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  • 1
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    Prediction of individual brain maturity using fMRI (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-11
    Description: Group functional connectivity magnetic resonance imaging (fcMRI) studies have documented reliable changes in human functional brain maturity over development. Here we show that support vector machine-based multivariate pattern analysis extracts sufficient information from fcMRI data to make accurate predictions about individuals' brain maturity across development. The use of only 5 minutes of resting-state fcMRI data from 238 scans of typically developing volunteers (ages 7 to 30 years) allowed prediction of individual brain maturity as a functional connectivity maturation index. The resultant functional maturation curve accounted for 55% of the sample variance and followed a nonlinear asymptotic growth curve shape. The greatest relative contribution to predicting individual brain maturity was made by the weakening of short-range functional connections between the adult brain's major functional networks.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135376/" 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/PMC3135376/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dosenbach, Nico U F -- Nardos, Binyam -- Cohen, Alexander L -- Fair, Damien A -- Power, Jonathan D -- Church, Jessica A -- Nelson, Steven M -- Wig, Gagan S -- Vogel, Alecia C -- Lessov-Schlaggar, Christina N -- Barnes, Kelly Anne -- Dubis, Joseph W -- Feczko, Eric -- Coalson, Rebecca S -- Pruett, John R Jr -- Barch, Deanna M -- Petersen, Steven E -- Schlaggar, Bradley L -- DA027046/DA/NIDA NIH HHS/ -- EY16336/EY/NEI NIH HHS/ -- HD057076/HD/NICHD NIH HHS/ -- MH62130/MH/NIMH NIH HHS/ -- NS00169011/NS/NINDS NIH HHS/ -- NS053425/NS/NINDS NIH HHS/ -- NS32979/NS/NINDS NIH HHS/ -- NS41255/NS/NINDS NIH HHS/ -- NS46424/NS/NINDS NIH HHS/ -- NS51281/NS/NINDS NIH HHS/ -- NS55582/NS/NINDS NIH HHS/ -- R01 HD057076/HD/NICHD NIH HHS/ -- R01 HD057076-04/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1358-61. doi: 10.1126/science.1194144.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA. ndosenbach@wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829489" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aging ; Algorithms ; Artificial Intelligence ; Brain/*growth & development/*physiology ; Brain Mapping ; Cerebellum/growth & development/physiology ; Child ; Female ; Frontal Lobe/growth & development/physiology ; Humans ; *Magnetic Resonance Imaging ; Male ; Multivariate Analysis ; Neural Pathways ; Occipital Lobe/growth & development/physiology ; Young Adult
    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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    Polarized notum activation at wounds inhibits Wnt function to promote planarian head regeneration (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-14
    Description: Regeneration requires initiation of programs tailored to the identity of missing parts. Head-versus-tail regeneration in planarians presents a paradigm for study of this phenomenon. After injury, Wnt signaling promotes tail regeneration. We report that wounding elicits expression of the Wnt inhibitor notum preferentially at anterior-facing wounds. This expression asymmetry occurs at essentially any wound, even if the anterior pole is intact. Inhibition of notum with RNA interference (RNAi) causes regeneration of an anterior-facing tail instead of a head, and double-RNAi experiments indicate that notum inhibits Wnt signaling to promote head regeneration. notum expression is itself controlled by Wnt signaling, suggesting that regulation of feedback inhibition controls the binary head-tail regeneration outcome. We conclude that local detection of wound orientation with respect to tissue axes results in distinct signaling environments that initiate appropriate regeneration responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320723/" 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/PMC3320723/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petersen, Christian P -- Reddien, Peter W -- R01 GM080639/GM/NIGMS NIH HHS/ -- R01 GM080639-04/GM/NIGMS NIH HHS/ -- R01GM080639/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 May 13;332(6031):852-5. doi: 10.1126/science.1202143.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21566195" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Feedback, Physiological ; Gene Expression Regulation ; Genes, Helminth ; Head ; Helminth Proteins/genetics/*metabolism ; Hydrolases/genetics/*metabolism ; Molecular Sequence Data ; Planarians/cytology/genetics/*physiology ; RNA Interference ; *Regeneration ; *Signal Transduction ; Tail ; Wnt Proteins/genetics/*metabolism ; Wnt1 Protein/genetics/metabolism ; beta Catenin/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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    Wild pollinators enhance fruit set of crops regardless of honey bee abundance (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-02
