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  • Cell Line  (47)
  • American Association for the Advancement of Science (AAAS)  (47)
  • Uppsala
  • 2010-2014  (25)
  • 1980-1984  (22)
  • 2012  (25)
  • 1981  (22)
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  • 2010-2014  (25)
  • 1980-1984  (22)
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  • 1
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    The ancient drug salicylate directly activates AMP-activated protein kinase (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-21
    Description: Salicylate, a plant product, has been in medicinal use since ancient times. More recently, it has been replaced by synthetic derivatives such as aspirin and salsalate, both of which are rapidly broken down to salicylate in vivo. At concentrations reached in plasma after administration of salsalate or of aspirin at high doses, salicylate activates adenosine monophosphate-activated protein kinase (AMPK), a central regulator of cell growth and metabolism. Salicylate binds at the same site as the synthetic activator A-769662 to cause allosteric activation and inhibition of dephosphorylation of the activating phosphorylation site, threonine-172. In AMPK knockout mice, effects of salicylate to increase fat utilization and to lower plasma fatty acids in vivo were lost. Our results suggest that AMPK activation could explain some beneficial effects of salsalate and aspirin in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399766/" 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/PMC3399766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hawley, Simon A -- Fullerton, Morgan D -- Ross, Fiona A -- Schertzer, Jonathan D -- Chevtzoff, Cyrille -- Walker, Katherine J -- Peggie, Mark W -- Zibrova, Darya -- Green, Kevin A -- Mustard, Kirsty J -- Kemp, Bruce E -- Sakamoto, Kei -- Steinberg, Gregory R -- Hardie, D Grahame -- 080982/Wellcome Trust/United Kingdom -- 097726/Wellcome Trust/United Kingdom -- MC_U127088492/Medical Research Council/United Kingdom -- Canadian Institutes of Health Research/Canada -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 May 18;336(6083):918-22. doi: 10.1126/science.1215327. Epub 2012 Apr 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Signalling and Immunology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22517326" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/genetics/*metabolism ; Amino Acid Substitution ; Animals ; Aspirin/pharmacology ; Binding Sites ; Carbohydrate Metabolism/drug effects ; Cell Line ; Enzyme Activation ; Enzyme Activators/pharmacology ; HEK293 Cells ; Humans ; Lipid Metabolism/drug effects ; Liver/drug effects/metabolism ; Mice ; Mice, Knockout ; Mutation ; Oxygen Consumption/drug effects ; Phosphorylation ; Pyrones/pharmacology ; Rats ; Salicylates/blood/*metabolism/*pharmacology ; Thiophenes/pharmacology
    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
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    Sedlin controls the ER export of procollagen by regulating the Sar1 cycle (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-29
    Description: Newly synthesized proteins exit the endoplasmic reticulum (ER) via coat protein complex II (COPII) vesicles. Procollagen (PC), however, forms prefibrils that are too large to fit into typical COPII vesicles; PC thus needs large transport carriers, which we term megacarriers. TANGO1 assists PC packing, but its role in promoting the growth of megacarriers is not known. We found that TANGO1 recruited Sedlin, a TRAPP component that is defective in spondyloepiphyseal dysplasia tarda (SEDT), and that Sedlin was required for the ER export of PC. Sedlin bound and promoted efficient cycling of Sar1, a guanosine triphosphatase that can constrict membranes, and thus allowed nascent carriers to grow and incorporate PC prefibrils. This joint action of TANGO1 and Sedlin sustained the ER export of PC, and its derangement may explain the defective chondrogenesis underlying SEDT.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471527/" 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/PMC3471527/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Venditti, Rossella -- Scanu, Tiziana -- Santoro, Michele -- Di Tullio, Giuseppe -- Spaar, Alexander -- Gaibisso, Renato -- Beznoussenko, Galina V -- Mironov, Alexander A -- Mironov, Alexander Jr -- Zelante, Leopoldo -- Piemontese, Maria Rosaria -- Notarangelo, Angelo -- Malhotra, Vivek -- Vertel, Barbara M -- Wilson, Cathal -- De Matteis, Maria Antonietta -- AR053696/AR/NIAMS NIH HHS/ -- GGP06166/Telethon/Italy -- GGP07075/Telethon/Italy -- GSP08002/Telethon/Italy -- GTF08001/Telethon/Italy -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1668-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Telethon Institute of Genetics and Medicine, Naples, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019651" target="_blank"〉PubMed〈/a〉
    Keywords: Aryl Hydrocarbon Receptor Nuclear Translocator/*metabolism ; COP-Coated Vesicles/metabolism ; Cell Line ; Chondrogenesis/genetics ; Endoplasmic Reticulum/*metabolism ; Golgi Apparatus/metabolism ; Humans ; Membrane Transport Proteins/genetics/*metabolism ; Monomeric GTP-Binding Proteins/*metabolism ; Mutation ; Osteochondrodysplasias/genetics/metabolism ; Procollagen/*metabolism ; Protein Transport ; Transcription Factors/genetics/*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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    GSK3-TIP60-ULK1 signaling pathway links growth factor deprivation to autophagy (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-28
    Description: In metazoans, cells depend on extracellular growth factors for energy homeostasis. We found that glycogen synthase kinase-3 (GSK3), when deinhibited by default in cells deprived of growth factors, activates acetyltransferase TIP60 through phosphorylating TIP60-Ser(86), which directly acetylates and stimulates the protein kinase ULK1, which is required for autophagy. Cells engineered to express TIP60(S86A) that cannot be phosphorylated by GSK3 could not undergo serum deprivation-induced autophagy. An acetylation-defective mutant of ULK1 failed to rescue autophagy in ULK1(-/-) mouse embryonic fibroblasts. Cells used signaling from GSK3 to TIP60 and ULK1 to regulate autophagy when deprived of serum but not glucose. These findings uncover an activating pathway that integrates protein phosphorylation and acetylation to connect growth factor deprivation to autophagy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Shu-Yong -- Li, Terytty Yang -- Liu, Qing -- Zhang, Cixiong -- Li, Xiaotong -- Chen, Yan -- Zhang, Shi-Meng -- Lian, Guili -- Liu, Qi -- Ruan, Ka -- Wang, Zhen -- Zhang, Chen-Song -- Chien, Kun-Yi -- Wu, Jiawei -- Li, Qinxi -- Han, Jiahuai -- Lin, Sheng-Cai -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):477-81. doi: 10.1126/science.1217032.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Fujian, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22539723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cell Line ; Cell Line, Tumor ; Culture Media ; Culture Media, Serum-Free ; Glucose/metabolism ; Glycogen Synthase Kinase 3/genetics/*metabolism ; HEK293 Cells ; Histone Acetyltransferases/genetics/*metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Intracellular Signaling Peptides and Proteins/genetics/*metabolism ; Mice ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Rats ; *Signal Transduction ; Trans-Activators/genetics/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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  • 4
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    Tumor necrosis factor signaling requires iRhom2 to promote trafficking and activation of TACE (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-17
    Description: The cytokine tumor necrosis factor (TNF) is the primary trigger of inflammation. Like many extracellular signaling proteins, TNF is synthesized as a transmembrane protein; the active signal is its ectodomain, which is shed from cells after cleavage by an ADAM family metalloprotease, ADAM17 (TNFalpha-converting enzyme, TACE). We report that iRhom2 (RHBDF2), a proteolytically inactive member of the rhomboid family, is required for TNF release in mice. iRhom2 binds TACE and promotes its exit from the endoplasmic reticulum. The failure of TACE to exit the endoplasmic reticulum in the absence of iRhom2 prevents the furin-mediated maturation and trafficking of TACE to the cell surface, the site of TNF cleavage. Given the role of TNF in autoimmune and inflammatory diseases, iRhom2 may represent an attractive therapeutic target.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3272371/" 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/PMC3272371/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adrain, Colin -- Zettl, Markus -- Christova, Yonka -- Taylor, Neil -- Freeman, Matthew -- MC_U105178780/Medical Research Council/United Kingdom -- U.1051.01.009(78780)/Medical Research Council/United Kingdom -- U105178780/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):225-8. doi: 10.1126/science.1214400.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246777" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/*metabolism ; Animals ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Endoplasmic Reticulum/metabolism ; Enzyme Activation ; Furin/metabolism ; Humans ; Lipopolysaccharides/immunology ; Macrophages/metabolism ; Mice ; Mice, Knockout ; Protein Binding ; Protein Transport ; *Signal Transduction ; Tumor Necrosis Factor-alpha/*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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  • 5
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    A DOC2 protein identified by mutational profiling is essential for apicomplexan parasite exocytosis (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-17
