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  • 1
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    Trim28 is required for epigenetic stability during mouse oocyte to embryo transition (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-24
    Description: Phenotypic variability in genetic disease is usually attributed to genetic background variation or environmental influence. Here, we show that deletion of a single gene, Trim28 (Kap1 or Tif1beta), from the maternal germ line alone, on an otherwise identical genetic background, results in severe phenotypic and epigenetic variability that leads to embryonic lethality. We identify early and minute epigenetic variations in blastomeres of the preimplantation embryo of these animals, suggesting that the embryonic lethality may result from the misregulation of genomic imprinting in mice lacking maternal Trim28. Our results reveal the long-range effects of a maternal gene deletion on epigenetic memory and illustrate the delicate equilibrium of maternal and zygotic factors during nuclear reprogramming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Messerschmidt, Daniel M -- de Vries, Wilhelmine -- Ito, Mitsuteru -- Solter, Davor -- Ferguson-Smith, Anne -- Knowles, Barbara B -- 079249/Wellcome Trust/United Kingdom -- 095606/Wellcome Trust/United Kingdom -- MR/J001597/1/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1499-502. doi: 10.1126/science.1216154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Development Group, Institute of Medical Biology, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/physiology ; DNA Methylation ; Down-Regulation ; *Embryo Loss ; Embryo, Mammalian/*physiology ; Embryonic Development ; *Epigenesis, Genetic ; Female ; Gene Expression Regulation, Developmental ; *Genomic Imprinting ; Insulin-Like Growth Factor II/genetics/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/*genetics/*physiology ; Oligonucleotide Array Sequence Analysis ; Oocytes/*physiology ; Phenotype ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/*genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Single-cell DNA-methylation analysis reveals epigenetic chimerism in preimplantation embryos (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-07
    Description: Epigenetic alterations are increasingly recognized as causes of human cancers and disease. These aberrations are likely to arise during genomic reprogramming in mammalian preimplantation embryos, when their epigenomes are most vulnerable. However, this process is only partially understood because of the experimental inaccessibility of early-stage embryos. Here, we introduce a methodologic advance, probing single cells for various DNA-methylation errors at multiple loci, to reveal failed maintenance of epigenetic mark results in chimeric mice, which display unpredictable phenotypes leading to developmental arrest. Yet we show that mouse pronuclear transfer can be used to ameliorate such reprogramming defects. This study not only details the epigenetic reprogramming dynamics in early mammalian embryos but also suggests diagnostic and potential future therapeutic applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lorthongpanich, Chanchao -- Cheow, Lih Feng -- Balu, Sathish -- Quake, Stephen R -- Knowles, Barbara B -- Burkholder, William F -- Solter, Davor -- Messerschmidt, Daniel M -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Sep 6;341(6150):1110-2. doi: 10.1126/science.1240617.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Development Group, Institute of Medical Biology, A*STAR, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24009393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*metabolism ; Cellular Reprogramming/*genetics ; *Chimerism ; *DNA Methylation ; *Epigenesis, Genetic ; Gene Deletion ; *Gene Expression Regulation, Developmental ; Genetic Loci ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nuclear Proteins/genetics ; Repressor Proteins/genetics ; Single-Cell Analysis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Nuclear transplantation in the mouse embryo by microsurgery and cell fusion (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-06-17
    Description: Nuclear transplantation in the mouse embryo was achieved by using a method that combines microsurgical removal of the zygote pronuclei with the introduction of a donor nucleus by a virus-mediated cell fusion technique. Survival of embryos was greater than 90 per cent in tests of this procedure. The embryos developed to term at a frequency not significantly different from that of nonmanipulated control embryos. Because nuclei and cytoplasm from genetically distinct inbred mouse strains can be efficiently interchanged, this procedure may be useful in characterizing possible cytoplasmic contributions to the embryonic and adult phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGrath, J -- Solter, D -- CA-10815/CA/NCI NIH HHS/ -- CA-25875/CA/NCI NIH HHS/ -- CA-27932/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Jun 17;220(4603):1300-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857250" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/physiology ; *Cell Fusion ; Embryo, Mammalian/*surgery ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Inbred ICR ; Microsurgery/*methods ; *Nuclear Transfer Techniques
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Raf, a trans-acting locus, regulates the alpha-fetoprotein gene in a cell-autonomous manner (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-17
    Description: Genetic analysis provides an approach for identifying regulatory loci that govern the expression of specific genes within the context of the entire organism. Such analyses have defined two unlinked regulatory loci, termed raf and Rif, that modulate the levels of alpha-fetoprotein in liver. Of primary importance for the isolation and characterization of the raf product is to determine whether it is produced by the hepatocyte or whether it is produced by a different cell type. By means of analysis of alpha-fetoprotein expression in livers of embryo aggregation chimeras derived from mice of different raf genotypes it was possible to conclude that the product of the raf locus is expressed as a hepatocyte autonomous function that acts in trans to regulate the level of alpha-fetoprotein messenger RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogt, T F -- Solter, D -- Tilghman, S M -- CA06927/CA/NCI NIH HHS/ -- CA28050/CA/NCI NIH HHS/ -- HD17720/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Apr 17;236(4799):301-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2436297" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chimera ; Crosses, Genetic ; Gene Expression Regulation ; *Genes ; *Genes, Regulator ; Genotype ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mosaicism ; Polymorphism, Restriction Fragment Length ; RNA, Messenger/genetics ; Species Specificity ; alpha-Fetoproteins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
    Electronic Resource
    Electronic Resource
    Characterization of a monoclonal antibody that binds equally to all apolipoprotein and lipoprotein forms of human plasma apolipoprotein B. I. Specificity and binding studies
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism 876 (1986), S. 91-100 
    Details
    ISSN: 0005-2760
    Keywords: (Human plasma) ; Apolipoprotein B ; Lipoprotein ; Monoclonal antibody
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0005-2760(86)90321-8
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    Paper (German National Licenses)
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