    Description: The diversity and abundance of wild insect pollinators have declined in many agricultural landscapes. Whether such declines reduce crop yields, or are mitigated by managed pollinators such as honey bees, is unclear. We found universally positive associations of fruit set with flower visitation by wild insects in 41 crop systems worldwide. In contrast, fruit set increased significantly with flower visitation by honey bees in only 14% of the systems surveyed. Overall, wild insects pollinated crops more effectively; an increase in wild insect visitation enhanced fruit set by twice as much as an equivalent increase in honey bee visitation. Visitation by wild insects and honey bees promoted fruit set independently, so pollination by managed honey bees supplemented, rather than substituted for, pollination by wild insects. Our results suggest that new practices for integrated management of both honey bees and diverse wild insect assemblages will enhance global crop yields.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garibaldi, Lucas A -- Steffan-Dewenter, Ingolf -- Winfree, Rachael -- Aizen, Marcelo A -- Bommarco, Riccardo -- Cunningham, Saul A -- Kremen, Claire -- Carvalheiro, Luisa G -- Harder, Lawrence D -- Afik, Ohad -- Bartomeus, Ignasi -- Benjamin, Faye -- Boreux, Virginie -- Cariveau, Daniel -- Chacoff, Natacha P -- Dudenhoffer, Jan H -- Freitas, Breno M -- Ghazoul, Jaboury -- Greenleaf, Sarah -- Hipolito, Juliana -- Holzschuh, Andrea -- Howlett, Brad -- Isaacs, Rufus -- Javorek, Steven K -- Kennedy, Christina M -- Krewenka, Kristin M -- Krishnan, Smitha -- Mandelik, Yael -- Mayfield, Margaret M -- Motzke, Iris -- Munyuli, Theodore -- Nault, Brian A -- Otieno, Mark -- Petersen, Jessica -- Pisanty, Gideon -- Potts, Simon G -- Rader, Romina -- Ricketts, Taylor H -- Rundlof, Maj -- Seymour, Colleen L -- Schuepp, Christof -- Szentgyorgyi, Hajnalka -- Taki, Hisatomo -- Tscharntke, Teja -- Vergara, Carlos H -- Viana, Blandina F -- Wanger, Thomas C -- Westphal, Catrin -- Williams, Neal -- Klein, Alexandra M -- New York, N.Y. -- Science. 2013 Mar 29;339(6127):1608-11. doi: 10.1126/science.1230200. Epub 2013 Feb 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sede Andina, Universidad Nacional de Rio Negro (UNRN) and Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET), San Carlos de Bariloche, Rio Negro, Argentina. lgaribaldi@unrn.edu.ar〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23449997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bees/physiology ; Crops, Agricultural/*growth & development ; Flowers/physiology ; Fruit/*growth & development ; Insects/*physiology ; *Pollination
    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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    Hydrogen is an energy source for hydrothermal vent symbioses (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-08-13
    Description: The discovery of deep-sea hydrothermal vents in 1977 revolutionized our understanding of the energy sources that fuel primary productivity on Earth. Hydrothermal vent ecosystems are dominated by animals that live in symbiosis with chemosynthetic bacteria. So far, only two energy sources have been shown to power chemosynthetic symbioses: reduced sulphur compounds and methane. Using metagenome sequencing, single-gene fluorescence in situ hybridization, immunohistochemistry, shipboard incubations and in situ mass spectrometry, we show here that the symbionts of the hydrothermal vent mussel Bathymodiolus from the Mid-Atlantic Ridge use hydrogen to power primary production. In addition, we show that the symbionts of Bathymodiolus mussels from Pacific vents have hupL, the key gene for hydrogen oxidation. Furthermore, the symbionts of other vent animals such as the tubeworm Riftia pachyptila and the shrimp Rimicaris exoculata also have hupL. We propose that the ability to use hydrogen as an energy source is widespread in hydrothermal vent symbioses, particularly at sites where hydrogen is abundant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petersen, Jillian M -- Zielinski, Frank U -- Pape, Thomas -- Seifert, Richard -- Moraru, Cristina -- Amann, Rudolf -- Hourdez, Stephane -- Girguis, Peter R -- Wankel, Scott D -- Barbe, Valerie -- Pelletier, Eric -- Fink, Dennis -- Borowski, Christian -- Bach, Wolfgang -- Dubilier, Nicole -- England -- Nature. 