    Description: Exocytosis is essential to the lytic cycle of apicomplexan parasites and required for the pathogenesis of toxoplasmosis and malaria. DOC2 proteins recruit the membrane fusion machinery required for exocytosis in a Ca(2+)-dependent fashion. Here, the phenotype of a Toxoplasma gondii conditional mutant impaired in host cell invasion and egress was pinpointed to a defect in secretion of the micronemes, an apicomplexan-specific organelle that contains adhesion proteins. Whole-genome sequencing identified the etiological point mutation in TgDOC2.1. A conditional allele of the orthologous gene engineered into Plasmodium falciparum was also defective in microneme secretion. However, the major effect was on invasion, suggesting that microneme secretion is dispensable for Plasmodium egress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3354045/" 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/PMC3354045/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farrell, Andrew -- Thirugnanam, Sivasakthivel -- Lorestani, Alexander -- Dvorin, Jeffrey D -- Eidell, Keith P -- Ferguson, David J P -- Anderson-White, Brooke R -- Duraisingh, Manoj T -- Marth, Gabor T -- Gubbels, Marc-Jan -- AI057919/AI/NIAID NIH HHS/ -- AI081220/AI/NIAID NIH HHS/ -- AI087874/AI/NIAID NIH HHS/ -- AI088314/AI/NIAID NIH HHS/ -- HG004719/HG/NHGRI NIH HHS/ -- K08 AI087874/AI/NIAID NIH HHS/ -- K08 AI087874-02/AI/NIAID NIH HHS/ -- R01 AI057919/AI/NIAID NIH HHS/ -- R01 HG004719/HG/NHGRI NIH HHS/ -- R21 AI081220/AI/NIAID NIH HHS/ -- R21 AI088314/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):218-21. doi: 10.1126/science.1210829.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Boston College, Chestnut Hill, MA 02467, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246776" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Calcium/*metabolism ; Calcium-Binding Proteins/chemistry/genetics/*metabolism ; Cell Line ; *Exocytosis ; Genes, Protozoan ; Genetic Complementation Test ; Genome, Protozoan ; Humans ; Models, Molecular ; Molecular Sequence Data ; Movement ; Mutagenesis ; Organelles/*metabolism ; Plasmodium falciparum/genetics/growth & development/physiology ; Point Mutation ; Protein Structure, Tertiary ; Protozoan Proteins/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Toxoplasma/genetics/growth & development/*physiology/ultrastructure
    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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  • 6
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    An overlapping protein-coding region in influenza A virus segment 3 modulates the host response (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-30
    Description: Influenza A virus (IAV) infection leads to variable and imperfectly understood pathogenicity. We report that segment 3 of the virus contains a second open reading frame ("X-ORF"), accessed via ribosomal frameshifting. The frameshift product, termed PA-X, comprises the endonuclease domain of the viral PA protein with a C-terminal domain encoded by the X-ORF and functions to repress cellular gene expression. PA-X also modulates IAV virulence in a mouse infection model, acting to decrease pathogenicity. Loss of PA-X expression leads to changes in the kinetics of the global host response, which notably includes increases in inflammatory, apoptotic, and T lymphocyte-signaling pathways. Thus, we have identified a previously unknown IAV protein that modulates the host response to infection, a finding with important implications for understanding IAV pathogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552242/" 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/PMC3552242/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jagger, B W -- Wise, H M -- Kash, J C -- Walters, K-A -- Wills, N M -- Xiao, Y-L -- Dunfee, R L -- Schwartzman, L M -- Ozinsky, A -- Bell, G L -- Dalton, R M -- Lo, A -- Efstathiou, S -- Atkins, J F -- Firth, A E -- Taubenberger, J K -- Digard, P -- 073126/Wellcome Trust/United Kingdom -- 088789/Wellcome Trust/United Kingdom -- G0700815/Medical Research Council/United Kingdom -- G0700815(82260)/Medical Research Council/United Kingdom -- G9800943/Medical Research Council/United Kingdom -- MR/J002232/1/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):199-204. doi: 10.1126/science.1222213. Epub 2012 Jun 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Virology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745253" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Codon ; Conserved Sequence ; Female ; *Frameshifting, Ribosomal ; Gene Expression Regulation ; Genome, Viral ; HEK293 Cells ; Humans ; Influenza A Virus, H1N1 Subtype/*genetics/growth & development/pathogenicity ; Influenza A virus/*genetics/metabolism ; Lung/pathology/virology ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutation ; *Open Reading Frames ; Orthomyxoviridae Infections/genetics/immunology/pathology/*virology ; Protein Interaction Domains and Motifs ; Proteome ; RNA Replicase/chemistry/*genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; RNA, Viral/genetics/metabolism ; Reassortant Viruses/genetics ; Repressor Proteins/chemistry/*genetics/*metabolism ; Viral Nonstructural Proteins/chemistry/*genetics/*metabolism ; Viral Proteins/biosynthesis/chemistry/*genetics/*metabolism ; Virus Replication
    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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  • 7
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    Metabolite profiling identifies a key role for glycine in rapid cancer cell proliferation (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-26
    Description: Metabolic reprogramming has been proposed to be a hallmark of cancer, yet a systematic characterization of the metabolic pathways active in transformed cells is currently lacking. Using mass spectrometry, we measured the consumption and release (CORE) profiles of 219 metabolites from media across the NCI-60 cancer cell lines, and integrated these data with a preexisting atlas of gene expression. This analysis identified glycine consumption and expression of the mitochondrial glycine biosynthetic pathway as strongly correlated with rates of proliferation across cancer cells. Antagonizing glycine uptake and its mitochondrial biosynthesis preferentially impaired rapidly proliferating cells. Moreover, higher expression of this pathway was associated with greater mortality in breast cancer patients. Increased reliance on glycine may represent a metabolic vulnerability for selectively targeting rapid cancer cell proliferation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3526189/" 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/PMC3526189/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jain, Mohit -- Nilsson, Roland -- Sharma, Sonia -- Madhusudhan, Nikhil -- Kitami, Toshimori -- Souza, Amanda L -- Kafri, Ran -- Kirschner, Marc W -- Clish, Clary B -- Mootha, Vamsi K -- K08 HL107451/HL/NHLBI NIH HHS/ -- K08HL107451/HL/NHLBI NIH HHS/ -- R01 DK081457/DK/NIDDK NIH HHS/ -- R01 GM026875/GM/NIGMS NIH HHS/ -- R01DK081457/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 May 25;336(6084):1040-4. doi: 10.1126/science.1218595.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628656" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/genetics/metabolism/pathology ; Cell Cycle ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Cell Transformation, Neoplastic ; Chromatography, Liquid ; Culture Media ; Gene Expression ; Gene Expression Profiling ; Glycine/biosynthesis/*metabolism ; Humans ; Metabolic Networks and Pathways/genetics ; Metabolome ; Mitochondria/enzymology/metabolism ; Neoplasms/genetics/*metabolism/*pathology ; Purines/biosynthesis ; Tandem Mass Spectrometry
    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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  • 8
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    Extrachromosomal microDNAs and chromosomal microdeletions in normal tissues (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-10
    Description: We have identified tens of thousands of short extrachromosomal circular DNAs (microDNA) in mouse tissues as well as mouse and human cell lines. These microDNAs are 200 to 400 base pairs long, are derived from unique nonrepetitive sequence, and are enriched in the 5'-untranslated regions of genes, exons, and CpG islands. Chromosomal loci that are enriched sources of microDNA in the adult brain are somatically mosaic for microdeletions that appear to arise from the excision of microDNAs. Germline microdeletions identified by the "Thousand Genomes" project may also arise from the excision of microDNAs in the germline lineage. We have thus identified a previously unknown DNA entity in mammalian cells and provide evidence that their generation leaves behind deletions in different genomic loci.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3703515/" 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/PMC3703515/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shibata, Yoshiyuki -- Kumar, Pankaj -- Layer, Ryan -- Willcox, Smaranda -- Gagan, Jeffrey R -- Griffith, Jack D -- Dutta, Anindya -- ES013773/ES/NIEHS NIH HHS/ -- GM31819/GM/NIGMS NIH HHS/ -- GM84465/GM/NIGMS NIH HHS/ -- P30 CA016086/CA/NCI NIH HHS/ -- R01 CA060499/CA/NCI NIH HHS/ -- R01 CA060499-18/CA/NCI NIH HHS/ -- R01 CA60499/CA/NCI NIH HHS/ -- R01 ES013773/ES/NIEHS NIH HHS/ -- R01 GM031819/GM/NIGMS NIH HHS/ -- R01 GM084465/GM/NIGMS NIH HHS/ -- R01 GM084465-04/GM/NIGMS NIH HHS/ -- T32 GM008136/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 6;336(6077):82-6. doi: 10.1126/science.1213307. Epub 2012 Mar 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22403181" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions ; Animals ; Base Pairing ; Base Sequence ; Brain/*embryology ; Brain Chemistry ; Cell Line ; Cell Line, Tumor ; *Chromosome Deletion ; Chromosomes, Human/*genetics ; Chromosomes, Mammalian/*genetics ; CpG Islands ; DNA Replication ; *DNA, Circular/analysis/chemistry/isolation & purification/metabolism ; Exons ; Germ Cells/chemistry ; Heart/embryology ; Humans ; Liver/chemistry/embryology ; Mice ; Mice, Inbred C57BL ; Microscopy, Electron ; Molecular Sequence Data ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid
    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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  • 9
