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  • 1
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    An oestrogen-receptor-alpha-bound human chromatin interactome (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-11-06
    Description: Genomes are organized into high-level three-dimensional structures, and DNA elements separated by long genomic distances can in principle interact functionally. Many transcription factors bind to regulatory DNA elements distant from gene promoters. Although distal binding sites have been shown to regulate transcription by long-range chromatin interactions at a few loci, chromatin interactions and their impact on transcription regulation have not been investigated in a genome-wide manner. Here we describe the development of a new strategy, chromatin interaction analysis by paired-end tag sequencing (ChIA-PET) for the de novo detection of global chromatin interactions, with which we have comprehensively mapped the chromatin interaction network bound by oestrogen receptor alpha (ER-alpha) in the human genome. We found that most high-confidence remote ER-alpha-binding sites are anchored at gene promoters through long-range chromatin interactions, suggesting that ER-alpha functions by extensive chromatin looping to bring genes together for coordinated transcriptional regulation. We propose that chromatin interactions constitute a primary mechanism for regulating transcription in mammalian genomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2774924/" 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/PMC2774924/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fullwood, Melissa J -- Liu, Mei Hui -- Pan, You Fu -- Liu, Jun -- Xu, Han -- Mohamed, Yusoff Bin -- Orlov, Yuriy L -- Velkov, Stoyan -- Ho, Andrea -- Mei, Poh Huay -- Chew, Elaine G Y -- Huang, Phillips Yao Hui -- Welboren, Willem-Jan -- Han, Yuyuan -- Ooi, Hong Sain -- Ariyaratne, Pramila N -- Vega, Vinsensius B -- Luo, Yanquan -- Tan, Peck Yean -- Choy, Pei Ye -- Wansa, K D Senali Abayratna -- Zhao, Bing -- Lim, Kar Sian -- Leow, Shi Chi -- Yow, Jit Sin -- Joseph, Roy -- Li, Haixia -- Desai, Kartiki V -- Thomsen, Jane S -- Lee, Yew Kok -- Karuturi, R Krishna Murthy -- Herve, Thoreau -- Bourque, Guillaume -- Stunnenberg, Hendrik G -- Ruan, Xiaoan -- Cacheux-Rataboul, Valere -- Sung, Wing-Kin -- Liu, Edison T -- Wei, Chia-Lin -- Cheung, Edwin -- Ruan, Yijun -- 1U54HG004557-01/HG/NHGRI NIH HHS/ -- R01 HG004456/HG/NHGRI NIH HHS/ -- R01 HG004456-01/HG/NHGRI NIH HHS/ -- R01 HG004456-02/HG/NHGRI NIH HHS/ -- R01 HG004456-03/HG/NHGRI NIH HHS/ -- R01HG003521-01/HG/NHGRI NIH HHS/ -- R01HG004456-01/HG/NHGRI NIH HHS/ -- U54 HG004557/HG/NHGRI NIH HHS/ -- U54 HG004557-01/HG/NHGRI NIH HHS/ -- U54 HG004557-02/HG/NHGRI NIH HHS/ -- U54 HG004557-03/HG/NHGRI NIH HHS/ -- U54 HG004557-04/HG/NHGRI NIH HHS/ -- England -- Nature. 2009 Nov 5;462(7269):58-64. doi: 10.1038/nature08497.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genome Institute of Singapore, Agency for Science, Technology and Research, Singapore 138672.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19890323" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Line ; Chromatin/*genetics/*metabolism ; Chromatin Immunoprecipitation ; Cross-Linking Reagents ; Estrogen Receptor alpha/*metabolism ; Formaldehyde ; Genome, Human/*genetics ; Humans ; Promoter Regions, Genetic/genetics ; Protein Binding ; Reproducibility of Results ; Sequence Analysis, DNA ; Transcription, Genetic ; Transcriptional Activation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    The genomic landscapes of human breast and colorectal cancers (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-13
    Description: Human cancer is caused by the accumulation of mutations in oncogenes and tumor suppressor genes. To catalog the genetic changes that occur during tumorigenesis, we isolated DNA from 11 breast and 11 colorectal tumors and determined the sequences of the genes in the Reference Sequence database in these samples. Based on analysis of exons representing 20,857 transcripts from 18,191 genes, we conclude that the genomic landscapes of breast and colorectal cancers are composed of a handful of commonly mutated gene "mountains" and a much larger number of gene "hills" that are mutated at low frequency. We describe statistical and bioinformatic tools that may help identify mutations with a role in tumorigenesis. These results have implications for understanding the nature and heterogeneity of human cancers and for using personal genomics for tumor diagnosis and therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wood, Laura D -- Parsons, D Williams -- Jones, Sian -- Lin, Jimmy -- Sjoblom, Tobias -- Leary, Rebecca J -- Shen, Dong -- Boca, Simina M -- Barber, Thomas -- Ptak, Janine -- Silliman, Natalie -- Szabo, Steve -- Dezso, Zoltan -- Ustyanksky, Vadim -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Karchin, Rachel -- Wilson, Paul A -- Kaminker, Joshua S -- Zhang, Zemin -- Croshaw, Randal -- Willis, Joseph -- Dawson, Dawn -- Shipitsin, Michail -- Willson, James K V -- Sukumar, Saraswati -- Polyak, Kornelia -- Park, Ben Ho -- Pethiyagoda, Charit L -- Pant, P V Krishna -- Ballinger, Dennis G -- Sparks, Andrew B -- Hartigan, James -- Smith, Douglas R -- Suh, Erick -- Papadopoulos, Nickolas -- Buckhaults, Phillip -- Markowitz, Sanford D -- Parmigiani, Giovanni -- Kinzler, Kenneth W -- Velculescu, Victor E -- Vogelstein, Bert -- CA 43460/CA/NCI NIH HHS/ -- CA 57345/CA/NCI NIH HHS/ -- CA109274/CA/NCI NIH HHS/ -- CA112828/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM070219/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- P30-CA43703/CA/NCI NIH HHS/ -- RR017698/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1108-13. Epub 2007 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*genetics/metabolism ; Cell Line ; Chromosome Mapping ; Colorectal Neoplasms/*genetics/metabolism ; Computational Biology ; DNA, Neoplasm ; Databases, Genetic ; Genes, Neoplasm ; Genome, Human ; Humans ; Metabolic Networks and Pathways/genetics ; Mice ; Mutation ; Neoplasm Proteins/genetics/metabolism ; Sequence Analysis, DNA
    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
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    An aneuploid mouse strain carrying human chromosome 21 with Down syndrome phenotypes (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-24
    Description: Aneuploidies are common chromosomal defects that result in growth and developmental deficits and high levels of lethality in humans. To gain insight into the biology of aneuploidies, we manipulated mouse embryonic stem cells and generated a trans-species aneuploid mouse line that stably transmits a freely segregating, almost complete human chromosome 21 (Hsa21). This "transchromosomic" mouse line, Tc1, is a model of trisomy 21, which manifests as Down syndrome (DS) in humans, and has phenotypic alterations in behavior, synaptic plasticity, cerebellar neuronal number, heart development, and mandible size that relate to human DS. Transchromosomic mouse lines such as Tc1 may represent useful genetic tools for dissecting other human aneuploidies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1378183/" 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/PMC1378183/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Doherty, Aideen -- Ruf, Sandra -- Mulligan, Claire -- Hildreth, Victoria -- Errington, Mick L -- Cooke, Sam -- Sesay, Abdul -- Modino, Sonie -- Vanes, Lesley -- Hernandez, Diana -- Linehan, Jacqueline M -- Sharpe, Paul T -- Brandner, Sebastian -- Bliss, Timothy V P -- Henderson, Deborah J -- Nizetic, Dean -- Tybulewicz, Victor L J -- Fisher, Elizabeth M C -- 076700/Wellcome Trust/United Kingdom -- MC_U117512674/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):2033-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16179473" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Animals ; Behavior, Animal ; Brain/pathology ; Cell Count ; Cell Line ; Chimera ; *Chromosomes, Human, Pair 21 ; *Disease Models, Animal ; *Down Syndrome/genetics/physiopathology ; Embryo, Mammalian/cytology ; Facial Bones/pathology ; Female ; Gene Expression ; *Genetic Engineering ; Genetic Markers ; Heart Defects, Congenital/embryology ; Hippocampus/physiopathology ; Humans ; Long-Term Potentiation ; Lymphocyte Activation ; Male ; Maze Learning ; Memory ; Mice ; Mice, Inbred Strains ; *Mice, Transgenic ; Neurons/cytology ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Skull/pathology ; Stem Cells ; Synaptic Transmission ; T-Lymphocytes/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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  • 4
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    Somatic and germline activating mutations of the ALK kinase receptor in neuroblastoma (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-10-17
