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  • 1
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    MHC class I deficiency: susceptibility to natural killer (NK) cells and impaired NK activity (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-12
    Description: The role of major histocompatibility complex (MHC) class I expression in natural killer (NK) cell target recognition is controversial. Normal T cell blasts from MHC class I-deficient mutant mice were found to serve as target cells for NK cells in vitro, which suggests that MHC class I molecules are directly involved in NK cell recognition. Spleen cells from the mutant mice were deficient in their ability to lyse MHC class I-deficient target cells or NK-susceptible tumor targets, and mutant mice could not reject allogeneic bone marrow. Thus, class I molecules may participate in the positive selection or tolerance induction of NK cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liao, N S -- Bix, M -- Zijlstra, M -- Jaenisch, R -- Raulet, D -- R01 AI30171/AI/NIAID NIH HHS/ -- R35 CA44339/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):199-202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1853205" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytotoxicity, Immunologic ; Histocompatibility Antigens Class I/*immunology ; *Immunity, Cellular ; *Immunity, Innate ; Killer Cells, Natural/*immunology ; Major Histocompatibility Complex ; Mice ; Mice, Inbred Strains ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Cytotoxic/immunology ; beta 2-Microglobulin/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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    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
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Germ line transmission of a yeast artificial chromosome spanning the murine alpha 1(I) collagen locus (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-26
    Description: Molecular complementation of mutant phenotypes by transgenic technology is a potentially important tool for gene identification. A technology was developed that allows the transfer of a physically intact yeast artificial chromosome (YAC) into the germ line of the mouse. A purified 150-kilobase YAC encompassing the murine gene Col1a1 was efficiently introduced into embryonic stem (ES) cells via lipofection. Chimeric founder mice were derived from two transfected ES cell clones. These chimeras transmitted the full length transgene through the germ line, generating two transgenic mouse strains. Transgene expression was visualized as nascent transcripts in interphase nuclei and quantitated by ribonuclease protection analysis. Both assays indicated that the transgene was expressed at levels comparable to the endogenous collagen gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, W M -- Dausman, J -- Beard, C -- Johnson, C -- Lawrence, J B -- Jaenisch, R -- 5 F32 GM13756-02/GM/NIGMS NIH HHS/ -- 5 R35 CA44339-05/CA/NCI NIH HHS/ -- HG00198-01/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Mar 26;259(5103):1904-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8096090" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism ; Blotting, Southern ; Chromosomes, Fungal ; Collagen/*genetics ; *Gene Expression ; Gene Library ; In Situ Hybridization ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutagenesis, Insertional ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Transfection
    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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    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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  • 5
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    Parkinson-associated risk variant in distal enhancer of alpha-synuclein modulates target gene expression (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-04-21
    Description: Genome-wide association studies (GWAS) have identified numerous genetic variants associated with complex diseases, but mechanistic insights are impeded by a lack of understanding of how specific risk variants functionally contribute to the underlying pathogenesis. It has been proposed that cis-acting effects of non-coding risk variants on gene expression are a major factor for phenotypic variation of complex traits and disease susceptibility. Recent genome-scale epigenetic studies have highlighted the enrichment of GWAS-identified variants in regulatory DNA elements of disease-relevant cell types. Furthermore, single nucleotide polymorphism (SNP)-specific changes in transcription factor binding are correlated with heritable alterations in chromatin state and considered a major mediator of sequence-dependent regulation of gene expression. Here we describe a novel strategy to functionally dissect the cis-acting effect of genetic risk variants in regulatory elements on gene expression by combining genome-wide epigenetic information with clustered regularly-interspaced short palindromic repeats (CRISPR)/Cas9 genome editing in human pluripotent stem cells. By generating a genetically precisely controlled experimental system, we identify a common Parkinson's disease associated risk variant in a non-coding distal enhancer element that regulates the expression of alpha-synuclein (SNCA), a key gene implicated in the pathogenesis of Parkinson's disease. Our data suggest that the transcriptional deregulation of SNCA is associated with sequence-dependent binding of the brain-specific transcription factors EMX2 and NKX6-1. This work establishes an experimental paradigm to functionally connect genetic variation with disease-relevant phenotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soldner, Frank -- Stelzer, Yonatan -- Shivalila, Chikdu S -- Abraham, Brian J -- Latourelle, Jeanne C -- Barrasa, M Inmaculada -- Goldmann, Johanna -- Myers, Richard H -- Young, Richard A -- Jaenisch, Rudolf -- 1R01NS088538-01/NS/NINDS NIH HHS/ -- 2R01MH104610-15/MH/NIMH NIH HHS/ -- R01 NS088538/NS/NINDS NIH HHS/ -- England -- Nature. 2016 May 5;533(7601):95-9. doi: 10.1038/nature17939. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Whitehead Institute, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA. ; Department of Biology, Massachusetts Institute of Technology, 31 Ames Street, Cambridge, Massachusetts 02139, USA. ; Department of Neurology, Boston University School of Medicine, Boston, Masssachusetts 02118, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096366" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Brain/metabolism ; CRISPR-Cas Systems/genetics ; Enhancer Elements, Genetic/*genetics ; Epigenesis, Genetic/genetics ; *Gene Expression Regulation ; Genetic Engineering ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; Homeodomain Proteins/metabolism ; Humans ; Models, Genetic ; Parkinson Disease/*genetics ; Pluripotent Stem Cells/metabolism ; Risk ; Transcription Factors/metabolism ; alpha-Synuclein/*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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  • 6
