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  • 1
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    Quantitative sequencing of 5-methylcytosine and 5-hydroxymethylcytosine at single-base resolution (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-28
    Description: 5-Methylcytosine can be converted to 5-hydroxymethylcytosine (5hmC) in mammalian DNA by the ten-eleven translocation (TET) enzymes. We introduce oxidative bisulfite sequencing (oxBS-Seq), the first method for quantitative mapping of 5hmC in genomic DNA at single-nucleotide resolution. Selective chemical oxidation of 5hmC to 5-formylcytosine (5fC) enables bisulfite conversion of 5fC to uracil. We demonstrate the utility of oxBS-Seq to map and quantify 5hmC at CpG islands (CGIs) in mouse embryonic stem (ES) cells and identify 800 5hmC-containing CGIs that have on average 3.3% hydroxymethylation. High levels of 5hmC were found in CGIs associated with transcriptional regulators and in long interspersed nuclear elements, suggesting that these regions might undergo epigenetic reprogramming in ES cells. Our results open new questions on 5hmC dynamics and sequence-specific targeting by TETs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Booth, Michael J -- Branco, Miguel R -- Ficz, Gabriella -- Oxley, David -- Krueger, Felix -- Reik, Wolf -- Balasubramanian, Shankar -- 095645/Wellcome Trust/United Kingdom -- 11961/Cancer Research UK/United Kingdom -- G0801156/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 May 18;336(6083):934-7. doi: 10.1126/science.1220671. Epub 2012 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Cambridge, Cambridge CB2 1EW, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22539555" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/*analysis ; Animals ; *CpG Islands ; Cytosine/*analogs & derivatives/analysis/chemistry ; DNA/*chemistry/genetics ; DNA Methylation ; *Embryonic Stem Cells/physiology ; Epigenesis, Genetic ; Genes, Intracisternal A-Particle ; High-Throughput Nucleotide Sequencing ; Long Interspersed Nucleotide Elements ; Mice ; Oxidation-Reduction ; Rhenium/chemistry ; *Sequence Analysis, DNA ; Sulfites ; Transcription, Genetic ; Uracil/chemistry
    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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    Caspases 3 and 7: key mediators of mitochondrial events of apoptosis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-14
    Description: The current model of apoptosis holds that upstream signals lead to activation of downstream effector caspases. We generated mice deficient in the two effectors, caspase 3 and caspase 7, which died immediately after birth with defects in cardiac development. Fibroblasts lacking both enzymes were highly resistant to both mitochondrial and death receptor-mediated apoptosis, displayed preservation of mitochondrial membrane potential, and had defective nuclear translocation of apoptosis-inducing factor (AIF). Furthermore, the early apoptotic events of Bax translocation and cytochrome c release were also delayed. We conclude that caspases 3 and 7 are critical mediators of mitochondrial events of apoptosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738210/" 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/PMC3738210/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lakhani, Saquib A -- Masud, Ali -- Kuida, Keisuke -- Porter, George A Jr -- Booth, Carmen J -- Mehal, Wajahat Z -- Inayat, Irteza -- Flavell, Richard A -- 1 K08 HD044580/HD/NICHD NIH HHS/ -- 5 K12 HD01401/HD/NICHD NIH HHS/ -- K08 DK002965/DK/NIDDK NIH HHS/ -- K08 DK002965-04/DK/NIDDK NIH HHS/ -- K12 HD00850/HD/NICHD NIH HHS/ -- NIDDK P30-34989/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 10;311(5762):847-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16469926" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Inducing Factor/metabolism ; Caspase 3 ; Caspase 7 ; Caspases/deficiency/*metabolism ; Cell Nucleus/metabolism ; Cell Shape ; Cell Survival ; Cells, Cultured ; Cytochromes c/metabolism ; DNA Fragmentation ; Female ; Fibroblasts/cytology ; Heart/embryology ; Heart Defects, Congenital/etiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/metabolism/*physiology ; Mitochondrial Membranes/physiology ; Permeability ; T-Lymphocytes/cytology ; bcl-2-Associated X Protein/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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  • 3