    Description: Neuroblastoma, a tumour derived from the peripheral sympathetic nervous system, is one of the most frequent solid tumours in childhood. It usually occurs sporadically but familial cases are observed, with a subset of cases occurring in association with congenital malformations of the neural crest being linked to germline mutations of the PHOX2B gene. Here we conducted genome-wide comparative genomic hybridization analysis on a large series of neuroblastomas. Copy number increase at the locus encoding the anaplastic lymphoma kinase (ALK) tyrosine kinase receptor was observed recurrently. One particularly informative case presented a high-level gene amplification that was strictly limited to ALK, indicating that this gene may contribute on its own to neuroblastoma development. Through subsequent direct sequencing of cell lines and primary tumour DNAs we identified somatic mutations of the ALK kinase domain that mainly clustered in two hotspots. Germline mutations were observed in two neuroblastoma families, indicating that ALK is a neuroblastoma predisposition gene. Mutated ALK proteins were overexpressed, hyperphosphorylated and showed constitutive kinase activity. The knockdown of ALK expression in ALK-mutated cells, but also in cell lines overexpressing a wild-type ALK, led to a marked decrease of cell proliferation. Altogether, these data identify ALK as a critical player in neuroblastoma development that may hence represent a very attractive therapeutic target in this disease that is still frequently fatal with current treatments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Janoueix-Lerosey, Isabelle -- Lequin, Delphine -- Brugieres, Laurence -- Ribeiro, Agnes -- de Pontual, Loic -- Combaret, Valerie -- Raynal, Virginie -- Puisieux, Alain -- Schleiermacher, Gudrun -- Pierron, Gaelle -- Valteau-Couanet, Dominique -- Frebourg, Thierry -- Michon, Jean -- Lyonnet, Stanislas -- Amiel, Jeanne -- Delattre, Olivier -- England -- Nature. 2008 Oct 16;455(7215):967-70. doi: 10.1038/nature07398.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Curie, Centre de Recherche, and Inserm, U830, 26 rue d'Ulm, Paris F-75248, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18923523" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division ; Cell Line ; Cell Line, Tumor ; Child ; Gene Dosage ; Genome, Human/genetics ; Germ-Line Mutation/*genetics ; Humans ; Neuroblastoma/enzymology/*genetics ; Nucleic Acid Hybridization ; Phosphorylation ; Point Mutation/*genetics ; Polymorphism, Single Nucleotide/genetics ; Protein-Tyrosine Kinases/chemistry/deficiency/*genetics/metabolism ; Receptor Protein-Tyrosine Kinases
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Biodiversity and biogeography of phages in modern stromatolites and thrombolites (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-03-04
    Description: Viruses, and more particularly phages (viruses that infect bacteria), represent one of the most abundant living entities in aquatic and terrestrial environments. The biogeography of phages has only recently been investigated and so far reveals a cosmopolitan distribution of phage genetic material (or genotypes). Here we address this cosmopolitan distribution through the analysis of phage communities in modern microbialites, the living representatives of one of the most ancient life forms on Earth. On the basis of a comparative metagenomic analysis of viral communities associated with marine (Highborne Cay, Bahamas) and freshwater (Pozas Azules II and Rio Mesquites, Mexico) microbialites, we show that some phage genotypes are geographically restricted. The high percentage of unknown sequences recovered from the three metagenomes (〉97%), the low percentage similarities with sequences from other environmental viral (n = 42) and microbial (n = 36) metagenomes, and the absence of viral genotypes shared among microbialites indicate that viruses are genetically unique in these environments. Identifiable sequences in the Highborne Cay metagenome were dominated by single-stranded DNA microphages that were not detected in any other samples examined, including sea water, fresh water, sediment, terrestrial, extreme, metazoan-associated and marine microbial mats. Finally, a marine signature was present in the phage community of the Pozas Azules II microbialites, even though this environment has not been in contact with the ocean for tens of millions of years. Taken together, these results prove that viruses in modern microbialites display biogeographical variability and suggest that they may be derived from an ancient community.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Desnues, Christelle -- Rodriguez-Brito, Beltran -- Rayhawk, Steve -- Kelley, Scott -- Tran, Tuong -- Haynes, Matthew -- Liu, Hong -- Furlan, Mike -- Wegley, Linda -- Chau, Betty -- Ruan, Yijun -- Hall, Dana -- Angly, Florent E -- Edwards, Robert A -- Li, Linlin -- Thurber, Rebecca Vega -- Reid, R Pamela -- Siefert, Janet -- Souza, Valeria -- Valentine, David L -- Swan, Brandon K -- Breitbart, Mya -- Rohwer, Forest -- England -- Nature. 2008 Mar 20;452(7185):340-3. doi: 10.1038/nature06735. Epub 2008 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, San Diego State University, San Diego, California 92182, USA. cdesnues@yahoo.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18311127" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteriophages/classification/genetics/*isolation & purification/*physiology ; Bahamas ; *Biodiversity ; Capsid/chemistry ; Computational Biology ; DNA, Viral/analysis/genetics ; *Ecosystem ; Fresh Water/microbiology/virology ; Genome, Viral/genetics ; Genomics ; *Geography ; Geologic Sediments/microbiology/virology ; Mexico ; Molecular Sequence Data ; Phylogeny ; Proteome/metabolism ; Seawater/microbiology/virology ; *Water Microbiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Bone-marrow adipocytes as negative regulators of the haematopoietic microenvironment (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-06-12
