What's new for 'JKB_daily1' in PubMed

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Tuesday, 2010 May 18
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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PubMed Results

Items 1 - 3 of 3

1.	Nature. 2010 Apr 8;464(7290):831. PhD: routine technical work of sequencing is no substitute. Chen Y. Comment on: Nature. 2010 Mar 4;464(7285):7.
	PMID: 20376128 [PubMed - indexed for MEDLINE]
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	Publication Types: Comment Letter MeSH Terms: China Creativeness Education, Graduate/standards* Genomics/education Genomics/manpower Genomics/methods Logic Research Personnel/education* Research Personnel/standards* Sequence Analysis, DNA*

2.	Nature. 2010 Apr 8;464(7290):831. PhD: still necessary for independent research leaders. Li Y. Comment on: Nature. 2010 Mar 4;464(7285):7.
	PMID: 20376127 [PubMed - indexed for MEDLINE]
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	Publication Types: Comment Letter MeSH Terms: China Education, Graduate* Genomics/manpower Leadership* Research Personnel/education* Research Personnel/standards

3.	Nature. 2010 Apr 8;464(7290):927-31. Epub 2010 Feb 17. Proviral silencing in embryonic stem cells requires the histone methyltransferase ESET. Matsui T, Leung D, Miyashita H, Maksakova IA, Miyachi H, Kimura H, Tachibana M, Lorincz MC, Shinkai Y. Experimental Research Center for Infectious Diseases, Institute for Virus Research, Kyoto University, 53 Shogoin, Kawara-cho, Sakyo-ku, Kyoto 606-8507, Japan. Abstract Endogenous retroviruses (ERVs), retrovirus-like elements with long terminal repeats, are widely dispersed in the euchromatic compartment in mammalian cells, comprising approximately 10% of the mouse genome. These parasitic elements are responsible for >10% of spontaneous mutations. Whereas DNA methylation has an important role in proviral silencing in somatic and germ-lineage cells, an additional DNA-methylation-independent pathway also functions in embryonal carcinoma and embryonic stem (ES) cells to inhibit transcription of the exogenous gammaretrovirus murine leukaemia virus (MLV). Notably, a recent genome-wide study revealed that ERVs are also marked by histone H3 lysine 9 trimethylation (H3K9me3) and H4K20me3 in ES cells but not in mouse embryonic fibroblasts. However, the role that these marks have in proviral silencing remains unexplored. Here we show that the H3K9 methyltransferase ESET (also called SETDB1 or KMT1E) and the Krüppel-associated box (KRAB)-associated protein 1 (KAP1, also called TRIM28) are required for H3K9me3 and silencing of endogenous and introduced retroviruses specifically in mouse ES cells. Furthermore, whereas ESET enzymatic activity is crucial for HP1 binding and efficient proviral silencing, the H4K20 methyltransferases Suv420h1 and Suv420h2 are dispensable for silencing. Notably, in DNA methyltransferase triple knockout (Dnmt1(-/-)Dnmt3a(-/-)Dnmt3b(-/-)) mouse ES cells, ESET and KAP1 binding and ESET-mediated H3K9me3 are maintained and ERVs are minimally derepressed. We propose that a DNA-methylation-independent pathway involving KAP1 and ESET/ESET-mediated H3K9me3 is required for proviral silencing during the period early in embryogenesis when DNA methylation is dynamically reprogrammed.
	PMID: 20164836 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, Non-U.S. Gov't MeSH Terms: Animals Cell Line DNA (Cytosine-5-)-Methyltransferase/deficiency DNA (Cytosine-5-)-Methyltransferase/genetics DNA (Cytosine-5-)-Methyltransferase/metabolism DNA Methylation/genetics Embryonic Stem Cells/enzymology* Embryonic Stem Cells/metabolism Embryonic Stem Cells/virology* Endogenous Retroviruses/genetics* Fibroblasts Gene Deletion Gene Silencing* Histone-Lysine N-Methyltransferase/deficiency Histone-Lysine N-Methyltransferase/genetics Histone-Lysine N-Methyltransferase/metabolism* Mice Nuclear Proteins/metabolism Protein Methyltransferases/deficiency Protein Methyltransferases/genetics Protein Methyltransferases/metabolism* Proviruses/genetics* Repressor Proteins/metabolism Substances: Nuclear Proteins Repressor Pr oteins Trim28 protein, mouse DNA methyltransferase 3B Protein Methyltransferases SETDB1 protein, mouse histone methyltransferase DNA (Cytosine-5-)-Methyltransferase DNA (cytosine-5-)-methyltransferase 1 DNA methyltransferase 3A Histone-Lysine N-Methyltransferase Grant Support: 77805/Canadian Institutes of Health Research/Canada 92090/Canadian Institutes of Health Research/Canada