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    IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-10-19
    Description: Chronic mucosal inflammation and tissue damage predisposes patients to the development of colorectal cancer. This association could be explained by the hypothesis that the same factors and pathways important for wound healing also promote tumorigenesis. A sensor of tissue damage should induce these factors to promote tissue repair and regulate their action to prevent development of cancer. Interleukin 22 (IL-22), a cytokine of the IL-10 superfamily, has an important role in colonic epithelial cell repair, and its levels are increased in the blood and intestine of inflammatory bowel disease patients. This cytokine can be neutralized by the soluble IL-22 receptor, known as the IL-22 binding protein (IL-22BP, also known as IL22RA2); however, the significance of endogenous IL-22BP in vivo and the pathways that regulate this receptor are unknown. Here we describe that IL-22BP has a crucial role in controlling tumorigenesis and epithelial cell proliferation in the colon. IL-22BP is highly expressed by dendritic cells in the colon in steady-state conditions. Sensing of intestinal tissue damage via the NLRP3 or NLRP6 inflammasomes led to an IL-18-dependent downregulation of IL-22BP, thereby increasing the ratio of IL-22/IL-22BP. IL-22, which is induced during intestinal tissue damage, exerted protective properties during the peak of damage, but promoted tumour development if uncontrolled during the recovery phase. Thus, the IL-22-IL-22BP axis critically regulates intestinal tissue repair and tumorigenesis in the colon.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3493690/" 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/PMC3493690/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huber, Samuel -- Gagliani, Nicola -- Zenewicz, Lauren A -- Huber, Francis J -- Bosurgi, Lidia -- Hu, Bo -- Hedl, Matija -- Zhang, Wei -- O'Connor, William Jr -- Murphy, Andrew J -- Valenzuela, David M -- Yancopoulos, George D -- Booth, Carmen J -- Cho, Judy H -- Ouyang, Wenjun -- Abraham, Clara -- Flavell, Richard A -- DK-P30-34989/DK/NIDDK NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- R01 DK077905/DK/NIDDK NIH HHS/ -- R01DK077905/DK/NIDDK NIH HHS/ -- U19 AI082713/AI/NIAID NIH HHS/ -- U19-AI082713/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Nov 8;491(7423):259-63. doi: 10.1038/nature11535. Epub 2012 Oct 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23075849" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Colitis/complications/metabolism/pathology ; Colon/metabolism/pathology ; Colonic Neoplasms/complications/metabolism/pathology ; Disease Models, Animal ; Down-Regulation ; Epithelial Cells/metabolism/pathology ; Genes, APC ; Inflammasomes/*metabolism ; Interleukin-18/metabolism ; Interleukins/deficiency/genetics/metabolism ; Intestines/*metabolism/*pathology ; Mice ; Mice, Knockout ; Receptors, Interleukin/deficiency/genetics/*metabolism ; Time Factors ; Weight Loss
    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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  • 4
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    GBP5 promotes NLRP3 inflammasome assembly and immunity in mammals (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: Inflammasomes are sensory complexes that alert the immune system to the presence of infection or tissue damage. These complexes assemble NLR (nucleotide binding and oligomerization, leucine-rich repeat) or ALR (absent in melanoma 2-like receptor) proteins to activate caspase-1 cleavage and interleukin (IL)-1beta/IL-18 secretion. Here, we identified a non-NLR/ALR human protein that stimulates inflammasome assembly: guanylate binding protein 5 (GBP5). GBP5 promoted selective NLRP3 inflammasome responses to pathogenic bacteria and soluble but not crystalline inflammasome priming agents. Generation of Gbp5(-/-) mice revealed pronounced caspase-1 and IL-1beta/IL-18 cleavage defects in vitro and impaired host defense and Nlrp3-dependent inflammatory responses in vivo. Thus, GBP5 serves as a unique rheostat for NLRP3 inflammasome activation and extends our understanding of the inflammasome complex beyond its core machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shenoy, Avinash R -- Wellington, David A -- Kumar, Pradeep -- Kassa, Hilina -- Booth, Carmen J -- Cresswell, Peter -- MacMicking, John D -- R01 AI068041-06/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):481-5. doi: 10.1126/science.1217141. Epub 2012 Mar 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461501" target="_blank"〉PubMed〈/a〉
