neuroscience Center and Department of Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22879516" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Cerebral Cortex/*cytology/embryology ; Homeodomain Proteins/genetics ; Mice ; Neural Stem Cells/*cytology/physiology ; *Neurogenesis ; Neuroglia/*cytology ; Neurons/*cytology/physiology ; Recombination, Genetic
    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
    Publication Date: 1999-08-07
    Description: There is a long-standing controversy regarding the mechanisms that generate the functional subdivisions of the cerebral neocortex. One model proposes that thalamic axonal input specifies these subdivisions; the competing model postulates that patterning mechanisms intrinsic to the dorsal telencephalon generate neocortical regions. Gbx-2 mutant mice, whose thalamic differentiation is disrupted, were investigated. Despite the lack of cortical innervation by thalamic axons, neocortical region-specific gene expression (Cadherin-6, EphA-7, Id-2, and RZR-beta) developed normally. This provides evidence that patterning mechanisms intrinsic to the neocortex specify the basic organization of its functional subdivisions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyashita-Lin, E M -- Hevner, R -- Wassarman, K M -- Martinez, S -- Rubenstein, J L -- NS34661-01A1/NS/NINDS NIH HHS/ -- R01 MH49428-01/MH/NIMH NIH HHS/ -- R01 MH51561-01A1/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):906-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nina Ireland Laboratory of Developmental Neurobiology, Department of Psychiatry, School of Medicine, University of California San Francisco, San Francisco, CA 94143-0984, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10436162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/chemistry/*physiology ; Cadherins/genetics ; Calbindin 2 ; Carbocyanines ; DNA-Binding Proteins/genetics ; Gene Expression ; Homeodomain Proteins/genetics/physiology ; Immunohistochemistry ; In Situ Hybridization ; Inhibitor of Differentiation Proteins ; Lymphoid Enhancer-Binding Factor 1 ; Mice ; Mutation ; Neocortex/anatomy & histology/*embryology/growth & development/metabolism ; Nerve Fibers/physiology/ultrastructure ; Proteins/genetics ; Receptors, Cell Surface/genetics ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Melatonin ; S100 Calcium Binding Protein G/analysis ; Steroid 17-alpha-Hydroxylase/analysis ; Telencephalon/embryology/growth & development/physiology ; Thalamus/anatomy & histology/*embryology/growth & development/metabolism ; Transcription Factors/genetics
    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
    Publication Date: 2009-07-25
    Description: A fundamental function of CD4+ helper T (T(H)) cells is the regulation of B cell-mediated humoral immunity. Development of T follicular helper (T(FH)) cells that provide help to B cells is mediated by the cytokines interleukin-6 and interleukin-21 but is independent of TH1, TH2, and TH17 effector cell lineages. Here, we characterize the function of Bcl6, a transcription factor selectively expressed in T(FH) cells. Bcl6 expression is regulated by interleukin-6 and interleukin-21. Bcl6 overexpression induced T(FH)-related gene expression and inhibited other T(H) lineage cell differentiation in a DNA binding-dependent manner. Moreover, Bcl6 deficiency in T cells resulted in impaired T(FH) cell development and germinal center reactions, and altered production of other effector T cell subsets. Our data thus illustrate that Bcl6 is required for programming of T(FH) cell generation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2857334/" 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/PMC2857334/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nurieva, Roza I -- Chung, Yeonseok -- Martinez, Gustavo J -- Yang, Xuexian O -- Tanaka, Shinya -- Matskevitch, Tatyana D -- Wang, Yi-Hong -- Dong, Chen -- R01 AI050746/AI/NIAID NIH HHS/ -- R01 AI050746-05/AI/NIAID NIH HHS/ -- R01 AI050761/AI/NIAID NIH HHS/ -- R01 AI050761-05/AI/NIAID NIH HHS/ -- R01 AI050761-06/AI/NIAID NIH HHS/ -- R01 AI050761-07A1/AI/NIAID NIH HHS/ -- R01 AI083761/AI/NIAID NIH HHS/ -- R01 AR050772/AR/NIAMS NIH HHS/ -- R01 AR050772-07/AR/NIAMS NIH HHS/ -- R01 AR050772-08/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 21;325(5943):1001-5. doi: 10.1126/science.1176676. Epub 2009 Jul 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, M. D. Anderson Cancer Center, Houston, TX 77030, USA. rnurieva@mdanderson.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19628815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Formation ; B-Lymphocytes/immunology ; Cell Differentiation ; Cell Lineage ; Cytokines/immunology/metabolism ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Germinal Center/cytology/*immunology ; Immunoglobulins/biosynthesis ; Interleukin-6/immunology/metabolism ; Interleukins/immunology/metabolism ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; RNA, Messenger/genetics/metabolism ; T-Lymphocyte Subsets/cytology/*immunology ; T-Lymphocytes, Helper-Inducer/cytology/*immunology ; Transcription Factors/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 8
    Publication Date: 2006-01-28
    Description: The transition of DNA secondary structure from an analogous B to Z conformation modulates the dielectric environment of the single-walled carbon nanotube (SWNT) around which it is adsorbed. The SWNT band-gap fluorescence undergoes a red shift when an encapsulating 30-nucleotide oligomer is exposed to counter ions that screen the charged backbone. The transition is thermodynamically identical for DNA on and off the nanotube, except that the propagation length of the former is shorter by five-sixths. The magnitude of the energy shift is described by using an effective medium model and the DNA geometry on the nanotube sidewall. We demonstrate the detection of the B-Z change in whole blood, tissue, and from within living mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heller, Daniel A -- Jeng, Esther S -- Yeung, Tsun-Kwan -- Martinez, Brittany M -- Moll, Anthonie E -- Gastala, Joseph B -- Strano, Michael S -- New York, N.Y. -- Science. 2006 Jan 27;311(5760):508-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439657" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Absorption ; Adsorption ; Animals ; Cations, Divalent/chemistry ; Chickens ; Circular Dichroism ; DNA/blood/*chemistry ; DNA, Z-Form/blood/*chemistry ; Fluorescence ; Mathematics ; Mercury/analysis ; Mice ; Models, Molecular ; Muscle, Skeletal/chemistry ; *Nanotubes, Carbon ; *Nucleic Acid Conformation ; Oligodeoxyribonucleotides/chemistry ; Spectrometry, Fluorescence ; Thermodynamics