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    Genomics. ENCODE project writes eulogy for junk DNA (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2012 Sep 7;337(6099):1159, 1161. doi: 10.1126/science.337.6099.1159.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22955811" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Conserved Sequence ; *DNA, Intergenic/genetics/metabolism ; DNA-Binding Proteins/genetics/metabolism ; Gene Expression Regulation ; Gene Regulatory Networks ; Genetic Predisposition to Disease ; Genome ; *Genome, Human ; *Genomics ; Humans ; Mammals/genetics ; RNA, Untranslated/genetics/metabolism ; Sequence Analysis, DNA ; Transcription Factors/genetics/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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  • 10
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    Drosophila dosage compensation involves enhanced Pol II recruitment to male X-linked promoters (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-24
    Description: Through hyperacetylation of histone H4 lysine 16 (H4K16), the male-specific lethal (MSL) complex in Drosophila approximately doubles transcription from the single male X chromosome in order to match X-linked expression in females and expression from diploid autosomes. By obtaining accurate measurements of RNA polymerase II (Pol II) occupancies and short promoter-proximal RNA production, we detected a consistent, genome-scale increase in Pol II activity at the promoters of male X-linked genes. Moreover, we found that enhanced Pol II recruitment to male X-linked promoters is largely dependent on the MSL complex. These observations provide insights into how global modulation of chromatin structure by histone acetylation contributes to the precise control of Pol II function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conrad, Thomas -- Cavalli, Florence M G -- Vaquerizas, Juan M -- Luscombe, Nicholas M -- Akhtar, Asifa -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2012 Aug 10;337(6095):742-6. doi: 10.1126/science.1221428. Epub 2012 Jul 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Immunobiology and Epigenetics, 79108 Freiburg im Breisgau, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22821985" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Cell Line ; Chromatin Immunoprecipitation ; DNA Polymerase II/*metabolism ; *Dosage Compensation, Genetic ; Drosophila/*genetics/metabolism ; Drosophila Proteins/*metabolism ; Female ; Genes, Insect ; *Genes, X-Linked ; Histones/metabolism ; Male ; Multigene Family ; *Promoter Regions, Genetic ; Sex Characteristics ; Transcription, Genetic ; X Chromosome/*genetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    iRhom2 regulation of TACE controls TNF-mediated protection against Listeria and responses to LPS (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-17
    Description: Innate immune responses are vital for pathogen defense but can result in septic shock when excessive. A key mediator of septic shock is tumor necrosis factor-alpha (TNFalpha), which is shed from the plasma membrane after cleavage by the TNFalpha convertase (TACE). We report that the rhomboid family member iRhom2 interacted with TACE and regulated TNFalpha shedding. iRhom2 was critical for TACE maturation and trafficking to the cell surface in hematopoietic cells. Gene-targeted iRhom2-deficient mice showed reduced serum TNFalpha in response to lipopolysaccharide (LPS) and could survive a lethal LPS dose. Furthermore, iRhom2-deficient mice failed to control the replication of Listeria monocytogenes. Our study has identified iRhom2 as a regulator of innate immunity that may be an important target for modulating sepsis and pathogen defense.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4250273/" 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/PMC4250273/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McIlwain, David R -- Lang, Philipp A -- Maretzky, Thorsten -- Hamada, Koichi -- Ohishi, Kazuhito -- Maney, Sathish Kumar -- Berger, Thorsten -- Murthy, Aditya -- Duncan, Gordon -- Xu, Haifeng C -- Lang, Karl S -- Haussinger, Dieter -- Wakeham, Andrew -- Itie-Youten, Annick -- Khokha, Rama -- Ohashi, Pamela S -- Blobel, Carl P -- Mak, Tak W -- GM64750/GM/NIGMS NIH HHS/ -- R01 GM064750/GM/NIGMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):229-32. doi: 10.1126/science.1214448.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Campell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network (UHN), 620 University Avenue, Toronto, Ontario M5G 2C1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22246778" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/genetics/*metabolism ; Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology/metabolism ; Base Sequence ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Gene Deletion ; *Immunity, Innate ; Lipopolysaccharides/*immunology ; Listeria monocytogenes/immunology/physiology ; Listeriosis/*immunology/metabolism/microbiology/pathology ; Macrophages/immunology/metabolism ; Macrophages, Peritoneal/immunology/metabolism/microbiology ; Mice ; Molecular Sequence Data ; Protein Transport ; Shock, Septic/*immunology/metabolism ; Spleen/cytology ; Tumor Necrosis Factor-alpha/blood/genetics/*metabolism
    Print ISSN: 0036-8075
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    Medicine. iPSC disease modeling (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soldner, Frank -- Jaenisch, Rudolf -- R01 CA084198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 30;338(6111):1155-6. doi: 10.1126/science.1227682.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Whitehead Institute, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23197518" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cell Differentiation/genetics ; Cell Line ; Cellular Reprogramming/*genetics ; Disease/*genetics ; *Epigenesis, Genetic ; Genetic Engineering/*methods ; Humans ; Induced Pluripotent Stem Cells/*physiology ; *Models, Genetic ; Transfection/methods
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  • 13
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    Recurrent hemizygous deletions in cancers may optimize proliferative potential (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-26
    Description: Tumors exhibit numerous recurrent hemizygous focal deletions that contain no known tumor suppressors and are poorly understood. To investigate whether these regions contribute to tumorigenesis, we searched genetically for genes with cancer-relevant properties within these hemizygous deletions. We identified STOP and GO genes, which negatively and positively regulate proliferation, respectively. STOP genes include many known tumor suppressors, whereas GO genes are enriched for essential genes. Analysis of their chromosomal distribution revealed that recurring deletions preferentially overrepresent STOP genes and underrepresent GO genes. We propose a hypothesis called the cancer gene island model, whereby gene islands encompassing high densities of STOP genes and low densities of GO genes are hemizygously deleted to maximize proliferative fitness through cumulative haploinsufficiencies. Because hundreds to thousands of genes are hemizygously deleted per tumor, this mechanism may help to drive tumorigenesis across many cancer types.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4027969/" 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/PMC4027969/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solimini, Nicole L -- Xu, Qikai -- Mermel, Craig H -- Liang, Anthony C -- Schlabach, Michael R -- Luo, Ji -- Burrows, Anna E -- Anselmo, Anthony N -- Bredemeyer, Andrea L -- Li, Mamie Z -- Beroukhim, Rameen -- Meyerson, Matthew -- Elledge, Stephen J -- T32 GM007753/GM/NIGMS NIH HHS/ -- T32GM07753/GM/NIGMS NIH HHS/ -- U54CA143798/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 6;337(6090):104-9. doi: 10.1126/science.1219580. Epub 2012 May 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard University Medical School, and Division of Genetics, Howard Hughes Medical Institute, Brigham and Women's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22628553" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; *Cell Transformation, Neoplastic ; Chromosome Mapping ; Genes, Essential ; *Genes, Neoplasm ; Genes, Recessive ; Genes, Tumor Suppressor ; *Haploinsufficiency ; Hemizygote ; Humans ; Models, Genetic ; Neoplasms/*genetics/*pathology ; Oncogenes ; *Sequence Deletion
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    miRNA-mediated gene silencing by translational repression followed by mRNA deadenylation and decay (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-14
    Description: microRNAs (miRNAs) regulate gene expression through translational repression and/or messenger RNA (mRNA) deadenylation and decay. Because translation, deadenylation, and decay are closely linked processes, it is important to establish their ordering and thus to define the molecular mechanism of silencing. We have investigated the kinetics of these events in miRNA-mediated gene silencing by using a Drosophila S2 cell-based controllable expression system and show that mRNAs with both natural and engineered 3' untranslated regions with miRNA target sites are first subject to translational inhibition, followed by effects on deadenylation and decay. We next used a natural translational elongation stall to show that miRNA-mediated silencing inhibits translation at an early step, potentially translation initiation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3971879/" 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/PMC3971879/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Djuranovic, Sergej -- Nahvi, Ali -- Green, Rachel -- R01 GM059425/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Apr 13;336(6078):237-40. doi: 10.1126/science.1215691.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute (HHMI) and Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22499947" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Cell Line ; Drosophila Proteins/genetics ; Drosophila melanogaster/*genetics/metabolism ; *Gene Silencing ; Kinetics ; MicroRNAs/*genetics/metabolism ; Peptide Chain Elongation, Translational ; Peptide Chain Initiation, Translational ; *Protein Biosynthesis ; *RNA Stability ; RNA, Messenger/genetics/*metabolism
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    Tuning of natural killer cell reactivity by NKp46 and Helios calibrates T cell responses (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-24