2011 Aug 10;476(7359):176-80. doi: 10.1038/nature10325.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Marine Microbiology, Celsiusstrasse 1, 28359 Bremen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21833083" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atlantic Ocean ; Bivalvia/drug effects/metabolism/*microbiology ; Dose-Response Relationship, Drug ; *Ecosystem ; *Energy Metabolism ; Geologic Sediments/chemistry ; Gills/drug effects/metabolism/microbiology ; Hot Springs/*chemistry/microbiology ; Hydrogen/analysis/*metabolism/pharmacology ; Hydrogenase/genetics/metabolism ; Molecular Sequence Data ; Oxidation-Reduction ; Partial Pressure ; Seawater/chemistry/microbiology ; Sulfides/metabolism ; Sulfur/metabolism ; Symbiosis/drug effects/genetics/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Human metabolic individuality in biomedical and pharmaceutical research (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-09-03
    Description: Genome-wide association studies (GWAS) have identified many risk loci for complex diseases, but effect sizes are typically small and information on the underlying biological processes is often lacking. Associations with metabolic traits as functional intermediates can overcome these problems and potentially inform individualized therapy. Here we report a comprehensive analysis of genotype-dependent metabolic phenotypes using a GWAS with non-targeted metabolomics. We identified 37 genetic loci associated with blood metabolite concentrations, of which 25 show effect sizes that are unusually high for GWAS and account for 10-60% differences in metabolite levels per allele copy. Our associations provide new functional insights for many disease-related associations that have been reported in previous studies, including those for cardiovascular and kidney disorders, type 2 diabetes, cancer, gout, venous thromboembolism and Crohn's disease. The study advances our knowledge of the genetic basis of metabolic individuality in humans and generates many new hypotheses for biomedical and pharmaceutical research.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3832838/" 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/PMC3832838/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suhre, Karsten -- Shin, So-Youn -- Petersen, Ann-Kristin -- Mohney, Robert P -- Meredith, David -- Wagele, Brigitte -- Altmaier, Elisabeth -- CARDIoGRAM -- Deloukas, Panos -- Erdmann, Jeanette -- Grundberg, Elin -- Hammond, Christopher J -- de Angelis, Martin Hrabe -- Kastenmuller, Gabi -- Kottgen, Anna -- Kronenberg, Florian -- Mangino, Massimo -- Meisinger, Christa -- Meitinger, Thomas -- Mewes, Hans-Werner -- Milburn, Michael V -- Prehn, Cornelia -- Raffler, Johannes -- Ried, Janina S -- Romisch-Margl, Werner -- Samani, Nilesh J -- Small, Kerrin S -- Wichmann, H-Erich -- Zhai, Guangju -- Illig, Thomas -- Spector, Tim D -- Adamski, Jerzy -- Soranzo, Nicole -- Gieger, Christian -- 091746/Wellcome Trust/United Kingdom -- 091746/Z/10/Z/Wellcome Trust/United Kingdom -- 1R01HL103931-01/HL/NHLBI NIH HHS/ -- HL087647/HL/NHLBI NIH HHS/ -- MOP172605/Canadian Institutes of Health Research/Canada -- MOP77682/Canadian Institutes of Health Research/Canada -- MOP-82810/Canadian Institutes of Health Research/Canada -- N01-AG-12100/AG/NIA NIH HHS/ -- N01-HC-55015/HC/NHLBI NIH HHS/ -- N01-HC-55016/HC/NHLBI NIH HHS/ -- N01-HC-55018/HC/NHLBI NIH HHS/ -- N01-HC-55019/HC/NHLBI NIH HHS/ -- N01-HC-55020/HC/NHLBI NIH HHS/ -- N01-HC-55021/HC/NHLBI NIH HHS/ -- N01-HC-55022/HC/NHLBI NIH HHS/ -- P01 HL098055/HL/NHLBI NIH HHS/ -- P01HL076491-06/HL/NHLBI NIH HHS/ -- P01HL087018/HL/NHLBI NIH HHS/ -- R01 HL087647/HL/NHLBI NIH HHS/ -- R01 HL087676/HL/NHLBI NIH HHS/ -- R01DK080732/DK/NIDDK NIH HHS/ -- R01HL089650-02/HL/NHLBI NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- British Heart Foundation/United Kingdom -- Cancer Research UK/United Kingdom -- Intramural NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2011 Aug 31;477(7362):54-60. doi: 10.1038/nature10354.