    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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  • 9
    Publication Date: 2010-04-10
    Description: Transcription factors (TFs) direct gene expression by binding to DNA regulatory regions. To explore the evolution of gene regulation, we used chromatin immunoprecipitation with high-throughput sequencing (ChIP-seq) to determine experimentally the genome-wide occupancy of two TFs, CCAAT/enhancer-binding protein alpha and hepatocyte nuclear factor 4 alpha, in the livers of five vertebrates. Although each TF displays highly conserved DNA binding preferences, most binding is species-specific, and aligned binding events present in all five species are rare. Regions near genes with expression levels that are dependent on a TF are often bound by the TF in multiple species yet show no enhanced DNA sequence constraint. Binding divergence between species can be largely explained by sequence changes to the bound motifs. Among the binding events lost in one lineage, only half are recovered by another binding event within 10 kilobases. Our results reveal large interspecies differences in transcriptional regulation and provide insight into regulatory evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008766/" 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/PMC3008766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmidt, Dominic -- Wilson, Michael D -- Ballester, Benoit -- Schwalie, Petra C -- Brown, Gordon D -- Marshall, Aileen -- Kutter, Claudia -- Watt, Stephen -- Martinez-Jimenez, Celia P -- Mackay, Sarah -- Talianidis, Iannis -- Flicek, Paul -- Odom, Duncan T -- 062023/Wellcome Trust/United Kingdom -- 079643/Wellcome Trust/United Kingdom -- 15603/Cancer Research UK/United Kingdom -- 202218/European Research Council/International -- A15603/Cancer Research UK/United Kingdom -- WT062023/Wellcome Trust/United Kingdom -- WT079643/Wellcome Trust/United Kingdom -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2010 May 21;328(5981):1036-40. doi: 10.1126/science.1186176. Epub 2010 Apr 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20378774" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Base Sequence ; Binding Sites ; Biological Evolution ; CCAAT-Enhancer-Binding Protein-alpha/*metabolism ; Chickens/genetics ; Chromatin Immunoprecipitation ; DNA/genetics/metabolism ; Dogs ; *Evolution, Molecular ; *Gene Expression Regulation ; *Genome ; Genome, Human ; Hepatocyte Nuclear Factor 4/*metabolism ; Humans ; Liver/*metabolism ; Mice ; Opossums/genetics ; Protein Binding ; Regulatory Sequences, Nucleic Acid ; Sequence Analysis, DNA ; Species Specificity ; Vertebrates/*genetics/metabolism
    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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  • 10
    Publication Date: 2011-06-02
    Description: The retrovirus XMRV (xenotropic murine leukemia virus-related virus) has been detected in human prostate tumors and in blood samples from patients with chronic fatigue syndrome, but these findings have not been replicated. We hypothesized that an understanding of when and how XMRV first arose might help explain the discrepant results. We studied human prostate cancer cell lines CWR22Rv1 and CWR-R1, which produce XMRV virtually identical to the viruses recently found in patient samples, as well as their progenitor human prostate tumor xenograft (CWR22) that had been passaged in mice. We detected XMRV infection in the two cell lines and in the later passage xenografts, but not in the early passages. In particular, we found that the host mice contained two proviruses, PreXMRV-1 and PreXMRV-2, which share 99.92% identity with XMRV over 〉3.2-kilobase stretches of their genomes. We conclude that XMRV was not present in the original CWR22 tumor but was generated by recombination of two proviruses during tumor passaging in mice. The probability that an identical recombinant was generated independently is negligible (~10(-12)); our results suggest that the association of XMRV with human disease is due to contamination of human samples with virus originating from this recombination event.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278917/" 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/PMC3278917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paprotka, Tobias -- Delviks-Frankenberry, Krista A -- Cingoz, Oya -- Martinez, Anthony -- Kung, Hsing-Jien -- Tepper, Clifford G -- Hu, Wei-Shau -- Fivash, Matthew J Jr -- Coffin, John M -- Pathak, Vinay K -- P30 CA093373/CA/NCI NIH HHS/ -- R01CA150197/CA/NCI NIH HHS/ -- R37 CA 089441/CA/NCI NIH HHS/ -- R37 CA089441/CA/NCI NIH HHS/ -- R37 CA089441-11/CA/NCI NIH HHS/ -- ZIA BC011339-02/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):97-101. doi: 10.1126/science.1205292. Epub 2011 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Viral Mutation Section, HIV Drug Resistance Program, National Cancer Institute at Frederick, Frederick, MD 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21628392" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor/*virology ; DNA Contamination ; DNA, Viral/analysis ; Endogenous Retroviruses/genetics ; Fatigue Syndrome, Chronic/virology ; Gammaretrovirus/*genetics ; Genes, env ; Genes, gag ; Humans ; Male ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Polymerase Chain Reaction ; Prostatic Neoplasms/*virology ; Proviruses/genetics/isolation & purification ; *Recombination, Genetic ; Transplantation, Heterologous ; Xenotropic murine leukemia virus-related virus/*genetics/*isolation & ; purification
    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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