    Keywords: Alum Compounds ; Animals ; Apoptosis Regulatory Proteins ; Carrier Proteins/genetics/*metabolism ; Caspase 1/metabolism ; Cell Line ; Cytoskeletal Proteins/metabolism ; GTP-Binding Proteins/chemistry/genetics/*metabolism ; Humans ; Inflammasomes/*metabolism ; Interferon-gamma/immunology ; Interleukin-1beta/secretion ; Lipopolysaccharides/immunology ; Listeria monocytogenes ; Listeriosis/immunology ; Macrophages/immunology/*metabolism ; Mice ; Protein Multimerization ; RNA Interference ; Salmonella typhimurium/immunology ; Uric Acid
    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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  • 5
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    Gut microbiota. Antimicrobial peptide resistance mediates resilience of prominent gut commensals during inflammation (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-01-13
    Description: Resilience to host inflammation and other perturbations is a fundamental property of gut microbial communities, yet the underlying mechanisms are not well understood. We have found that human gut microbes from all dominant phyla are resistant to high levels of inflammation-associated antimicrobial peptides (AMPs) and have identified a mechanism for lipopolysaccharide (LPS) modification in the phylum Bacteroidetes that increases AMP resistance by four orders of magnitude. Bacteroides thetaiotaomicron mutants that fail to remove a single phosphate group from their LPS were displaced from the microbiota during inflammation triggered by pathogen infection. These findings establish a mechanism that determines the stability of prominent members of a healthy microbiota during perturbation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388331/" 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/PMC4388331/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cullen, T W -- Schofield, W B -- Barry, N A -- Putnam, E E -- Rundell, E A -- Trent, M S -- Degnan, P H -- Booth, C J -- Yu, H -- Goodman, A L -- AI064184/AI/NIAID NIH HHS/ -- AI76322/AI/NIAID NIH HHS/ -- DK089121/DK/NIDDK NIH HHS/ -- DP2 GM105456/GM/NIGMS NIH HHS/ -- GM103574/GM/NIGMS NIH HHS/ -- GM105456/GM/NIGMS NIH HHS/ -- R01 GM103574/GM/NIGMS NIH HHS/ -- T32 AI007640/AI/NIAID NIH HHS/ -- UL1 TR000142/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2015 Jan 9;347(6218):170-5. doi: 10.1126/science.1260580.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA. Microbial Sciences Institute, Yale University School of Medicine, New Haven, CT 06520, USA. ; Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA. ; Department of Molecular Biosciences and Institute of Cell and Molecular Biology, University of Texas, Austin, TX 78712, USA. ; Department of Microbiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA. ; Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA. ; Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA. ; Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA. Microbial Sciences Institute, Yale University School of Medicine, New Haven, CT 06520, USA. andrew.goodman@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25574022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimicrobial Cationic Peptides ; Bacteroides/*drug effects/genetics/physiology ; Colitis/*microbiology ; Drug Resistance, Bacterial/*genetics ; Escherichia coli/drug effects/physiology ; Gastrointestinal Tract/*microbiology ; Germ-Free Life ; Humans ; Lipid A/metabolism ; Mice ; Microbiota/*drug effects/genetics/physiology ; Phosphoric Monoester Hydrolases/genetics/*physiology ; Polymyxin B/*pharmacology ; Symbiosis
    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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