    Description: Natural killer (NK) cells are lymphocytes involved in antimicrobial and antitumoral immune responses. Using N-ethyl-N-nitrosourea mutagenesis in mice, we identified a mutant with increased resistance to viral infections because of the presence of hyperresponsive NK cells. Whole-genome sequencing and functional analysis revealed a loss-of-function mutation in the Ncr1 gene encoding the activating receptor NKp46. The down-regulation of NK cell activity by NKp46 was associated with the silencing of the Helios transcription factor in NK cells. NKp46 was critical for the subsequent development of antiviral and antibacterial T cell responses, which suggests that the regulation of NK cell function by NKp46 allows for the optimal development of adaptive immune responses. NKp46 blockade enhanced NK cell reactivity in vivo, which could enable the design of immunostimulation strategies in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Narni-Mancinelli, Emilie -- Jaeger, Baptiste N -- Bernat, Claire -- Fenis, Aurore -- Kung, Sam -- De Gassart, Aude -- Mahmood, Sajid -- Gut, Marta -- Heath, Simon C -- Estelle, Jordi -- Bertosio, Elodie -- Vely, Frederic -- Gastinel, Louis N -- Beutler, Bruce -- Malissen, Bernard -- Malissen, Marie -- Gut, Ivo G -- Vivier, Eric -- Ugolini, Sophie -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):344-8. doi: 10.1126/science.1215621.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie de Marseille-Luminy, Aix-Marseille University, Campus de Luminy case 906, 13288 Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22267813" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Amino Acid Substitution ; Animals ; Antibodies, Blocking/immunology ; Antibodies, Monoclonal/immunology ; Antigens, Ly/genetics/immunology/*physiology ; CD8-Positive T-Lymphocytes/immunology ; Cell Line ; DNA-Binding Proteins/*genetics/physiology ; Down-Regulation ; Genetic Complementation Test ; Herpesviridae Infections/*immunology/virology ; Immunologic Memory ; Killer Cells, Natural/*immunology ; Listeriosis/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muromegalovirus/physiology ; Mutagenesis ; Natural Cytotoxicity Triggering Receptor 1/antagonists & ; inhibitors/genetics/immunology/*physiology ; T-Lymphocytes/*immunology ; Transcription Factors/*genetics/physiology ; Transcription, Genetic ; Viral Load
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    ESCRT-III governs the Aurora B-mediated abscission checkpoint through CHMP4C (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-17
    Description: The endosomal sorting complex required for transport (ESCRT) machinery plays an evolutionarily conserved role in cytokinetic abscission, the final step of cell division where daughter cells are physically separated. Here, we show that charged multivesicular body (MVB) protein 4C (CHMP4C), a human ESCRT-III subunit, is involved in abscission timing. This function correlated with its differential spatiotemporal distribution during late stages of cytokinesis. Accordingly, CHMP4C functioned in the Aurora B-dependent abscission checkpoint to prevent both premature resolution of intercellular chromosome bridges and accumulation of DNA damage. CHMP4C engaged the chromosomal passenger complex (CPC) via interaction with Borealin, which suggested a model whereby CHMP4C inhibits abscission upon phosphorylation by Aurora B. Thus, the ESCRT machinery may protect against genetic damage by coordinating midbody resolution with the abscission checkpoint.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998087/" 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/PMC3998087/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlton, Jeremy G -- Caballe, Anna -- Agromayor, Monica -- Kloc, Magdalena -- Martin-Serrano, Juan -- 092429/Z/10/Z/Wellcome Trust/United Kingdom -- 093056/Wellcome Trust/United Kingdom -- G0802777/Medical Research Council/United Kingdom -- WT093056MA/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Apr 13;336(6078):220-5. doi: 10.1126/science.1217180. Epub 2012 Mar 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Diseases, King's College London School of Medicine, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22422861" target="_blank"〉PubMed〈/a〉
    Keywords: Aurora Kinase B ; Aurora Kinases ; Cell Cycle Checkpoints ; Cell Cycle Proteins/metabolism ; Cell Line ; Chromosomes, Human/metabolism ; *Cytokinesis ; DNA Damage ; Endosomal Sorting Complexes Required for Transport/*metabolism ; Endosomes/metabolism ; HeLa Cells ; Histocompatibility Antigens Class I/metabolism ; Humans ; Mitosis ; Phosphorylation ; Protein Transport ; Protein-Serine-Threonine Kinases/*metabolism ; Recombinant Fusion Proteins/metabolism
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    Transcription-independent function of Polycomb group protein PSC in cell cycle control (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-12
    Description: Polycomb group (PcG) proteins control development and cell proliferation through chromatin-mediated transcriptional repression. We describe a transcription-independent function for PcG protein Posterior sex combs (PSC) in regulating the destruction of cyclin B (CYC-B). A substantial portion of PSC was found outside canonical PcG complexes, instead associated with CYC-B and the anaphase-promoting complex (APC). Cell-based experiments and reconstituted reactions established that PSC and Lemming (LMG, also called APC11) associate and ubiquitylate CYC-B cooperatively, marking it for proteosomal degradation. Thus, PSC appears to mediate both developmental gene silencing and posttranslational control of mitosis. Direct regulation of cell cycle progression might be a crucial part of the PcG system's function in development and cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mohd-Sarip, Adone -- Lagarou, Anna -- Doyen, Cecile M -- van der Knaap, Jan A -- Aslan, Ulku -- Bezstarosti, Karel -- Yassin, Yasmin -- Brock, Hugh W -- Demmers, Jeroen A A -- Verrijzer, C Peter -- New York, N.Y. -- Science. 2012 May 11;336(6082):744-7. doi: 10.1126/science.1215927. Epub 2012 Apr 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Centre for Biomedical Genetics, Erasmus University Medical Centre, Post Office Box 1738, 3000 DR, Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22491092" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase-Promoting Complex-Cyclosome ; Animals ; Apc11 Subunit, Anaphase-Promoting Complex-Cyclosome ; Carrier Proteins/metabolism ; *Cell Cycle Checkpoints ; Cell Line ; Compound Eye, Arthropod/growth & development/metabolism ; Cyclin B/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/cytology/embryology/metabolism ; G2 Phase Cell Cycle Checkpoints ; Gene Silencing ; Imaginal Discs/metabolism ; *Mitosis ; Phenotype ; Polycomb Repressive Complex 1 ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; RNA Interference ; Transcription, Genetic ; Ubiquitin-Protein Ligase Complexes/metabolism ; Ubiquitination ; Wings, Animal/growth & development
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    Evolutionarily assembled cis-regulatory module at a human ciliopathy locus (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-28
    Description: Neighboring genes are often coordinately expressed within cis-regulatory modules, but evidence that nonparalogous genes share functions in mammals is lacking. Here, we report that mutation of either TMEM138 or TMEM216 causes a phenotypically indistinguishable human ciliopathy, Joubert syndrome. Despite a lack of sequence homology, the genes are aligned in a head-to-tail configuration and joined by chromosomal rearrangement at the amphibian-to-reptile evolutionary transition. Expression of the two genes is mediated by a conserved regulatory element in the noncoding intergenic region. Coordinated expression is important for their interdependent cellular role in vesicular transport to primary cilia. Hence, during vertebrate evolution of genes involved in ciliogenesis, nonparalogous genes were arranged to a functional gene cluster with shared regulatory elements.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671610/" 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/PMC3671610/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Jeong Ho -- Silhavy, Jennifer L -- Lee, Ji Eun -- Al-Gazali, Lihadh -- Thomas, Sophie -- Davis, Erica E -- Bielas, Stephanie L -- Hill, Kiley J -- Iannicelli, Miriam -- Brancati, Francesco -- Gabriel, Stacey B -- Russ, Carsten -- Logan, Clare V -- Sharif, Saghira Malik -- Bennett, Christopher P -- Abe, Masumi -- Hildebrandt, Friedhelm -- Diplas, Bill H -- Attie-Bitach, Tania -- Katsanis, Nicholas -- Rajab, Anna -- Koul, Roshan -- Sztriha, Laszlo -- Waters, Elizabeth R -- Ferro-Novick, Susan -- Woods, C Geoffrey -- Johnson, Colin A -- Valente, Enza Maria -- Zaki, Maha S -- Gleeson, Joseph G -- DK068306/DK/NIDDK NIH HHS/ -- DK072301/DK/NIDDK NIH HHS/ -- DK075972/DK/NIDDK NIH HHS/ -- DK090917/DK/NIDDK NIH HHS/ -- EY021872/EY/NEI NIH HHS/ -- G0700073/Medical Research Council/United Kingdom -- GGP08145/Telethon/Italy -- HD042601/HD/NICHD NIH HHS/ -- NS04843/NS/NINDS NIH HHS/ -- NS052455/NS/NINDS NIH HHS/ -- P30 CA023100/CA/NCI NIH HHS/ -- P30NS047101/NS/NINDS NIH HHS/ -- R01 DK068306/DK/NIDDK NIH HHS/ -- R01 DK072301/DK/NIDDK NIH HHS/ -- R01 DK075972/DK/NIDDK NIH HHS/ -- R01 EY021872/EY/NEI NIH HHS/ -- R01 HD042601/HD/NICHD NIH HHS/ -- R01 NS048453/NS/NINDS NIH HHS/ -- R01 NS052455/NS/NINDS NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Feb 24;335(6071):966-9. doi: 10.1126/science.1213506. Epub 2012 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Laboratory, Howard Hughes Medical Institute (HHMI), Department of Neurosciences, University of California, San Diego, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22282472" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cerebellar Diseases/*genetics/metabolism/pathology ; Cilia/metabolism/*ultrastructure ; Conserved Sequence ; DNA, Intergenic ; *Evolution, Molecular ; Eye Abnormalities/*genetics/metabolism/pathology ; Gene Expression Profiling ; *Gene Expression Regulation ; Genetic Heterogeneity ; *Genetic Loci ; Humans ; Kidney Diseases, Cystic/*genetics/metabolism/pathology ; Membrane Proteins/chemistry/*genetics/metabolism ; Molecular Sequence Data ; Multigene Family ; Mutation ; Mutation, Missense ; Phenotype ; Protein Transport ; *Regulatory Sequences, Nucleic Acid ; Retina/abnormalities/metabolism/pathology ; Transport Vesicles/metabolism/ultrastructure
