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  • 1
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    Chromosomal instability and tumors promoted by DNA hypomethylation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eden, Amir -- Gaudet, Francois -- Waghmare, Alpana -- Jaenisch, Rudolf -- CA87869/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 18;300(5618):455.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Mammalian/*genetics/physiology ; DNA (Cytosine-5-)-Methyltransferase/genetics/metabolism ; *DNA Methylation ; Fibroblasts/metabolism ; Genes, Neurofibromatosis 1 ; Genes, p53 ; Humans ; *Loss of Heterozygosity ; Mice ; Mutation ; Neoplasms/genetics ; Recombination, Genetic ; Sarcoma/*genetics ; Soft Tissue Neoplasms/*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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  • 2
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    Genome-scale DNA methylation maps of pluripotent and differentiated cells (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-07-05
    Description: DNA methylation is essential for normal development and has been implicated in many pathologies including cancer. Our knowledge about the genome-wide distribution of DNA methylation, how it changes during cellular differentiation and how it relates to histone methylation and other chromatin modifications in mammals remains limited. Here we report the generation and analysis of genome-scale DNA methylation profiles at nucleotide resolution in mammalian cells. Using high-throughput reduced representation bisulphite sequencing and single-molecule-based sequencing, we generated DNA methylation maps covering most CpG islands, and a representative sampling of conserved non-coding elements, transposons and other genomic features, for mouse embryonic stem cells, embryonic-stem-cell-derived and primary neural cells, and eight other primary tissues. Several key findings emerge from the data. First, DNA methylation patterns are better correlated with histone methylation patterns than with the underlying genome sequence context. Second, methylation of CpGs are dynamic epigenetic marks that undergo extensive changes during cellular differentiation, particularly in regulatory regions outside of core promoters. Third, analysis of embryonic-stem-cell-derived and primary cells reveals that 'weak' CpG islands associated with a specific set of developmentally regulated genes undergo aberrant hypermethylation during extended proliferation in vitro, in a pattern reminiscent of that reported in some primary tumours. More generally, the results establish reduced representation bisulphite sequencing as a powerful technology for epigenetic profiling of cell populations relevant to developmental biology, cancer and regenerative medicine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896277/" 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/PMC2896277/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meissner, Alexander -- Mikkelsen, Tarjei S -- Gu, Hongcang -- Wernig, Marius -- Hanna, Jacob -- Sivachenko, Andrey -- Zhang, Xiaolan -- Bernstein, Bradley E -- Nusbaum, Chad -- Jaffe, David B -- Gnirke, Andreas -- Jaenisch, Rudolf -- Lander, Eric S -- R01 HG004401/HG/NHGRI NIH HHS/ -- R01 HG004401-02/HG/NHGRI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-04/HG/NHGRI NIH HHS/ -- U54 HG003067-06/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Aug 7;454(7205):766-70. doi: 10.1038/nature07107. Epub 2008 Jul 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18600261" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cells, Cultured ; Conserved Sequence ; CpG Islands/genetics ; *DNA Methylation ; Embryonic Stem Cells/cytology/metabolism ; Fibroblasts/cytology ; Genome/genetics ; *Genomics ; Histones/genetics/metabolism ; Male ; Mice ; Neurons/cytology ; Pluripotent Stem Cells/*cytology/*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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  • 3
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    Dissecting direct reprogramming through integrative genomic analysis (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-05-30
    Description: Somatic cells can be reprogrammed to a pluripotent state through the ectopic expression of defined transcription factors. Understanding the mechanism and kinetics of this transformation may shed light on the nature of developmental potency and suggest strategies with improved efficiency or safety. Here we report an integrative genomic analysis of reprogramming of mouse fibroblasts and B lymphocytes. Lineage-committed cells show a complex response to the ectopic expression involving induction of genes downstream of individual reprogramming factors. Fully reprogrammed cells show gene expression and epigenetic states that are highly similar to embryonic stem cells. In contrast, stable partially reprogrammed cell lines show reactivation of a distinctive subset of stem-cell-related genes, incomplete repression of lineage-specifying transcription factors, and DNA hypermethylation at pluripotency-related loci. These observations suggest that some cells may become trapped in partially reprogrammed states owing to incomplete repression of transcription factors, and that DNA de-methylation is an inefficient step in the transition to pluripotency. We demonstrate that RNA inhibition of transcription factors can facilitate reprogramming, and that treatment with DNA methyltransferase inhibitors can improve the overall efficiency of the reprogramming process.