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  • 1
    Publication Date: 2003-03-22
    Description: The Polycomb group (PcG) protein Eed is implicated in regulation of imprinted X-chromosome inactivation in extraembryonic cells but not of random X inactivation in embryonic cells. The Drosophila homolog of the Eed-Ezh2 PcG protein complex achieves gene silencing through methylation of histone H3 on lysine 27 (H3-K27), which suggests a role for H3-K27 methylation in imprinted X inactivation. Here we demonstrate that transient recruitment of the Eed-Ezh2 complex to the inactive X chromosome (Xi) occurs during initiation of X inactivation in both extraembryonic and embryonic cells and is accompanied by H3-K27 methylation. Recruitment of the complex and methylation on the Xi depend on Xist RNA but are independent of its silencing function. Together, our results suggest a role for Eed-Ezh2-mediated H3-K27 methylation during initiation of both imprinted and random X inactivation and demonstrate that H3-K27 methylation is not sufficient for silencing of the Xi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plath, Kathrin -- Fang, Jia -- Mlynarczyk-Evans, Susanna K -- Cao, Ru -- Worringer, Kathleen A -- Wang, Hengbin -- de la Cruz, Cecile C -- Otte, Arie P -- Panning, Barbara -- Zhang, Yi -- New York, N.Y. -- Science. 2003 Apr 4;300(5616):131-5. Epub 2003 Mar 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12649488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism/*physiology ; Cell Differentiation ; Cell Nucleus/metabolism ; Cells, Cultured ; *Dosage Compensation, Genetic ; Female ; Fluorescent Antibody Technique ; Genomic Imprinting ; HeLa Cells ; Histones/*metabolism ; Humans ; In Situ Hybridization, Fluorescence ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mutation ; Polycomb Repressive Complex 2 ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/metabolism ; Stem Cells/metabolism/*physiology ; Transgenes ; Trophoblasts/*physiology ; X Chromosome/*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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  • 2
    Publication Date: 2009-07-10
    Description: An open chromatin largely devoid of heterochromatin is a hallmark of stem cells. It remains unknown whether an open chromatin is necessary for the differentiation potential of stem cells, and which molecules are needed to maintain open chromatin. Here we show that the chromatin remodelling factor Chd1 is required to maintain the open chromatin of pluripotent mouse embryonic stem cells. Chd1 is a euchromatin protein that associates with the promoters of active genes, and downregulation of Chd1 leads to accumulation of heterochromatin. Chd1-deficient embryonic stem cells are no longer pluripotent, because they are incapable of giving rise to primitive endoderm and have a high propensity for neural differentiation. Furthermore, Chd1 is required for efficient reprogramming of fibroblasts to the pluripotent stem cell state. Our results indicate that Chd1 is essential for open chromatin and pluripotency of embryonic stem cells, and for somatic cell reprogramming to the pluripotent state.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891576/" 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/PMC3891576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gaspar-Maia, Alexandre -- Alajem, Adi -- Polesso, Fanny -- Sridharan, Rupa -- Mason, Mike J -- Heidersbach, Amy -- Ramalho-Santos, Joao -- McManus, Michael T -- Plath, Kathrin -- Meshorer, Eran -- Ramalho-Santos, Miguel -- DP2 OD004698/OD/NIH HHS/ -- R01 GM080783/GM/NIGMS NIH HHS/ -- R01 GM080783-01/GM/NIGMS NIH HHS/ -- R01 GM080783-02/GM/NIGMS NIH HHS/ -- R01 GM080783-03/GM/NIGMS NIH HHS/ -- R01 GM080783-04/GM/NIGMS NIH HHS/ -- R01 GM080783-05/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Aug 13;460(7257):863-8. doi: 10.1038/nature08212. Epub 2009 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ob/Gyn and Pathology, Center for Reproductive Sciences and Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, California 94143-0525, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19587682" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers ; Cell Proliferation ; Cells, Cultured ; Cellular Reprogramming ; *Chromatin Assembly and Disassembly ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Embryonic Stem Cells/*cytology/*metabolism ; Endoderm/metabolism ; Euchromatin/genetics/*metabolism ; Fibroblasts/cytology/metabolism ; GATA6 Transcription Factor/genetics/metabolism ; Histones/metabolism ; Methylation ; Mice ; Neurogenesis ; Neurons/cytology/metabolism ; Octamer Transcription Factor-3/genetics ; Pluripotent Stem Cells/*cytology/*metabolism ; Promoter Regions, Genetic/genetics ; RNA Interference
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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