    Description: Osteoblasts and endothelium constitute functional niches that support haematopoietic stem cells in mammalian bone marrow. Adult bone marrow also contains adipocytes, the number of which correlates inversely with the haematopoietic activity of the marrow. Fatty infiltration of haematopoietic red marrow follows irradiation or chemotherapy and is a diagnostic feature in biopsies from patients with marrow aplasia. To explore whether adipocytes influence haematopoiesis or simply fill marrow space, we compared the haematopoietic activity of distinct regions of the mouse skeleton that differ in adiposity. Here we show, by flow cytometry, colony-forming activity and competitive repopulation assay, that haematopoietic stem cells and short-term progenitors are reduced in frequency in the adipocyte-rich vertebrae of the mouse tail relative to the adipocyte-free vertebrae of the thorax. In lipoatrophic A-ZIP/F1 'fatless' mice, which are genetically incapable of forming adipocytes, and in mice treated with the peroxisome proliferator-activated receptor-gamma inhibitor bisphenol A diglycidyl ether, which inhibits adipogenesis, marrow engraftment after irradiation is accelerated relative to wild-type or untreated mice. These data implicate adipocytes as predominantly negative regulators of the bone-marrow microenvironment, and indicate that antagonizing marrow adipogenesis may enhance haematopoietic recovery in clinical bone-marrow transplantation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831539/" 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/PMC2831539/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naveiras, Olaia -- Nardi, Valentina -- Wenzel, Pamela L -- Hauschka, Peter V -- Fahey, Frederic -- Daley, George Q -- DP1 OD000256/OD/NIH HHS/ -- DP1 OD000256-01/OD/NIH HHS/ -- R01 DK059279/DK/NIDDK NIH HHS/ -- R01 DK059279-06/DK/NIDDK NIH HHS/ -- R01 DK070055/DK/NIDDK NIH HHS/ -- R01 DK070055-01/DK/NIDDK NIH HHS/ -- T32- HL -7623/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jul 9;460(7252):259-63. doi: 10.1038/nature08099. Epub 2009 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pediatric Hematology/Oncology, Children's Hospital Boston and Dana Farber Cancer Institute, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19516257" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/drug effects/*physiology ; Adipogenesis/drug effects ; Adiposity/physiology ; Animals ; Benzhydryl Compounds ; Bone Marrow Cells/*cytology/*metabolism ; Bone Marrow Transplantation ; Cell Line ; Epoxy Compounds/pharmacology ; Femur ; *Hematopoiesis/drug effects ; Hematopoietic Stem Cells/cytology/metabolism ; Homeostasis ; Mice ; Mice, Inbred C57BL ; Osteogenesis ; Spine/cytology/metabolism ; Stromal Cells ; Tail ; Thorax ; Tibia
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Early-warning signals for critical transitions (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-09-04
    Description: Complex dynamical systems, ranging from ecosystems to financial markets and the climate, can have tipping points at which a sudden shift to a contrasting dynamical regime may occur. Although predicting such critical points before they are reached is extremely difficult, work in different scientific fields is now suggesting the existence of generic early-warning signals that may indicate for a wide class of systems if a critical threshold is approaching.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheffer, Marten -- Bascompte, Jordi -- Brock, William A -- Brovkin, Victor -- Carpenter, Stephen R -- Dakos, Vasilis -- Held, Hermann -- van Nes, Egbert H -- Rietkerk, Max -- Sugihara, George -- England -- Nature. 2009 Sep 3;461(7260):53-9. doi: 10.1038/nature08227.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Environmental Sciences, Wageningen University, PO Box 47, 6700 AA Wageningen, The Netherlands. marten.scheffer@wur.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19727193" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/physiopathology ; Climate ; *Ecosystem ; Eutrophication ; Extinction, Biological ; Humans ; *Models, Biological ; *Models, Economic ; Seizures/physiopathology ; Stochastic Processes