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754827/" 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/PMC2754827/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mikkelsen, Tarjei S -- Hanna, Jacob -- Zhang, Xiaolan -- Ku, Manching -- Wernig, Marius -- Schorderet, Patrick -- Bernstein, Bradley E -- Jaenisch, Rudolf -- Lander, Eric S -- Meissner, Alexander -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-04/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Jul 3;454(7200):49-55. doi: 10.1038/nature07056. Epub 2008 May 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18509334" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azacitidine/pharmacology ; Cell Line ; Cell Lineage ; Cellular Reprogramming/*genetics ; Chromatin/metabolism ; DNA (Cytosine-5-)-Methyltransferase/antagonists & inhibitors/genetics/metabolism ; DNA Methylation ; Embryonic Stem Cells/metabolism ; Enzyme Inhibitors/pharmacology ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genome/genetics ; *Genomics ; Mice ; Pluripotent Stem Cells/cytology/*metabolism ; Transcription Factors/deficiency/genetics
    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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  • 4
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    Uracil DNA glycosylase activity is dispensable for immunoglobulin class switch (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-08-25
    Description: Activation-induced cytidine deaminase (AID) is required for the DNA cleavage step in immunoglobulin class switch recombination (CSR). AID is proposed to deaminate cytosine to generate uracil (U) in either mRNA or DNA. In the second instance, DNA cleavage depends on uracil DNA glycosylase (UNG) for removal of U. Using phosphorylated histone gamma-H2AX focus formation as a marker of DNA cleavage, we found that the UNG inhibitor Ugi did not inhibit DNA cleavage in immunoglobulin heavy chain (IgH) locus during CSR, even though Ugi blocked UNG binding to DNA and strongly inhibited CSR. Strikingly, UNG mutants that had lost the capability of removing U rescued CSR in UNG-/- B cells. These results indicate that UNG is involved in the repair step of CSR yet by an unknown mechanism. The dispensability of U removal in the DNA cleavage step of CSR requires a reconsideration of the model of DNA deamination by AID.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Begum, Nasim A -- Kinoshita, Kazuo -- Kakazu, Naoki -- Muramatsu, Masamichi -- Nagaoka, Hitoshi -- Shinkura, Reiko -- Biniszkiewicz, Detlev -- Boyer, Laurie A -- Jaenisch, Rudolf -- Honjo, Tasuku -- New York, N.Y. -- Science. 2004 Aug 20;305(5687):1160-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry and Molecular Biology, Graduate School of Medicine, Kyoto University, Yoshida Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15326357" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/enzymology/immunology/*physiology ; Cell Line, Tumor ; Cytidine Deaminase/metabolism ; DNA/*metabolism ; DNA Glycosylases/antagonists & inhibitors/genetics/*metabolism ; DNA Repair ; *Genes, Immunoglobulin ; *Immunoglobulin Class Switching ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Switch Region ; Mice ; Mutation ; Precipitin Tests ; Recombination, Genetic ; Transfection ; Uracil/metabolism ; Uracil-DNA Glycosidase ; Viral Proteins/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
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    Dependence on p75 for innervation of some sympathetic targets (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The low-affinity neurotrophin receptor p75 binds all neurotrophins with similar affinity. For elucidation of its function, mice bearing a null mutation in the p75 locus were generated. Examination of sympathetic innervation of target tissues revealed that pineal glands lacked innervation and sweat gland innervation was absent or reduced in particular footpads. The absence of adult innervation reflects the failure of axons to reach these targets during development rather than a target deficit. These results indicate that p75 facilitates development of specific populations of sympathetic neurons, for which it may support axon growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, K F -- Bachman, K -- Landis, S -- Jaenisch, R -- 5 R35 CA44339/CA/NCI NIH HHS/ -- NS 023678/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1447-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128229" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic Fibers/*physiology/ultrastructure ; Animals ; Axons/physiology/ultrastructure ; Mice ; Mutation ; Pilocarpine/pharmacology ; Pineal Gland/*innervation ; Receptors, Nerve Growth Factor/genetics/*physiology ; Sweat Glands/chemistry/drug effects/*innervation/physiology ; Sweating ; Vasoactive Intestinal Peptide/analysis