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    The dorsal aorta initiates a molecular cascade that instructs sympatho-adrenal specification (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: The autonomic nervous system, which includes the sympathetic neurons and adrenal medulla, originates from the neural crest. Combining avian blood vessel-specific gene manipulation and mouse genetics, we addressed a long-standing question of how neural crest cells (NCCs) generate sympathetic and medullary lineages during embryogenesis. We found that the dorsal aorta acts as a morphogenetic signaling center that coordinates NCC migration and cell lineage segregation. Bone morphogenetic proteins (BMPs) produced by the dorsal aorta are critical for the production of the chemokine stromal cell-derived factor-1 (SDF -1) and Neuregulin 1 in the para-aortic region, which act as chemoattractants for early migration. Later, BMP signaling is directly involved in the sympatho-medullary segregation. This study provides insights into the complex developmental signaling cascade that instructs one of the earliest events of neurovascular interactions guiding embryonic development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saito, Daisuke -- Takase, Yuta -- Murai, Hidetaka -- Takahashi, Yoshiko -- New York, N.Y. -- Science. 2012 Jun 22;336(6088):1578-81. doi: 10.1126/science.1222369.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22723422" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/embryology/metabolism ; Adrenal Medulla/*cytology/embryology ; Animals ; Aorta/*embryology/*metabolism ; Avian Proteins/metabolism ; Bone Morphogenetic Proteins/*metabolism ; Cell Line ; Cell Lineage ; Cell Movement ; Chemokine CXCL12/metabolism ; Chemotactic Factors/metabolism ; Chick Embryo ; Coculture Techniques ; Embryonic Development ; Ganglia, Sympathetic/*cytology ; Mice ; Mice, Knockout ; Morphogenesis ; Neural Crest/*cytology/physiology ; Neuregulin-1/metabolism ; Signal Transduction ; Stem Cells/cytology/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Adenylate cyclases of Trypanosoma brucei inhibit the innate immune response of the host (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-16
    Description: The parasite Trypanosoma brucei possesses a large family of transmembrane receptor-like adenylate cyclases. Activation of these enzymes requires the dimerization of the catalytic domain and typically occurs under stress. Using a dominant-negative strategy, we found that reducing adenylate cyclase activity by about 50% allowed trypanosome growth but reduced the parasite's ability to control the early innate immune defense of the host. Specifically, activation of trypanosome adenylate cyclase resulting from parasite phagocytosis by liver myeloid cells inhibited the synthesis of the trypanosome-controlling cytokine tumor necrosis factor-alpha through activation of protein kinase A in these cells. Thus, adenylate cyclase activity of lyzed trypanosomes favors early host colonization by live parasites. The role of adenylate cyclases at the host-parasite interface could explain the expansion and polymorphism of this gene family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salmon, Didier -- Vanwalleghem, Gilles -- Morias, Yannick -- Denoeud, Julie -- Krumbholz, Carsten -- Lhomme, Frederic -- Bachmaier, Sabine -- Kador, Markus -- Gossmann, Jasmin -- Dias, Fernando Braga Stehling -- De Muylder, Geraldine -- Uzureau, Pierrick -- Magez, Stefan -- Moser, Muriel -- De Baetselier, Patrick -- Van Den Abbeele, Jan -- Beschin, Alain -- Boshart, Michael -- Pays, Etienne -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):463-6. doi: 10.1126/science.1222753. Epub 2012 Jun 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Parasitology, Institute for Molecular Biology and Medicine, Universite Libre de Bruxelles, 12, rue des Professeurs Jeener et Brachet, B6041 Gosselies, Belgium. salmon@bioqmed.ufrj.br〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22700656" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/chemistry/genetics/*metabolism ; Animals ; Catalytic Domain ; Cell Line ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Enzyme Activation ; Host-Parasite Interactions ; *Immunity, Innate ; Liver/cytology ; Mice ; Mice, Inbred C57BL ; Mutagenesis, Site-Directed ; Myeloid Cells/immunology ; Parasitemia ; Phagocytosis ; Protozoan Proteins/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Trypanosoma brucei brucei/*enzymology/growth & development/*immunology ; Trypanosomiasis, African/*immunology/metabolism/parasitology ; Tumor Necrosis Factor-alpha/biosynthesis/blood
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Human alpha-defensin 6 promotes mucosal innate immunity through self-assembled peptide nanonets (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-23
    Description: Defensins are antimicrobial peptides that contribute broadly to innate immunity, including protection of mucosal tissues. Human alpha-defensin (HD) 6 is highly expressed by secretory Paneth cells of the small intestine. However, in contrast to the other defensins, it lacks appreciable bactericidal activity. Nevertheless, we report here that HD6 affords protection against invasion by enteric bacterial pathogens in vitro and in vivo. After stochastic binding to bacterial surface proteins, HD6 undergoes ordered self-assembly to form fibrils and nanonets that surround and entangle bacteria. This self-assembly mechanism occurs in vivo, requires histidine-27, and is consistent with x-ray crystallography data. These findings support a key role for HD6 in protecting the small intestine against invasion by diverse enteric pathogens and may explain the conservation of HD6 throughout Hominidae evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4332406/" 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/PMC4332406/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chu, Hiutung -- Pazgier, Marzena -- Jung, Grace -- Nuccio, Sean-Paul -- Castillo, Patricia A -- de Jong, Maarten F -- Winter, Maria G -- Winter, Sebastian E -- Wehkamp, Jan -- Shen, Bo -- Salzman, Nita H -- Underwood, Mark A -- Tsolis, Renee M -- Young, Glenn M -- Lu, Wuyuan -- Lehrer, Robert I -- Baumler, Andreas J -- Bevins, Charles L -- AI032738/AI/NIAID NIH HHS/ -- AI040124/AI/NIAID NIH HHS/ -- AI044170/AI/NIAID NIH HHS/ -- AI050843/AI/NIAID NIH HHS/ -- AI057757/AI/NIAID NIH HHS/ -- AI070726/AI/NIAID NIH HHS/ -- AI072732/AI/NIAID NIH HHS/ -- AI073120/AI/NIAID NIH HHS/ -- AI076246/AI/NIAID NIH HHS/ -- AI082320/AI/NIAID NIH HHS/ -- AI088122/AI/NIAID NIH HHS/ -- HD059127/HD/NICHD NIH HHS/ -- R01 AI032738/AI/NIAID NIH HHS/ -- R01 AI050843/AI/NIAID NIH HHS/ -- R01 AI057757/AI/NIAID NIH HHS/ -- R01 AI076246/AI/NIAID NIH HHS/ -- R01 GM099526/GM/NIGMS NIH HHS/ -- T32AI060555/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):477-81. doi: 10.1126/science.1218831. Epub 2012 Jun 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, School of Medicine, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722251" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/metabolism ; Animals ; Bacterial Proteins/metabolism ; Cell Line ; Humans ; *Immunity, Innate ; *Immunity, Mucosal ; Intestinal Mucosa/immunology/microbiology/ultrastructure ; Intestine, Small/*immunology/microbiology/ultrastructure ; Macromolecular Substances/chemistry/immunology/metabolism ; Mice ; Mice, Transgenic ; Microscopy, Electron, Scanning ; Models, Molecular ; Nanostructures ; Paneth Cells/immunology/metabolism ; Peptides/chemistry/metabolism ; Protein Binding ; Protein Multimerization ; Protein Structure, Quaternary ; Salmonella Infections, Animal/immunology/microbiology ; Salmonella typhimurium/immunology/pathogenicity/ultrastructure ; Yersinia enterocolitica/immunology/pathogenicity ; alpha-Defensins/*chemistry/immunology/*metabolism ; env Gene Products, Human Immunodeficiency Virus/metabolism
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  • 22
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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
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  • 23
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    Phosphofructokinase 1 glycosylation regulates cell growth and metabolism (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-28
    Description: Cancer cells must satisfy the metabolic demands of rapid cell growth within a continually changing microenvironment. We demonstrated that the dynamic posttranslational modification of proteins by O-linked beta-N-acetylglucosamine (O-GlcNAcylation) is a key metabolic regulator of glucose metabolism. O-GlcNAcylation was induced at serine 529 of phosphofructokinase 1 (PFK1) in response to hypoxia. Glycosylation inhibited PFK1 activity and redirected glucose flux through the pentose phosphate pathway, thereby conferring a selective growth advantage on cancer cells. Blocking glycosylation of PFK1 at serine 529 reduced cancer cell proliferation in vitro and impaired tumor formation in vivo. These studies reveal a previously uncharacterized mechanism for the regulation of metabolic pathways in cancer and a possible target for therapeutic intervention.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3534962/" 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/PMC3534962/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yi, Wen -- Clark, Peter M -- Mason, Daniel E -- Keenan, Marie C -- Hill, Collin -- Goddard, William A 3rd -- Peters, Eric C -- Driggers, Edward M -- Hsieh-Wilson, Linda C -- R01 GM084724/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Aug 24;337(6097):975-80. doi: 10.1126/science.1222278.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22923583" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylglucosamine/metabolism ; Acylation ; Adenosine Triphosphate/metabolism ; Animals ; Cell Hypoxia ; Cell Line ; Cell Line, Tumor ; *Cell Proliferation ; Glucose/*metabolism ; Glycolysis ; Glycosylation ; Humans ; Lactic Acid/metabolism ; Mice ; Mice, Nude ; N-Acetylglucosaminyltransferases/genetics/metabolism ; NADP/metabolism ; Neoplasms/*metabolism/*pathology ; Pentose Phosphate Pathway ; Phosphofructokinase-1, Liver Type/antagonists & inhibitors/chemistry/*metabolism