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    Corrigendum: Failure to replicate the STAP cell phenomenon (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Los Angeles, Alejandro -- Ferrari, Francesco -- Fujiwara, Yuko -- Mathieu, Ronald -- Lee, Soohyun -- Lee, Semin -- Tu, Ho-Chou -- Ross, Samantha -- Chou, Stephanie -- Nguyen, Minh -- Wu, Zhaoting -- Theunissen, Thorold W -- Powell, Benjamin E -- Imsoonthornruksa, Sumeth -- Chen, Jiekai -- Borkent, Marti -- Krupalnik, Vladislav -- Lujan, Ernesto -- Wernig, Marius -- Hanna, Jacob H -- Hochedlinger, Konrad -- Pei, Duanqing -- Jaenisch, Rudolf -- Deng, Hongkui -- Orkin, Stuart H -- Park, Peter J -- Daley, George Q -- Nature. 2015 Dec 16. doi: 10.1038/nature16479.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26675720" target="_blank"〉PubMed〈/a〉
    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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  • 7
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    Failure to replicate the STAP cell phenomenon (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Los Angeles, Alejandro -- Ferrari, Francesco -- Fujiwara, Yuko -- Mathieu, Ronald -- Lee, Soohyun -- Lee, Semin -- Tu, Ho-Chou -- Ross, Samantha -- Chou, Stephanie -- Nguyen, Minh -- Wu, Zhaoting -- Theunissen, Thorold W -- Powell, Benjamin E -- Imsoonthornruksa, Sumeth -- Chen, Jiekai -- Borkent, Marti -- Krupalnik, Vladislav -- Lujan, Ernesto -- Wernig, Marius -- Hanna, Jacob H -- Hochedlinger, Konrad -- Pei, Duanqing -- Jaenisch, Rudolf -- Deng, Hongkui -- Orkin, Stuart H -- Park, Peter J -- Daley, George Q -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Sep 24;525(7570):E6-9. doi: 10.1038/nature15513.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Transplantation Program, Division of Pediatric Hematology Oncology, Children's Hospital Boston, and Dana-Farber Cancer Institute, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA. ; Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USApeter_park@hms.harvard.edu. ; Children's Hospital &Harvard Stem Cell Institute Flow Cytometry Research Facility, Children's Hospital Boston, Boston, Massachusetts 02115, USA. ; Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA. ; South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, China. ; Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Boston, Massachusetts 02114, USA. ; Department of Development and Reproduction, Erasmus Medical Center, 3015 CN Rotterdam, Netherlands. ; Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, California 94305, USA. ; College of Life Sciences and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26399835" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Corrigendum: Hallmarks of pluripotency (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Los Angeles, Alejandro -- Ferrari, Francesco -- Xi, Ruibin -- Fujiwara, Yuko -- Benvenisty, Nissim -- Deng, Hongkui -- Hochedlinger, Konrad -- Jaenisch, Rudolf -- Lee, Soohyun -- Leitch, Harry G -- Lensch, M William -- Lujan, Ernesto -- Pei, Duanqing -- Rossant, Janet -- Wernig, Marius -- Park, Peter J -- Daley, George Q -- Nature. 2015 Dec 16. doi: 10.1038/nature16470.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26675727" target="_blank"〉PubMed〈/a〉
    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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    Hallmarks of pluripotency (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-09-25
    Description: Stem cells self-renew and generate specialized progeny through differentiation, but vary in the range of cells and tissues they generate, a property called developmental potency. Pluripotent stem cells produce all cells of an organism, while multipotent or unipotent stem cells regenerate only specific lineages or tissues. Defining stem-cell potency relies upon functional assays and diagnostic transcriptional, epigenetic and metabolic states. Here we describe functional and molecular hallmarks of pluripotent stem cells, propose a checklist for their evaluation, and illustrate how forensic genomics can validate their provenance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Los Angeles, Alejandro -- Ferrari, Francesco -- Xi, Ruibin -- Fujiwara, Yuko -- Benvenisty, Nissim -- Deng, Hongkui -- Hochedlinger, Konrad -- Jaenisch, Rudolf -- Lee, Soohyun -- Leitch, Harry G -- Lensch, M William -- Lujan, Ernesto -- Pei, Duanqing -- Rossant, Janet -- Wernig, Marius -- Park, Peter J -- Daley, George Q -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Sep 24;525(7570):469-78. doi: 10.1038/nature15515.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Transplantation Program, Division of Pediatric Hematology Oncology, Children's Hospital Boston, and Dana-Farber Cancer Institute; Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA. ; Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, Massachusetts 02115, USA. ; School of Mathematical Sciences and Center for Statistical Science, Peking University, Beijing 100871, China. ; Stem Cell Unit, Department of Genetics, Institute of Life Sciences, The Hebrew University, Jerusalem 91904, Israel. ; College of Life Sciences and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China. ; Massachusetts General Hospital Cancer Center and Center for Regenerative Medicine, Boston, Massachusetts 02114, USA. ; Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA. ; Medical Research Council Clinical Sciences Centre, Imperial College London, London W12 0NN, United Kingdom. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, California 94305, USA. ; South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510530, China. ; The Hospital for Sick Children Research Institute, Toronto, Ontario ON M5G 0A4, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26399828" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Embryonic Stem Cells/cytology/metabolism ; Genomics ; Humans ; 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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  • 10
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    Mice lacking major histocompatibility complex class I and class II molecules. (1993)
    National Academy of Sciences
    Details
    Publication Date: 1993-05-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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