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Bioinformatics and Systems Biology, Helmholtz Zentrum Munchen, German Research Center for Environmental Health, Ingolstadter Landstrasse 1, 85764 Neuherberg, Germany. karsten@suhre.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21886157" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Aged, 80 and over ; *Biomedical Research ; Blood/metabolism ; Child ; Chronic Disease ; Coronary Artery Disease/genetics ; Diabetes Mellitus/genetics ; *Drug Industry ; Female ; Genetic Loci/genetics ; *Genetic Variation ; *Genome-Wide Association Study ; Genotype ; Humans ; Male ; Metabolism/*genetics ; Metabolomics ; Middle Aged ; Pharmacogenetics ; Renal Insufficiency/genetics ; Risk Factors ; Venous Thromboembolism/genetics ; Young Adult
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-10-30
    Description: Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3530898/" 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/PMC3530898/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biankin, Andrew V -- Waddell, Nicola -- Kassahn, Karin S -- Gingras, Marie-Claude -- Muthuswamy, Lakshmi B -- Johns, Amber L -- Miller, David K -- Wilson, Peter J -- Patch, Ann-Marie -- Wu, Jianmin -- Chang, David K -- Cowley, Mark J -- Gardiner, Brooke B -- Song, Sarah -- Harliwong, Ivon -- Idrisoglu, Senel -- Nourse, Craig -- Nourbakhsh, Ehsan -- Manning, Suzanne -- Wani, Shivangi -- Gongora, Milena -- Pajic, Marina -- Scarlett, Christopher J -- Gill, Anthony J -- Pinho, Andreia V -- Rooman, Ilse -- Anderson, Matthew -- Holmes, Oliver -- Leonard, Conrad -- Taylor, Darrin -- Wood, Scott -- Xu, Qinying -- Nones, Katia -- Fink, J Lynn -- Christ, Angelika -- Bruxner, Tim -- Cloonan, Nicole -- Kolle, Gabriel -- Newell, Felicity -- Pinese, Mark -- Mead, R Scott -- Humphris, Jeremy L -- Kaplan, Warren -- Jones, Marc D -- Colvin, Emily K -- Nagrial, Adnan M -- Humphrey, Emily S -- Chou, Angela -- Chin, Venessa T -- Chantrill, Lorraine A -- Mawson, Amanda -- Samra, Jaswinder S -- Kench, James G -- Lovell, Jessica A -- Daly, Roger J -- Merrett, Neil D -- Toon, Christopher -- Epari, Krishna -- Nguyen, Nam Q -- Barbour, Andrew -- Zeps, Nikolajs -- Australian Pancreatic Cancer Genome Initiative -- Kakkar, Nipun -- Zhao, Fengmei -- Wu, Yuan Qing -- Wang, Min -- Muzny, Donna M -- Fisher, William E -- Brunicardi, F Charles -- Hodges, Sally E -- Reid, Jeffrey G -- Drummond, Jennifer -- Chang, Kyle -- Han, Yi -- Lewis, Lora R -- Dinh, Huyen -- Buhay, Christian J -- Beck, Timothy -- Timms, Lee -- Sam, Michelle -- Begley, Kimberly -- Brown, Andrew -- Pai, Deepa -- Panchal, Ami -- Buchner, Nicholas -- De Borja, Richard -- Denroche, Robert E -- Yung, Christina K -- Serra, Stefano -- Onetto, Nicole -- Mukhopadhyay, Debabrata -- Tsao, Ming-Sound -- Shaw, Patricia A -- Petersen, Gloria M -- Gallinger, Steven -- Hruban, Ralph H -- Maitra, Anirban -- Iacobuzio-Donahue, Christine A -- Schulick, Richard D -- Wolfgang, Christopher L -- Morgan, Richard A -- Lawlor, Rita T -- Capelli, Paola -- Corbo, Vincenzo -- Scardoni, Maria -- Tortora, Giampaolo -- Tempero, Margaret A -- Mann, Karen M -- Jenkins, Nancy A -- Perez-Mancera, Pedro A -- Adams, David J -- Largaespada, David A -- Wessels, Lodewyk F A -- Rust, Alistair G -- Stein, Lincoln D -- Tuveson, David A -- Copeland, Neal G -- Musgrove, Elizabeth A -- Scarpa, Aldo -- Eshleman, James R -- Hudson, Thomas J -- Sutherland, Robert L -- Wheeler, David A -- Pearson, John V -- McPherson, John D -- Gibbs, Richard A -- Grimmond, Sean M -- 13031/Cancer Research UK/United Kingdom -- 2P50CA101955/CA/NCI NIH HHS/ -- P01CA134292/CA/NCI NIH HHS/ -- P50 CA101955/CA/NCI NIH HHS/ -- P50 CA102701/CA/NCI NIH HHS/ -- P50CA062924/CA/NCI NIH HHS/ -- R01 CA097075/CA/NCI NIH HHS/ -- R01 CA97075/CA/NCI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2012 Nov 15;491(7424):399-405. doi: 10.1038/nature11547. Epub 2012 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kinghorn Cancer Centre, 370 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Carcinoma, Pancreatic Ductal/*genetics/*pathology ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genome/*genetics ; Humans ; Kaplan-Meier Estimate ; Mice ; Mutation ; Pancreatic Neoplasms/*genetics/*pathology ; Proteins/genetics ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Severe malaria is associated with parasite binding to endothelial protein C receptor (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-06-07