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  • 24
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    AID-driven deletion causes immunoglobulin heavy chain locus suicide recombination in B cells (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-04-28
    Description: Remodeling of immunoglobulin genes by activation-induced deaminase (AID) is required for affinity maturation and class-switch recombination in mature B lymphocytes. In the immunoglobulin heavy chain locus, these processes are predominantly controlled by the 3' cis-regulatory region. We now show that this region is transcribed and undergoes AID-mediated mutation and recombination around phylogenetically conserved switchlike DNA repeats. Such recombination, which we term locus suicide recombination, deletes the whole constant region gene cluster and thus stops expression of the immunoglobulin of the B cell surface, which is critical for B cell survival. The frequency of this event is approaching that of class switching and makes it a potential regulator of B cell homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peron, Sophie -- Laffleur, Brice -- Denis-Lagache, Nicolas -- Cook-Moreau, Jeanne -- Tinguely, Aurelien -- Delpy, Laurent -- Denizot, Yves -- Pinaud, Eric -- Cogne, Michel -- New York, N.Y. -- Science. 2012 May 18;336(6083):931-4. doi: 10.1126/science.1218692. Epub 2012 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Limoges University, CNRS, 2 rue Marcland, 87025 Limoges Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22539552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology/*physiology ; Base Sequence ; Cell Line ; Cell Survival ; Cytidine Deaminase/*metabolism ; *Gene Deletion ; *Gene Rearrangement, B-Lymphocyte, Heavy Chain ; *Genes, Immunoglobulin Heavy Chain ; Homeostasis ; Humans ; Immunoglobulin Class Switching ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; *Recombination, Genetic ; Regulatory Sequences, Nucleic Acid ; Repetitive Sequences, Nucleic Acid ; Transcription, Genetic
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  • 25
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    Cyclic GMP-AMP is an endogenous second messenger in innate immune signaling by cytosolic DNA (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-22
    Description: Cytosolic DNA induces type I interferons and other cytokines that are important for antimicrobial defense but can also result in autoimmunity. This DNA signaling pathway requires the adaptor protein STING and the transcription factor IRF3, but the mechanism of DNA sensing is unclear. We found that mammalian cytosolic extracts synthesized cyclic guanosine monophosphate-adenosine monophosphate (cyclic GMP-AMP, or cGAMP) in vitro from adenosine triphosphate and guanosine triphosphate in the presence of DNA but not RNA. DNA transfection or DNA virus infection of mammalian cells also triggered cGAMP production. cGAMP bound to STING, leading to the activation of IRF3 and induction of interferon-beta. Thus, cGAMP functions as an endogenous second messenger in metazoans and triggers interferon production in response to cytosolic DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3855410/" 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/PMC3855410/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Jiaxi -- Sun, Lijun -- Chen, Xiang -- Du, Fenghe -- Shi, Heping -- Chen, Chuo -- Chen, Zhijian J -- AI-093967/AI/NIAID NIH HHS/ -- GM-079554/GM/NIGMS NIH HHS/ -- R01 AI093967/AI/NIAID NIH HHS/ -- R01 GM079554/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Feb 15;339(6121):826-30. doi: 10.1126/science.1229963. Epub 2012 Dec 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23258412" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Extracts/chemistry ; Cell Line ; Cyclic AMP/*metabolism ; Cyclic GMP/*metabolism ; Cytosol/*immunology ; DNA/*immunology ; HEK293 Cells ; Herpesvirus 1, Human/immunology ; Humans ; *Immunity, Innate ; Interferon Regulatory Factor-3/metabolism ; Interferon-beta/biosynthesis ; Membrane Proteins/genetics/metabolism ; Mice ; Nucleotides, Cyclic/*metabolism ; RNA Interference ; Second Messenger Systems/*immunology ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 26
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    Renin and angiotensin: the complete system within the neuroblastoma x glioma cell (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-11-20
    Description: Cells of the homogeneous hybrid line neuroblastoma x glioma (NG108-15) have many neuronal properties. Immunocytochemical tests show that they contain both immunoreactive renin and angiotensin; direct radioimmunoassays show that they are positive for renin, angiotensin I, and angiotensin II; enzymatic assays show that they contain angiotensinogen and converting enzyme as well. The renin appears to be present in an enzymatically inactive form that can be activated by trypsin and then blocked by antiserum to purified mouse submaxillary renin. Renin concentration and activity are increased by enhancing cellular differentiation with dibutyryl cyclic adenosine monophosphate or by serum withdrawal. These findings demonstrate a complete renin-angiotensin system within these neuron-like cells, and suggest that activation of intracellular renin could generate angiotensin II.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fishman, M C -- Zimmerman, E A -- Slater, E E -- HL-21247/HL/NHLBI NIH HHS/ -- HL-24105/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1981 Nov 20;214(4523):921-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6272392" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin I/*analysis ; Angiotensin II/*analysis ; Angiotensins/*analysis ; Animals ; Cell Line ; Cricetinae ; Glioma/*metabolism ; Hybrid Cells/*metabolism ; Mice ; Neuroblastoma/*metabolism ; Peptidyl-Dipeptidase A/metabolism ; Radioimmunoassay ; Rats ; Renin/*metabolism
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  • 27
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    Malignant potential of murine stromal cells after transplantation of human tumors into nude mice (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-04-03
    Description: Human malignant cancer tumors grafted into nude mice produce tumors containing both human cancer cells and the host's stromal cells. After short-term propagation of these tumors in vitro, the murine mesenchymal cells appear transformed and are tumorigenic in nude mice. However, established human cancer cell lines fail to similarly after adjacent murine stromal cells when used to produce tumors in nude mice. These experiments suggest that cancer cells may recruit normal cells to become malignant, qualifying the view of the clonal (unicellular) origin of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldenberg, D M -- Pavia, R A -- 1R01 CA17198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):65-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209521" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/pathology ; Animals ; Cell Line ; Cells, Cultured ; Colonic Neoplasms/pathology ; Fibrosarcoma/*etiology ; Humans ; Karyotyping ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Transplantation ; Neoplasms, Experimental/*etiology ; Transplantation, Heterologous
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  • 28
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    Insulin as a potent, specific growth factor in a rat hepatoma cell line (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-02-27
    Description: A line or rat hepatoma cells in culture which, in response to serum starvation, become arrested in the early G1 phase of growth, can be stimulated by insulin alone to enter the cell cycle and traverse S phase. A half-maximum response is observed at 30 to 70 picomolar concentrations and the maximum response is essentially identical to that found with optimum serum concentrations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koontz, J W -- Iwahashi, M -- AM 24047/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Feb 27;211(4485):947-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7008195" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Division/drug effects ; Cell Line ; *Growth Substances ; Insulin/*pharmacology ; Liver Neoplasms, Experimental/*pathology ; Mitosis/drug effects ; Proinsulin/pharmacology ; Rats ; Structure-Activity Relationship
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  • 29
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    A monosialoganglioside is a monoclonal antibody-defined antigen of colon carcinoma (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-04-03
    Description: The antigen of a monoclonal antibody that is specific for cells of human carcinoma of the colon is a monosialoganglioside as determined by the direct binding of antibody to thin-layer chromatograms of total lipid extracts of tissues. Binding of antibody to chromatograms is detected by autoradiography after the application of iodine-125-labeled F(ab')2 of rabbit immunoglobulin G antibodies to mouse immunoglobulins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magnani, J L -- Brockhaus, M -- Smith, D F -- Ginsburg, V -- Blaszczyk, M -- Mitchell, K F -- Steplewski, Z -- Koprowski, H -- CA-10815/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- RR-05540/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):55-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209516" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*immunology ; Antibodies, Neoplasm/*immunology ; Antibody Specificity ; Antigens, Neoplasm/*immunology/isolation & purification ; Cell Line ; Chromatography, Thin Layer ; Colonic Neoplasms/*immunology ; Gangliosides/*immunology/isolation & purification ; Humans ; Melanoma/immunology ; Neuraminidase/pharmacology
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    Growth inhibition by adenosine 3',5-monophosphate derivatives does not require 3',5' phosphodiester linkage (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-09-04
