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  • 1
    Publication Date: 2003-11-01
    Description: Mutations in MeCP2, which encodes a protein that has been proposed to function as a global transcriptional repressor, are the cause of Rett syndrome (RT T), an X-linked progressive neurological disorder. Although the selective inactivation of MeCP2 in neurons is sufficient to confer a Rett-like phenotype in mice, the specific functions of MeCP2 in postmitotic neurons are not known. We find that MeCP2 binds selectively to BDNF promoter III and functions to repress expression of the BDNF gene. Membrane depolarization triggers the calcium-dependent phosphorylation and release of MeCP2 from BDNF promoter III, thereby facilitating transcription. These studies indicate that MeCP2 plays a key role in the control of neuronal activity-dependent gene regulation and suggest that the deregulation of this process may underlie the pathology of RT T.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wen G -- Chang, Qiang -- Lin, Yingxi -- Meissner, Alexander -- West, Anne E -- Griffith, Eric C -- Jaenisch, Rudolf -- Greenberg, Michael E -- HD 18655/HD/NICHD NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):885-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593183" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/*genetics ; Calcium/*metabolism ; Cell Membrane/physiology ; Cells, Cultured ; *Chromosomal Proteins, Non-Histone ; Cloning, Molecular ; CpG Islands ; DNA Methylation ; DNA-Binding Proteins/*metabolism ; Electrophoretic Mobility Shift Assay ; *Gene Expression Regulation ; Gene Silencing ; Histones/metabolism ; Methyl-CpG-Binding Protein 2 ; Methylation ; Mice ; Mice, Knockout ; Neurons/metabolism/physiology ; Phosphorylation ; Potassium Chloride/pharmacology ; Precipitin Tests ; Promoter Regions, Genetic ; Rats ; *Repressor Proteins ; Rett Syndrome/genetics ; *Transcription, 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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  • 2
    Publication Date: 2007-12-08
    Description: It has recently been demonstrated that mouse and human fibroblasts can be reprogrammed into an embryonic stem cell-like state by introducing combinations of four transcription factors. However, the therapeutic potential of such induced pluripotent stem (iPS) cells remained undefined. By using a humanized sickle cell anemia mouse model, we show that mice can be rescued after transplantation with hematopoietic progenitors obtained in vitro from autologous iPS cells. This was achieved after correction of the human sickle hemoglobin allele by gene-specific targeting. Our results provide proof of principle for using transcription factor-induced reprogramming combined with gene and cell therapy for disease treatment in mice. The problems associated with using retroviruses and oncogenes for reprogramming need to be resolved before iPS cells can be considered for human therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanna, Jacob -- Wernig, Marius -- Markoulaki, Styliani -- Sun, Chiao-Wang -- Meissner, Alexander -- Cassady, John P -- Beard, Caroline -- Brambrink, Tobias -- Wu, Li-Chen -- Townes, Tim M -- Jaenisch, Rudolf -- 2-R01-HL057619/HL/NHLBI NIH HHS/ -- 5-R37-CA084198/CA/NCI NIH HHS/ -- 5-RO1-CA087869/CA/NCI NIH HHS/ -- 5-RO1-HDO45022/PHS HHS/ -- New York, N.Y. -- Science. 2007 Dec 21;318(5858):1920-3. Epub 2007 Dec 6.〈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/18063756" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/blood/physiopathology/*therapy ; Animals ; Cell Differentiation ; Cells, Cultured ; *Cellular Reprogramming ; DNA-Binding Proteins/genetics ; Disease Models, Animal ; Embryonic Stem Cells/cytology ; Erythrocyte Count ; Fibroblasts/*cytology ; Genes, myc ; Globins/genetics ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology ; Hemoglobin A/analysis ; Hemoglobin, Sickle/analysis ; Humans ; Kidney Concentrating Ability ; Kruppel-Like Transcription Factors/genetics ; Male ; Mice ; Octamer Transcription Factor-3/genetics ; Pluripotent Stem Cells/*cytology ; SOXB1 Transcription Factors ; Trans-Activators/genetics ; Transduction, 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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  • 3
    Publication Date: 2011-11-15
    Description: In the mammalian genome, 5'-CpG-3' dinucleotides are frequently methylated, correlating with transcriptional silencing. Genome-wide demethylation is thought to occur only twice during development, in primordial germ cells and in the pre-implantation embryo. These demethylation events are followed by de novo methylation, setting up a pattern inherited throughout development and modified only at tissue-specific loci. We studied DNA methylation in differentiating mouse erythroblasts in vivo by using genomic-scale reduced representation bisulfite sequencing (RRBS). Demethylation at the erythroid-specific beta-globin locus was coincident with global DNA demethylation at most genomic elements. Global demethylation was continuous throughout differentiation and required rapid DNA replication. Hence, DNA