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  • 1
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    GENE SILENCING. Epigenetic silencing by the HUSH complex mediates position-effect variegation in human cells (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-30
    Description: Forward genetic screens in Drosophila melanogaster for modifiers of position-effect variegation have revealed the basis of much of our understanding of heterochromatin. We took an analogous approach to identify genes required for epigenetic repression in human cells. A nonlethal forward genetic screen in near-haploid KBM7 cells identified the HUSH (human silencing hub) complex, comprising three poorly characterized proteins, TASOR, MPP8, and periphilin; this complex is absent from Drosophila but is conserved from fish to humans. Loss of HUSH components resulted in decreased H3K9me3 both at endogenous genomic loci and at retroviruses integrated into heterochromatin. Our results suggest that the HUSH complex is recruited to genomic loci rich in H3K9me3, where subsequent recruitment of the methyltransferase SETDB1 is required for further H3K9me3 deposition to maintain transcriptional silencing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4487827/" 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/PMC4487827/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tchasovnikarova, Iva A -- Timms, Richard T -- Matheson, Nicholas J -- Wals, Kim -- Antrobus, Robin -- Gottgens, Berthold -- Dougan, Gordon -- Dawson, Mark A -- Lehner, Paul J -- 100140/Wellcome Trust/United Kingdom -- 101835/Wellcome Trust/United Kingdom -- 101835/Z/13/Z/Wellcome Trust/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2015 Jun 26;348(6242):1481-5. doi: 10.1126/science.aaa7227. Epub 2015 May 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge CB2 0XY, UK. ; Department of Haematology, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge CB2 0XY, UK. ; Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge CB10 1SA, UK. ; Peter MacCallum Cancer Centre, East Melbourne, Victoria 3002, Australia. ; Department of Medicine, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge CB2 0XY, UK. pjl30@cam.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26022416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/genetics/*metabolism ; *Chromosomal Position Effects ; Conserved Sequence ; Drosophila melanogaster/genetics/metabolism ; Evolution, Molecular ; *Gene Silencing ; Genes, Reporter ; Genetic Loci ; Green Fluorescent Proteins/genetics ; HeLa Cells ; Heterochromatin/metabolism ; Histones/*metabolism ; Humans ; Immunoprecipitation ; Multiprotein Complexes/genetics/*metabolism ; Nuclear Proteins/genetics/*metabolism ; Phosphoproteins/genetics/*metabolism ; Protein Methyltransferases/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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  • 2
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    The pluripotency factor NANOG controls primitive hematopoiesis and directly regulates Tal1 (2019)
    Springer Nature
    Details
    Publication Date: 2019
    Description: 〈sec〉〈st〉Synopsis〈/st〉〈p〉〈textbox textbox-type="graphic"〉〈p〉〈inline-fig〉〈/inline-fig〉〈/p〉〈/textbox〉〈/p〉 〈p〉Mechanisms that specify primitive blood cells during embryonic development are largely unknown. Here, the stem cell factor NANOG is shown to exert important roles during specification from mesoderm to the first hematopoietic cells, instructing haematopoiesis by direct repression of critical lineage specifiers.〈/p〉 〈p〉 〈l type="unord"〉〈li〉〈p〉NANOG blocks erythroid differentiation in the gastrulating embryo in a cell-autonomous manner.〈/p〉〈/li〉 〈li〉〈p〉Loss of NANOG in embryonic stem cells increases expression of hematopoietic genes and shifts differentiation towards erythroid progenitors.〈/p〉〈/li〉 〈li〉〈p〉NANOG can block generation of megakaryocyte-erythroid progenitors in the adult bone marrow.〈/p〉〈/li〉 〈li〉〈p〉〈i〉Tal1〈/i〉, a key regulator of erythroid fate, is directly repressed by NANOG during gastrulation.〈/p〉〈/li〉〈/l〉 〈/p〉〈/sec〉
    Print ISSN: 0261-4189
    Electronic ISSN: 1460-2075
    Topics: Biology , Medicine
    Published by Springer Nature on behalf of The European Molecular Biology Organization (EMBO).
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  • 3
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    CODEX: a next-generation sequencing experiment database for the haematopoietic and embryonic stem cell communities (2015)
    Oxford University Press
    Details
    Publication Date: 2015-01-16
    Description: CODEX ( http://codex.stemcells.cam.ac.uk/ ) is a user-friendly database for the direct access and interrogation of publicly available next-generation sequencing (NGS) data, specifically aimed at experimental biologists. In an era of multi-centre genomic dataset generation, CODEX provides a single database where these samples are collected, uniformly processed and vetted. The main drive of CODEX is to provide the wider scientific community with instant access to high-quality NGS data, which, irrespective of the publishing laboratory, is directly comparable. CODEX allows users to immediately visualize or download processed datasets, or compare user-generated data against the database's cumulative knowledge-base. CODEX contains four types of NGS experiments: transcription factor chromatin immunoprecipitation coupled to high-throughput sequencing (ChIP-Seq), histone modification ChIP-Seq, DNase-Seq and RNA-Seq. These are largely encompassed within two specialized repositories, HAEMCODE and ESCODE, which are focused on haematopoiesis and embryonic stem cell samples, respectively. To date, CODEX contains over 1000 samples, including 221 unique TFs and 93 unique cell types. CODEX therefore provides one of the most complete resources of publicly available NGS data for the direct interrogation of transcriptional programmes that regulate cellular identity and fate in the context of mammalian development, homeostasis and disease.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 4
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    The pluripotency factor NANOG controls primitive hematopoiesis and directly regulates Tal1 (2019)
    Springer Nature
    Details
    Publication Date: 2019
    Description: 〈p〉Progenitors of the first hematopoietic cells in the mouse arise in the early embryo from 〈i〉Brachyury〈/i〉-positive multipotent cells in the posterior-proximal region of the epiblast, but the mechanisms that specify primitive blood cells are still largely unknown. Pluripotency factors maintain uncommitted cells of the blastocyst and embryonic stem cells in the pluripotent state. However, little is known about the role played by these factors during later development, despite being expressed in the postimplantation epiblast. Using a dual transgene system for controlled expression at postimplantation stages, we found that 〈i〉Nanog〈/i〉 blocks primitive hematopoiesis in the gastrulating embryo, resulting in a loss of red blood cells and downregulation of erythropoietic genes. Accordingly, 〈i〉Nanog〈/i〉-deficient embryonic stem cells are prone to erythropoietic differentiation. Moreover, 〈i〉Nanog〈/i〉 expression in adults prevents the maturation of erythroid cells. By analysis of previous data for NANOG binding during stem cell differentiation and CRISPR/Cas9 genome editing, we found that 〈i〉Tal1〈/i〉 is a direct NANOG target. Our results show that 〈i〉Nanog〈/i〉 regulates primitive hematopoiesis by directly repressing critical erythroid lineage specifiers.〈/p〉
    Print ISSN: 0261-4189
    Electronic ISSN: 1460-2075
    Topics: Biology , Medicine
    Published by Springer Nature on behalf of The European Molecular Biology Organization (EMBO).
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