    Description: Analogs of adenosine 3',5'-monophosphate (cyclic AMP) inhibit the growth of cultured cell lines. The effects of 8-bromo- and N6-butyryl-substituted analogs of cyclic and noncyclic AMP on six cell lines were examined and were equally inhibitory. Variant cell lines with altered cyclic AMP-dependent protein kinase were more resistant to both cyclic and noncyclic nucleotides. We conclude that growth inhibition by analogs of cyclic AMP (i) does not require a 3',5' phosphodiester bond and (ii) may be mediated by a pathway involving endogenous cyclic AMP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, T F -- Kowalchyk, J A -- AM 25861/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Sep 4;213(4512):1120-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6267695" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/*drug effects ; Cell Line ; Cricetinae ; Cyclic AMP/*pharmacology ; DNA/biosynthesis ; Growth Inhibitors/*pharmacology ; Mice ; Phosphodiesterase Inhibitors/pharmacology ; Structure-Activity Relationship
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    Human lupus inclusions and interferon (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-08-14
    Description: Raji cells, a human B lymphoblastoid cell line of Burkitt lymphoma origin, formed lupus inclusions when grown in a medium conditioned by the growth of Raji cells whose DNA thymidine residues had been unifilarly (single-strandedly) substituted with bromodeoxyuridine. Ultracentrifugation of this medium in excess of that required to remove Epstein-Barr virus and all other known mammalian viruses did not prevent the formation of the inclusions, and treatment of the conditioned medium with pronase destroyed the activity. These results demonstrate the presence of a protein that is secreted from bromodeoxyuridine-substituted Raji cells and is capable of inducing nonbromodeoxyuridine-substituted cells to form lupus inclusions. Interferon (100 units per milliliter) was found in the conditioned medium. Inclusions also formed in Raji cells grown in fresh medium supplemented with human leukocyte or fibroblast interferon (100 units per milliliter).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rich, S A -- New York, N.Y. -- Science. 1981 Aug 14;213(4509):772-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6166984" target="_blank"〉PubMed〈/a〉
    Keywords: Bromodeoxyuridine/*metabolism ; Burkitt Lymphoma ; Cell Line ; Culture Media ; Cytoplasmic Granules/ultrastructure ; DNA Replication ; Humans ; Interferons/*biosynthesis ; Lupus Erythematosus, Systemic/*pathology
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    Diameter of the cell-to-cell junctional membrane channels as probed with neutral molecules (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-07-31
    Description: The cell-to-cell channels in the junctions of an insect salivary gland and of insect and mammalian cells in culture were probed with fluorescent molecules-neutral linear oligosaccharides, neutral branched glycopeptides, and charged linear peptides. From the molecular dimensions of the largest permeants and smallest impermeants the permeation-limiting channel diameter was obtained: 16 to 20 angstroms for the mammalian cells and 20 to 30 angstroms for the insect cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwarzmann, G -- Wiegandt, H -- Rose, B -- Zimmerman, A -- Ben-Haim, D -- Loewenstein, W R -- CA 14464/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Jul 31;213(4507):551-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7244653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chironomidae ; Fluorescent Dyes ; Glycopeptides/*metabolism ; Intercellular Junctions/*ultrastructure ; Mice ; Mice, Inbred BALB C ; Models, Molecular ; Oligosaccharides/*metabolism ; Protein Conformation ; Salivary Glands/*ultrastructure ; Species Specificity
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    Tumor cell killing by phorbol ester--differentiated human leukemia cells (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-08-07
    Description: The tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate causes differentiation of cells of the human leukemia cell line HL60 to nondividing macrophage-like cells. These differentiated cells are cytotoxic for tumor cells (including parent, untreated HL60 cells) in vitro. Agents that induce this desirable differentiation to nondividing, antitumor effector cells may be useful in the experimental treatment of leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weinberg, J B -- 27070-02/PHS HHS/ -- New York, N.Y. -- Science. 1981 Aug 7;213(4508):655-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7196085" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/drug effects ; Cell Line ; *Cytotoxicity, Immunologic ; Humans ; Immunity, Cellular ; Leukemia, Experimental/immunology/*pathology ; Macrophages/cytology/*immunology ; Phorbols/*pharmacology ; Tetradecanoylphorbol Acetate/*pharmacology
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    Mesenchymal cells from the human embryonic palate are highly responsive to epidermal growth factor (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-07-31
    Description: An established line of mesenchymal cells from the human embryonic palate is highly sensitive to the stimulatory effect of epidermal growth factor on growth, labeled thymidine incorporation, and ornithine decarboxylase activity. The results suggest that epidermal growth factor may play a key role in development of various human embryonic and fetal tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoneda, T -- Pratt, R M -- New York, N.Y. -- Science. 1981 Jul 31;213(4507):563-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7017936" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; Cell Line ; DNA Replication/drug effects ; Embryo, Mammalian ; Epidermal Growth Factor/*pharmacology ; Female ; Humans ; Insulin/pharmacology ; Kinetics ; Organ Specificity ; Ornithine Decarboxylase/metabolism ; Palate/drug effects/*physiology ; Peptides/*pharmacology ; Pregnancy
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    Metastatic potential is positively correlated with cell surface sialylation of cultured murine tumor cell lines (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-06-26
    Description: The ability of murine tumor cells to metastasize spontaneously from subcutaneous sites is positively correlated with the total sialic acid content of the cells in culture, the degree to which the sialic acid is exposed on the tumor cell surface, and, most strongly, with the degree of sialylation of galactosyl and N-acetylgalactosaminyl residues in cell surface glycoconjugates. These findings suggest that sialic acid on the cell surface may play a role in tumor cell metastasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yogeeswaran, G -- Salk, P L -- CA19312-01/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Jun 26;212(4502):1514-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7233237" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/*physiology ; Cell Transformation, Neoplastic ; Cell Transformation, Viral ; Mice ; *Neoplasm Metastasis ; Neoplasms, Experimental/*physiopathology ; Sialic Acids/*analysis
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    Adenosine 3',5'-monophosphate modulates thyrotropin receptor clustering and thyrotropin activity in culture (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-12-11
    Description: A biologically active rhodamine conjugate of thyrotropin binds at 4 degrees C to diffusely distributed membrane thyrotropin receptors which patch and become endocytosed into thyroid cells in a temperature-sensitive process. When the cells are first incubated with 8-bromo-cyclic adenosine monophosphate at 37 degrees C, the conjugate also binds to clustered receptors at 4 degrees C. Furthermore, 8-bromo-cyclic adenosine monophosphate reduces the amount of adenosine 3',5'-monophosphate (cyclic AMP) induced by thyrotropin. Hence, increased intracellular cyclic AMP induces receptor patching and reduces the concentration of cyclic AMP normally induced by thyrotropin. This suggests that cyclic AMP acts both as the second messenger of thyrotropin and also as the regulator of the level of thyrotropin receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Avivi, A -- Tramontano, D -- Ambesi-Impiombato, F S -- Schlessinger, J -- CA-25820/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Dec 11;214(4526):1237-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6272396" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate ; Animals ; Cell Line ; Cell Membrane/drug effects/metabolism ; Cyclic AMP/*analogs & derivatives/*metabolism/pharmacology ; Rats ; Receptors, Cell Surface/drug effects/*metabolism ; Receptors, Thyrotropin ; Thyroid Gland/metabolism ; Thyrotropin/*metabolism/pharmacology
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    Korean hemorrhagic fever: propagation of the etiologic agent in a cell line of human origin (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-03-06
    Description: The etiologic agent of Korean hemorrhagic fever has been propagated in a human cultured cell line derived from a carcinoma of the lung. The cells, described as type II, alveolar epithelial, support replication of the agent and successive passages. Antigen of the Korean hemorrhagic fever agent is readily detected in infected cells by means of direct or indirect fluorescent antibody techniques. Previous attempts to propagate this agent in vitro had been unsuccessful.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉French, G R -- Foulke, R S -- Brand, O A -- Eddy, G A -- Lee, H W -- Lee, P W -- New York, N.Y. -- Science. 1981 Mar 6;211(4486):1046-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6110243" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Viral/analysis ; Cell Line ; Hantavirus/*growth & development/immunology ; Hemorrhagic Fever with Renal Syndrome/*microbiology ; Humans ; Pulmonary Alveoli/microbiology ; RNA Viruses/*growth & development
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    Somatic cell hybrids from frog lymphocytes and mouse myeloma cells (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-05-29