    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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    Histone modifications at human enhancers reflect global cell-type-specific gene expression (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-03-20
    Description: The human body is composed of diverse cell types with distinct functions. Although it is known that lineage specification depends on cell-specific gene expression, which in turn is driven by promoters, enhancers, insulators and other cis-regulatory DNA sequences for each gene, the relative roles of these regulatory elements in this process are not clear. We have previously developed a chromatin-immunoprecipitation-based microarray method (ChIP-chip) to locate promoters, enhancers and insulators in the human genome. Here we use the same approach to identify these elements in multiple cell types and investigate their roles in cell-type-specific gene expression. We observed that the chromatin state at promoters and CTCF-binding at insulators is largely invariant across diverse cell types. In contrast, enhancers are marked with highly cell-type-specific histone modification patterns, strongly correlate to cell-type-specific gene expression programs on a global scale, and are functionally active in a cell-type-specific manner. Our results define over 55,000 potential transcriptional enhancers in the human genome, significantly expanding the current catalogue of human enhancers and highlighting the role of these elements in cell-type-specific gene expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910248/" 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/PMC2910248/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heintzman, Nathaniel D -- Hon, Gary C -- Hawkins, R David -- Kheradpour, Pouya -- Stark, Alexander -- Harp, Lindsey F -- Ye, Zhen -- Lee, Leonard K -- Stuart, Rhona K -- Ching, Christina W -- Ching, Keith A -- Antosiewicz-Bourget, Jessica E -- Liu, Hui -- Zhang, Xinmin -- Green, Roland D -- Lobanenkov, Victor V -- Stewart, Ron -- Thomson, James A -- Crawford, Gregory E -- Kellis, Manolis -- Ren, Bing -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG004037-02/HG/NHGRI NIH HHS/ -- U01 HG003151/HG/NHGRI NIH HHS/ -- U01 HG003151-01/HG/NHGRI NIH HHS/ -- U01 HG003151-01S1/HG/NHGRI NIH HHS/ -- U01 HG003151-02/HG/NHGRI NIH HHS/ -- U01 HG003151-03/HG/NHGRI NIH HHS/ -- U01 HG003151-03S1/HG/NHGRI NIH HHS/ -- U01 HG003151-03S2/HG/NHGRI NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2009 May 7;459(7243):108-12. doi: 10.1038/nature07829. Epub 2009 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, UCSD School of Medicine, 9500 Gilman Drive, La Jolla, California 92093-0653, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19295514" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cell Line ; *Cell Physiological Phenomena ; Chromatin/genetics ; *Gene Expression Regulation ; Genome, Human/genetics ; HeLa Cells ; Histones/*metabolism ; Humans ; K562 Cells ; Promoter Regions, Genetic/genetics ; Transcription Factors/*genetics/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Role of the polycomb protein EED in the propagation of repressive histone marks (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-09-22
    Description: Polycomb group proteins have an essential role in the epigenetic maintenance of repressive chromatin states. The gene-silencing activity of the Polycomb repressive complex 2 (PRC2) depends on its ability to trimethylate lysine 27 of histone H3 (H3K27) by the catalytic SET domain of the EZH2 subunit, and at least two other subunits of the complex: SUZ12 and EED. Here we show that the carboxy-terminal domain of EED specifically binds to histone tails carrying trimethyl-lysine residues associated with repressive chromatin marks, and that this leads to the allosteric activation of the methyltransferase activity of PRC2. Mutations in EED that prevent it from recognizing repressive trimethyl-lysine marks abolish the activation of PRC2 in vitro and, in Drosophila, reduce global methylation and disrupt development. These findings suggest a model for the propagation of the H3K27me3 mark that accounts for the maintenance of repressive chromatin domains and for the transmission of a histone modification from mother to daughter cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772642/" 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/PMC3772642/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Margueron, Raphael -- Justin, Neil -- Ohno, Katsuhito -- Sharpe, Miriam L -- Son, Jinsook -- Drury, William J 3rd -- Voigt, Philipp -- Martin, Stephen R -- Taylor, William R -- De Marco, Valeria -- Pirrotta, Vincenzo -- Reinberg, Danny -- Gamblin, Steven J -- GM064844/GM/NIGMS NIH HHS/ -- GM37120/GM/NIGMS NIH HHS/ -- MC_U117584222/Medical Research Council/United Kingdom -- R01 GM064844/GM/NIGMS NIH HHS/ -- R01 GM064844-08/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- Medical Research Council/United Kingdom -- England -- Nature. 