    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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    Identification and rescue of alpha-synuclein toxicity in Parkinson patient-derived neurons (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-26
    Description: The induced pluripotent stem (iPS) cell field holds promise for in vitro disease modeling. However, identifying innate cellular pathologies, particularly for age-related neurodegenerative diseases, has been challenging. Here, we exploited mutation correction of iPS cells and conserved proteotoxic mechanisms from yeast to humans to discover and reverse phenotypic responses to alpha-synuclein (alphasyn), a key protein involved in Parkinson's disease (PD). We generated cortical neurons from iPS cells of patients harboring alphasyn mutations, who are at high risk of developing PD dementia. Genetic modifiers from unbiased screens in a yeast model of alphasyn toxicity led to identification of early pathogenic phenotypes in patient neurons. These included nitrosative stress, accumulation of endoplasmic reticulum (ER)-associated degradation substrates, and ER stress. A small molecule identified in a yeast screen (NAB2), and the ubiquitin ligase Nedd4 it affects, reversed pathologic phenotypes in these neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022187/" 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/PMC4022187/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, Chee Yeun -- Khurana, Vikram -- Auluck, Pavan K -- Tardiff, Daniel F -- Mazzulli, Joseph R -- Soldner, Frank -- Baru, Valeriya -- Lou, Yali -- Freyzon, Yelena -- Cho, Sukhee -- Mungenast, Alison E -- Muffat, Julien -- Mitalipova, Maisam -- Pluth, Michael D -- Jui, Nathan T -- Schule, Birgitt -- Lippard, Stephen J -- Tsai, Li-Huei -- Krainc, Dimitri -- Buchwald, Stephen L -- Jaenisch, Rudolf -- Lindquist, Susan -- 5 R01CA084198/CA/NCI NIH HHS/ -- K01 AG038546/AG/NIA NIH HHS/ -- P50 AG005134/AG/NIA NIH HHS/ -- R01 CA084198/CA/NCI NIH HHS/ -- R01 GM058160/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):983-7. doi: 10.1126/science.1245296. Epub 2013 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24158904" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzimidazoles/chemistry/*pharmacology ; Endoplasmic Reticulum Stress/drug effects ; Female ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; Mutation ; Neurogenesis ; Neurons/*drug effects/metabolism/pathology ; Parkinson Disease/genetics/*metabolism ; Rats ; alpha-Synuclein/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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  • 7
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    Activation of proto-oncogenes by disruption of chromosome neighborhoods (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-03-05
    Description: Oncogenes are activated through well-known chromosomal alterations such as gene fusion, translocation, and focal amplification. In light of recent evidence that the control of key genes depends on chromosome structures called insulated neighborhoods, we investigated whether proto-oncogenes occur within these structures and whether oncogene activation can occur via disruption of insulated neighborhood boundaries in cancer cells. We mapped insulated neighborhoods in T cell acute lymphoblastic leukemia (T-ALL) and found that tumor cell genomes contain recurrent microdeletions that eliminate the boundary sites of insulated neighborhoods containing prominent T-ALL proto-oncogenes. Perturbation of such boundaries in nonmalignant cells was sufficient to activate proto-oncogenes. Mutations affecting chromosome neighborhood boundaries were found in many types of cancer. Thus, oncogene activation can occur via genetic alterations that disrupt insulated neighborhoods in malignant cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hnisz, Denes -- Weintraub, Abraham S -- Day, Daniel S -- Valton, Anne-Laure -- Bak, Rasmus O -- Li, Charles H -- Goldmann, Johanna -- Lajoie, Bryan R -- Fan, Zi Peng -- Sigova, Alla A -- Reddy, Jessica -- Borges-Rivera, Diego -- Lee, Tong Ihn -- Jaenisch, Rudolf -- Porteus, Matthew H -- Dekker, Job -- Young, Richard A -- AI120766/AI/NIAID NIH HHS/ -- CA109901/CA/NCI NIH HHS/ -- HG002668/HG/NHGRI NIH HHS/ -- MH104610/MH/NIMH NIH HHS/ -- NS088538/NS/NINDS NIH HHS/ -- R01 GM 112720/GM/NIGMS NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R01 HG003143/HG/NHGRI NIH HHS/ -- R01 MH104610/MH/NIMH NIH HHS/ -- U01 DA 040588/DA/NIDA NIH HHS/ -- U01 HG007910/HG/NHGRI NIH HHS/ -- U01 R01 AI 117839/AI/NIAID NIH HHS/ -- U54 CA193419/CA/NCI NIH HHS/ -- U54 DK107980/DK/NIDDK NIH HHS/ -- U54 HG007010/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1454-8. doi: 