    Description: Stable somatic cell hybrids were obtained by fusing Xenopus lymphocytes with mouse myeloma cells. These hybrids contained one to four Xenopus chromosomes and expressed Xenopus gene products, one of which was a lymphocyte membrane protein of 85,000 daltons precipitated by a monoclonal antibody.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hengartner, H -- Du Pasquier, L -- New York, N.Y. -- Science. 1981 May 29;212(4498):1034-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6785884" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Antibodies, Monoclonal ; Cell Line ; Clone Cells ; Genes ; Hybrid Cells/*physiology ; Lymphocytes/*physiology ; Membrane Proteins/biosynthesis ; Mice ; Molecular Weight ; Neoplasms, Experimental/physiopathology ; Plasmacytoma/*physiopathology ; Xenopus
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    Purified reduced nicotinamide adenine dinucleotide: responses to lactate dehydrogenase isozymes from three cell sources (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-05-01
    Description: Lactate dehydrogenase (LDH, E.C. 1.1.1.27) isozymes from three single-cell sources reacted differently with reduced nicotinamide adenine dinucleotide (NADH) purified to published chromatographic and spectrophotometric specifications and free of inhibitors of LDH, when compared with a commercial preparation of NADH. The activity of LDH-1, purified from rabbit erythrocytes, increased the most with inhibitor-free NADH; the next most stimulated were the LDH isozymes from a control hepatocyte line; but hardly responsive at all were the same isozymes from chemically transformed cells. Thus isozyme composition alone did not account for the range of responses to purified NADH. The commercial preparation of NADH used in these studies contains the Strandjord-Clayson inhibitors, the most potent group identified in NADH preparations relative to LDH activity. The results suggest that specific molecular differences in individual isozymes contribute to the differential response to the Strandjord-Clayson inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, A E -- Weiss, E R -- Byrne, S T -- El-Torkey, N M -- Margolis, S A -- New York, N.Y. -- Science. 1981 May 1;212(4494):553-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209551" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic/metabolism ; Erythrocytes/enzymology ; Isoenzymes ; L-Lactate Dehydrogenase/antagonists & inhibitors/*metabolism ; Liver Neoplasms, Experimental/enzymology ; NAD/analysis/*metabolism ; Rabbits ; Rats
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    Owl monkey cell line (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-06-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, S J -- New York, N.Y. -- Science. 1981 Jun 12;212(4500):1214.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7233214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aotus trivirgatus ; Cell Line ; Hodgkin Disease/*pathology ; Humans ; Phenotype
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    Dissections and reconstructions of genes and chromosomes (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berg, P -- New York, N.Y. -- Science. 1981 Jul 17;213(4505):296-303.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6264595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosomes/*physiology/ultrastructure ; DNA Restriction Enzymes ; DNA, Recombinant ; DNA, Viral/genetics ; *Genes ; Histones ; Humans ; Plasmids ; RNA, Messenger/genetics ; Simian virus 40/genetics ; Transduction, Genetic
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    Hydra mesoglea: a model for investigating epithelial cell--basement membrane interactions (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-01-16
    Description: Isolated hydra mesoglea served as a suitable substrate for the attachment and spreading of hydra cells in vitro, irrespective of the species tested. Hydra cells did not attach and spread on substrates typically used for culturing mammalian cells. Mammalian and Drosophila cells attached and spread on plastic culture dishes but not on isolated mesoglea. Xenopus epithelial cells spread on both plastic and mesoglea. Because of the similarities of hydra mesoglea to vertebrate basement membranes, suggestions are offered for using mesoglea to study the interactions of epithelial cells with their basement membranes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Day, R M -- Lenhoff, H M -- New York, N.Y. -- Science. 1981 Jan 16;211(4479):291-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7444468" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basement Membrane/physiology ; Biological Evolution ; Cell Adhesion ; Cell Line ; Epithelial Cells ; Extracellular Space/physiology ; Hydra/*cytology ; Species Specificity
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    Inhibition of purine nucleoside phosphorylase by 8-aminoguanosine: selective toxicity for T lymphoblasts (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-12-04
    Description: The guanosine analog 8-aminoguanosine is an effective inhibitor of the purine degradative enzyme purine nucleoside phosphorylase, both in vitro and in intact lymphoid cells. In a human lymphoblast tissue culture system, 8-aminoguanosine, in combination with low concentrations of 2'-deoxyguanosine, causes toxicity toward T cells but not B cells. The selective T cell toxicity correlates with increased accumulation of deoxyguanosine triphosphate in the treated T lymphoblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kazmers, I S -- Mitchell, B S -- Dadonna, P E -- Wotring, L L -- Townsend, L B -- Kelley, W N -- AM 19045/AM/NIADDK NIH HHS/ -- CA 26032/CA/NCI NIH HHS/ -- CA 26284/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1981 Dec 4;214(4525):1137-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6795718" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/enzymology ; Cell Line ; Deoxyguanosine/pharmacology ; Guanosine/*analogs & derivatives/pharmacology ; Humans ; Kinetics ; Pentosyltransferases/*antagonists & inhibitors ; Purine-Nucleoside Phosphorylase/*antagonists & inhibitors ; T-Lymphocytes/drug effects/*enzymology
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    Plasminogen activator release at the neuronal growth cone (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-09-25
    Description: The site of plasminogen activator release by differentiated neuroblastoma clonal cell lines was determined with a fibrin overlay assay. Release of plasminogen activator was seen at the growth cone in 72 percent of the cells bearing neurites. For 21 percent of these cells the growth cone was the predominant or exclusive site of this enzyme activity. Selective release of protease at the "trailblazing" tip of the neurite may be important in neuron migration and neurite growth in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krystosek, A -- Seeds, N W -- New York, N.Y. -- Science. 1981 Sep 25;213(4515):1532-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7197054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; *Cell Movement ; Cytochalasin B/pharmacology ; Fibroblasts/metabolism ; Mice ; Neuroblastoma ; Neurons/cytology/*enzymology ; Plasminogen Activators/*metabolism/secretion ; Secretory Rate/drug effects
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    High levels of intracellular bombesin characterize human small-cell lung carcinoma (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-12-11
    Description: "Small cells" or "oat cells" characterize a virulent form of lung cancer and share many biochemical properties with peptide-secreting neurones. The neuropeptide bombesin is present in all small-cell lines examined, but not in other lung cancer cell lines, suggesting that bombesinergic precursor cells in lung may give rise to this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moody, T W -- Pert, C B -- Gazdar, A F -- Carney, D N -- Minna, J D -- New York, N.Y. -- Science. 1981 Dec 11;214(4526):1246-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6272398" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/analysis ; Bombesin/*analysis ; Carcinoma, Small Cell/*analysis ; Carcinoma, Squamous Cell/analysis ; Cell Line ; Humans ; Lung Neoplasms/*analysis ; Mesothelioma/analysis ; Peptides/*analysis
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    Induction of hemoglobin accumulation in human K562 cells by hemin is reversible (1981)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1981-04-24
    Description: Twenty micromolar hemin causes no change in the rate of division of K562 cells but results in accumulation of 11 to 14 picograms of embryonic and fetal hemoglobins per cell. This effect is reversible, and hemoglobin induction in response to hemin, and loss of hemoglobin upon removal of hemin, can be cyclically repeated. The cells can be indefinitely subcultured in the presence of the inducer. Thus, the control of hemoglobin levels in K562 cells does not depend on irreversible differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dean, A -- Erard, F -- Schneider, A P -- Schechter, A N -- AM 00103/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 24;212(4493):459-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6163216" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation/drug effects ; Cell Line ; Fetal Hemoglobin/biosynthesis ; Gene Expression Regulation/drug effects ; Heme/*analogs & derivatives ; Hemin/*pharmacology ; Hemoglobins/*biosynthesis ; Humans
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  • 47
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    Warburg effect revisited: merger of biochemistry and molecular biology (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Racker, E -- Spector, M -- CA-08964/CA/NCI NIH HHS/ -- CA-14454/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1981 Jul 17;213(4505):303-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6264596" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/*metabolism ; Animals ; Avian Sarcoma Viruses/metabolism ; Brain/*enzymology ; Carcinoma, Ehrlich Tumor/*metabolism ; Cell Line ; Cell Transformation, Neoplastic ; Electric Organ/enzymology ; Electrophorus ; *Glycolysis/drug effects ; Macromolecular Substances ; Mice ; Molecular Weight ; Neoplasms, Experimental/metabolism ; Ouabain/pharmacology ; Oxidation-Reduction ; Polyomavirus/metabolism ; Protein Kinases/metabolism ; Sodium-Potassium-Exchanging ATPase/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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