2009 Oct 8;461(7265):762-7. doi: 10.1038/nature08398. Epub 2009 Sep 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, New York University Medical School, 522 First Avenue, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19767730" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Animals ; Cell Line ; Chromatin/chemistry/*genetics/metabolism ; Crystallography, X-Ray ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/*genetics/growth & development/*metabolism ; Enzyme Activation ; *Gene Silencing ; Histone-Lysine N-Methyltransferase/chemistry/metabolism ; Histones/*chemistry/*metabolism ; Lysine/analogs & derivatives/metabolism ; Methylation ; Models, Biological ; Models, Molecular ; Nuclear Proteins/metabolism ; Nucleosomes/chemistry/genetics/metabolism ; Polycomb Repressive Complex 2 ; Protein Binding ; Protein Structure, Tertiary ; Repressor Proteins/chemistry/genetics/*metabolism ; Substrate Specificity
    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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    Pulsatile stimulation determines timing and specificity of NF-kappaB-dependent transcription (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-11
    Description: The nuclear factor kappaB (NF-kappaB) transcription factor regulates cellular stress responses and the immune response to infection. NF-kappaB activation results in oscillations in nuclear NF-kappaB abundance. To define the function of these oscillations, we treated cells with repeated short pulses of tumor necrosis factor-alpha at various intervals to mimic pulsatile inflammatory signals. At all pulse intervals that were analyzed, we observed synchronous cycles of NF-kappaB nuclear translocation. Lower frequency stimulations gave repeated full-amplitude translocations, whereas higher frequency pulses gave reduced translocation, indicating a failure to reset. Deterministic and stochastic mathematical models predicted how negative feedback loops regulate both the resetting of the system and cellular heterogeneity. Altering the stimulation intervals gave different patterns of NF-kappaB-dependent gene expression, which supports the idea that oscillation frequency has a functional role.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785900/" 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/PMC2785900/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ashall, Louise -- Horton, Caroline A -- Nelson, David E -- Paszek, Pawel -- Harper, Claire V -- Sillitoe, Kate -- Ryan, Sheila -- Spiller, David G -- Unitt, John F -- Broomhead, David S -- Kell, Douglas B -- Rand, David A -- See, Violaine -- White, Michael R H -- BB/C007158/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/C008219/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/C520471/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/D010748/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E004210/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E012965/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/F005938/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC0071581/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC0082191/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC5204711/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBD0107481/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBF0059381/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0500346/Medical Research Council/United Kingdom -- G0500346(73596)/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2009 Apr 10;324(5924):242-6. doi: 10.1126/science.1164860.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Cell Imaging, School of Biological Sciences, Bioscience Research Building, Crown Street, Liverpool, L69 7ZB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19359585" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; Feedback, Physiological ; *Gene Expression ; Humans ; I-kappa B Proteins/metabolism ; Mice ; Models, Biological ; Models, Statistical ; NF-kappa B/*metabolism ; Phosphorylation ; Recombinant Fusion Proteins/metabolism ; Stochastic Processes ; Transcription Factor RelA/*metabolism ; *Transcription, Genetic ; Transfection ; Tumor Necrosis Factor-alpha/*metabolism
    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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