10.1126/science.aad9024. Epub 2016 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. ; Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Program in Systems Biology, Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Pediatrics, Stanford University, Stanford, CA, USA. ; Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. Computational and Systems Biology Program, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Program in Systems Biology, Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. Howard Hughes Medical Institute. ; Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. young@wi.mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26940867" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Aberrations ; Chromosome Mapping ; *Gene Expression Regulation, Leukemic ; HEK293 Cells ; Humans ; Mutation ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/*genetics ; Proto-Oncogenes/*genetics ; *Sequence Deletion ; Transcriptional Activation ; *Translocation, 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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  • 8
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    Epigenetic memory in induced pluripotent stem cells (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-21
    Description: Somatic cell nuclear transfer and transcription-factor-based reprogramming revert adult cells to an embryonic state, and yield pluripotent stem cells that can generate all tissues. Through different mechanisms and kinetics, these two reprogramming methods reset genomic methylation, an epigenetic modification of DNA that influences gene expression, leading us to hypothesize that the resulting pluripotent stem cells might have different properties. Here we observe that low-passage induced pluripotent stem cells (iPSCs) derived by factor-based reprogramming of adult murine tissues harbour residual DNA methylation signatures characteristic of their somatic tissue of origin, which favours their differentiation along lineages related to the donor cell, while restricting alternative cell fates. Such an 'epigenetic memory' of the donor tissue could be reset by differentiation and serial reprogramming, or by treatment of iPSCs with chromatin-modifying drugs. In contrast, the differentiation and methylation of nuclear-transfer-derived pluripotent stem cells were more similar to classical embryonic stem cells than were iPSCs. Our data indicate that nuclear transfer is more effective at establishing the ground state of pluripotency than factor-based reprogramming, which can leave an epigenetic memory of the tissue of origin that may influence efforts at directed differentiation for applications in disease modelling or treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150836/" 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/PMC3150836/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, K -- Doi, A -- Wen, B -- Ng, K -- Zhao, R -- Cahan, P -- Kim, J -- Aryee, M J -- Ji, H -- Ehrlich, L I R -- Yabuuchi, A -- Takeuchi, A -- Cunniff, K C -- Hongguang, H -- McKinney-Freeman, S -- Naveiras, O -- Yoon, T J -- Irizarry, R A -- Jung, N -- Seita, J -- Hanna, J -- Murakami, P -- Jaenisch, R -- Weissleder, R -- Orkin, S H -- Weissman, I L -- Feinberg, A P -- Daley, G Q -- CA86065/CA/NCI NIH HHS/ -- DP1 OD000256/OD/NIH HHS/ -- DP1 OD000256-01/OD/NIH HHS/ -- HL099999/HL/NHLBI NIH HHS/ -- K99 HL093212/HL/NHLBI NIH HHS/ -- K99 HL093212-01/HL/NHLBI NIH HHS/ -- K99 HL093212-02/HL/NHLBI NIH HHS/ -- K99HL093212-01/HL/NHLBI NIH HHS/ -- P50HG003233/HG/NHGRI NIH HHS/ -- R01 CA086065/CA/NCI NIH HHS/ -- R01 DK059279/DK/NIDDK NIH HHS/ -- R01 DK059279-02/DK/NIDDK NIH HHS/ -- R01 DK059279-10/DK/NIDDK NIH HHS/ -- R01 DK070055/DK/NIDDK NIH HHS/ -- R01 DK070055-01/DK/NIDDK NIH HHS/ -- R01 GM083084/GM/NIGMS NIH HHS/ -- R01 GM083084-04/GM/NIGMS NIH HHS/ -- R01-DK59279/DK/NIDDK NIH HHS/ -- R01-DK70055/DK/NIDDK NIH HHS/ -- R01AI047457/AI/NIAID NIH HHS/ -- R01AI047458/AI/NIAID NIH HHS/ -- R37 HD045022/HD/NICHD NIH HHS/ -- R37CA054358/CA/NCI NIH HHS/ -- RC2 HL102815/HL/NHLBI NIH HHS/ -- RC2 HL102815-01/HL/NHLBI NIH HHS/ -- RC2-HL102815/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Sep 16;467(7313):285-90. doi: 10.1038/nature09342.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Transplantation Program, Division of Pediatric Hematology/Oncology, Manton Center for Orphan Disease Research, Howard Hughes Medical Institute, Children's Hospital Boston and Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20644535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Cellular Reprogramming/genetics ; DNA Methylation/genetics ; Embryonic Stem Cells/cytology/metabolism ; *Epigenesis, Genetic ; Genome/genetics ; Hematopoietic Stem Cells/cytology/metabolism ; Induced Pluripotent Stem Cells/*cytology/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Nuclear Transfer Techniques ; Transcription Factors/genetics/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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