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

Sent on Saturday, 2014 October 25
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. 2014 Aug 28;512(7515):400-5. doi: 10.1038/nature13497. Regulatory analysis of the C. elegans genome with spatiotemporal resolution. Araya CL1, Kawli T1, Kundaje A2, Jiang L1, Wu B1, Vafeados D3, Terrell R3, Weissdepp P3, Gevirtzman L3, Mace D3, Niu W4, Boyle AP1, Xie D1, Ma L5, Murray JI6, Reinke V4, Waterston RH3, Snyder M1. Author information: 1Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA. 2Department of Computer Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA. 3Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. 4Department of Genetics, Yale University School of Medicine, New Haven, Connecticut 06520, USA. 5Institute for Genomics and Systems Biology, University of Chicago, Chicago, Illinois 60637, USA. 6 Department of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. Comment in Genomics: Hiding in plain sight. [Nature. 2014] Genomics: Hiding in plain sight.Muerdter F, Stark A. Nature. 2014 Aug 28; 512(7515):374-5. Abstract Discovering the structure and dynamics of transcriptional regulatory events in the genome with cellular and temporal resolution is crucial to understanding the regulatory underpinnings of development and disease. We determined the genomic distribution of binding sites for 92 transcription factors and regulatory proteins across multiple stages of Caenorhabditis elegans development by performing 241 ChIP-seq (chromatin immunoprecipitation followed by sequencing) experiments. Integration of regulatory binding and cellular-resolution expression data produced a spatiotemporally resolved metazoan transcription factor binding map. Using this map, we explore developmental regulatory circuits that encode combinatorial logic at the levels of co-binding and co-expression of transcription factors, characterizing the genomic coverage and clustering of regulatory binding, the binding preferences of, and biological processes regulated by, transcription factors, the global transcription factor co-associations and genomic subdomains that suggest shared patterns of regulation, and identifying key transcription factors and transcription factor co-associations for fate specification of individual lineages and cell types.
	PMID: 25164749 [PubMed - indexed for MEDLINE]
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2.	Nature. 2014 Aug 28;512(7515):359. doi: 10.1038/512359a. Himalayan plants seek cooler climes. Padma TV.
	PMID: 25164731 [PubMed - indexed for MEDLINE]
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3.	Nature. 2014 Aug 28;512(7515):431-5. doi: 10.1038/nature13375. Epub 2014 Jun 25. miR-34a blocks osteoporosis and bone metastasis by inhibiting osteoclastogenesis and Tgif2. Krzeszinski JY1, Wei W1, Huynh H1, Jin Z1, Wang X1, Chang TC2, Xie XJ3, He L4, Mangala LS5, Lopez-Berestein G6, Sood AK7, Mendell JT8, Wan Y9. Author information: 1Department of Pharmacology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. 2Department of Molecular Biology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. 31] Simmons Cancer Center, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [2] Department of Clinical Sciences, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. 4Division of Cellular and Developmental Biology, Molecular and Cell Biology Department, University of California at Berkeley, Berkeley, California 94705, USA. 51] Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA [2] Center for RNA Interference and Non-coding RNA, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. 61] Center for RNA Interference and Non-coding RNA, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA [2] Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. 71] Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA [2] Center for RNA Interference and Non-coding RNA, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA [3] Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. 81] Department of Molecular Biology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [2] Simmons Cancer Center, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. 91] Department of Pharmacology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA [2] Simmons Cancer Center, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. Comment in Bone: micromanaging osteoporosis. [Nat Rev Rheumatol. 2014] Bone: micromanaging osteoporosis.Ray K. Nat Rev Rheumatol. 2014 Aug; 10(8):445. Epub 2014 Jul 8. Abstract Bone-resorbing osteoclasts significantly contribute to osteoporosis and bone metastases of cancer. MicroRNAs play important roles in physiology and disease, and present tremendous therapeutic potential. Nonetheless, how microRNAs regulate skeletal biology is underexplored. Here we identify miR-34a as a novel and critical suppressor of osteoclastogenesis, bone resorption and the bone metastatic niche. miR-34a is downregulated during osteoclast differentiation. Osteoclastic miR-34a-overexpressing transgenic mice exhibit lower bone resorption and higher bone mass. Conversely, miR-34a knockout and heterozygous mice exhibit elevated bone resorption and reduced bone mass. Consequently, ovariectomy-induced osteoporosis, as well as bone metastasis of breast and skin cancers, are diminished in osteoclastic miR-34a transgenic mice, and can be effectively attenuated by miR-34a nanoparticle treatment. Mechanistically, we identify transforming growth factor-β-induced factor 2 (Tgif2) as an essential direct miR-34a target that is pro-osteoclastogenic. Tgif2 deletion reduces bone resorption and abolishes miR-34a regulation. Together, using mouse genetic, pharmacological and disease models, we reveal miR-34a as a key osteoclast suppressor and a potential therapeutic strategy to confer skeletal protection and ameliorate bone metastasis of cancers. PMCID: PMC4149606 [Available on 2015/2/28]
	PMID: 25043055 [PubMed - indexed for MEDLINE]
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