demethylation can occur globally during somatic cell differentiation, providing an experimental model for its study in development and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230325/" 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/PMC3230325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shearstone, Jeffrey R -- Pop, Ramona -- Bock, Christoph -- Boyle, Patrick -- Meissner, Alexander -- Socolovsky, Merav -- DK32520/DK/NIDDK NIH HHS/ -- R01 HL084168/HL/NHLBI NIH HHS/ -- R01 HL084168-02/HL/NHLBI NIH HHS/ -- R01 HL084168-03/HL/NHLBI NIH HHS/ -- R01 HL084168-04/HL/NHLBI NIH HHS/ -- R01 HL084168-04S1/HL/NHLBI NIH HHS/ -- R01 HL084168-05/HL/NHLBI NIH HHS/ -- T32-130807/PHS HHS/ -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):799-802. doi: 10.1126/science.1207306.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22076376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CpG Islands ; *DNA Methylation ; DNA Replication ; Dinucleoside Phosphates/metabolism ; Embryo, Mammalian ; Erythroblasts/*metabolism ; *Erythropoiesis ; Gene Expression Regulation, Developmental ; Genome ; Liver/embryology ; Locus Control Region ; Long Interspersed Nucleotide Elements ; Mice ; S Phase ; Sequence Analysis, DNA ; Transcription, Genetic ; beta-Globins/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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  • 4
    Publication Date: 2009-09-05
    Description: Models of mammalian regulatory networks controlling gene expression have been inferred from genomic data but have largely not been validated. We present an unbiased strategy to systematically perturb candidate regulators and monitor cellular transcriptional responses. We applied this approach to derive regulatory networks that control the transcriptional response of mouse primary dendritic cells to pathogens. Our approach revealed the regulatory functions of 125 transcription factors, chromatin modifiers, and RNA binding proteins, which enabled the construction of a network model consisting of 24 core regulators and 76 fine-tuners that help to explain how pathogen-sensing pathways achieve specificity. This study establishes a broadly applicable, comprehensive, and unbiased approach to reveal the wiring and functions of a regulatory network controlling a major transcriptional response in primary mammalian cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879337/" 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/PMC2879337/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amit, Ido -- Garber, Manuel -- Chevrier, Nicolas -- Leite, Ana Paula -- Donner, Yoni -- Eisenhaure, Thomas -- Guttman, Mitchell -- Grenier, Jennifer K -- Li, Weibo -- Zuk, Or -- Schubert, Lisa A -- Birditt, Brian -- Shay, Tal -- Goren, Alon -- Zhang, Xiaolan -- Smith, Zachary -- Deering, Raquel -- McDonald, Rebecca C -- Cabili, Moran -- Bernstein, Bradley E -- Rinn, John L -- Meissner, Alex -- Root, David E -- Hacohen, Nir -- Regev, Aviv -- DP1 OD003958/OD/NIH HHS/ -- DP1 OD003958-01/OD/NIH HHS/ -- DP2 OD002230/OD/NIH HHS/ -- DP2 OD002230-01/OD/NIH HHS/ -- R21 AI071060/AI/NIAID NIH HHS/ -- R21 AI071060-01/AI/NIAID NIH HHS/ -- R21 AI71060/AI/NIAID NIH HHS/ -- S10 RR026688/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):257-63. doi: 10.1126/science.1179050. Epub 2009 Sep 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19729616" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*immunology ; Chromatin Assembly and Disassembly ; DNA, Single-Stranded/immunology ; Dendritic Cells/*immunology/*metabolism ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation ; *Gene Regulatory Networks ; Inflammation/immunology/*metabolism ; Lipopeptides/immunology ; Lipopolysaccharides/immunology ; Mice ; Mice, Inbred C57BL ; Poly I-C/immunology ; RNA-Binding Proteins/metabolism ; Toll-Like Receptors/agonists ; Transcription Factors/metabolism ; Transcription, Genetic ; Viruses/*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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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    The European physical journal 65 (1930), S. 158-166 
    ISSN: 1434-601X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Zusammenfassung Quarz als Isolator. — Struktur des Quarzes und des Metalls. — Ionenaufbau des Isolators. — Feststellung des Ionenaufbaus durch Formieren und piezoelektrische Messungen. — Bestimmung von polaren Eigenschaften am amorphen Quarz, Glimmer und an nach Erwärmung im Feld erstarrten Dielektrika. — Wechsel der Polarität des piezoelektrischen Moments.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 10 (1922), S. 810-814 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 10 (1922), S. 17-19 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 26 (1938), S. 188-191 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 17 (1929), S. 25-31 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Naturwissenschaften 23 (1935), S. 41-43 
    ISSN: 1432-1904
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General
    Type of Medium: Electronic Resource
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