    Description: Sequestration of Plasmodium falciparum-infected erythrocytes in host blood vessels is a key triggering event in the pathogenesis of severe childhood malaria, which is responsible for about one million deaths every year. Sequestration is mediated by specific interactions between members of the P. falciparum erythrocyte membrane protein 1 (PfEMP1) family and receptors on the endothelial lining. Severe childhood malaria is associated with expression of specific PfEMP1 subtypes containing domain cassettes (DCs) 8 and 13 (ref. 3), but the endothelial receptor for parasites expressing these proteins was unknown. Here we identify endothelial protein C receptor (EPCR), which mediates the cytoprotective effects of activated protein C, as the endothelial receptor for DC8 and DC13 PfEMP1. We show that EPCR binding is mediated through the amino-terminal cysteine-rich interdomain region (CIDRalpha1) of DC8 and group A PfEMP1 subfamilies, and that CIDRalpha1 interferes with protein C binding to EPCR. This PfEMP1 adhesive property links P. falciparum cytoadhesion to a host receptor involved in anticoagulation and endothelial cytoprotective pathways, and has implications for understanding malaria pathology and the development of new malaria interventions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3870021/" 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/PMC3870021/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turner, Louise -- Lavstsen, Thomas -- Berger, Sanne S -- Wang, Christian W -- Petersen, Jens E V -- Avril, Marion -- Brazier, Andrew J -- Freeth, Jim -- Jespersen, Jakob S -- Nielsen, Morten A -- Magistrado, Pamela -- Lusingu, John -- Smith, Joseph D -- Higgins, Matthew K -- Theander, Thor G -- G0901062/Medical Research Council/United Kingdom -- R01 AI047953/AI/NIAID NIH HHS/ -- R01 AI47953/AI/NIAID NIH HHS/ -- U19 AI089688/AI/NIAID NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2013 Jun 27;498(7455):502-5. doi: 10.1038/nature12216. Epub 2013 Jun 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Medical Parasitology, Department of International Health, Immunology & Microbiology, University of Copenhagen and Department of Infectious Diseases, Rigshospitalet, Copenhagen, Denmark. lturner@sund.ku.dk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23739325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*metabolism ; Blood Coagulation ; Brain/blood supply ; CHO Cells ; Cell Adhesion ; Cell Line ; Cricetinae ; Endothelial Cells/metabolism ; Erythrocyte Membrane/metabolism ; Humans ; Inflammation/complications/parasitology/pathology ; Malaria, Falciparum/complications/*parasitology/*pathology ; Microcirculation ; Plasmodium falciparum/chemistry/*metabolism/pathogenicity ; Protozoan Proteins/chemistry/metabolism ; Receptors, Cell Surface/*metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Is SIRT2 required for necroptosis? (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-02-28
    Description: Sirtuins can promote deacetylation of a wide range of substrates in diverse cellular compartments and regulate many cellular processes(1),(2). Recently Narayan et al., reported that SIRT2 was required for necroptosis based on their findings that SIRT2 inhibition, knock-down or knock-out prevented necroptosis. We sought to confirm and explore the role of SIRT2 in necroptosis and tested four different sources of the SIRT2 inhibitor AGK2, three independent siRNAs against SIRT2, and cells from two independently generated Sirt2-/- mouse strains, however we were unable to show that inhibiting or depleting SIRT2 protected cells from necroptosis. Furthermore, Sirt2-/- mice succumbed to TNF induced Systemic Inflammatory Response Syndrome (SIRS) more rapidly than wild type mice while Ripk3-/- mice were resistant. Our results therefore question the importance of SIRT2 in the necroptosis cell death pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005920/" 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/PMC4005920/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newton, Kim -- Hildebrand, Joanne M -- Shen, Zhirong -- Rodriguez, Diego -- Alvarez-Diaz, Silvia -- Petersen, Sean -- Shah, Saumil -- Dugger, Debra L -- Huang, Chunzi -- Auwerx, Johan -- Vandenabeele, Peter -- Green, Douglas R -- Ashkenazi, Avi -- Dixit, Vishva M -- Kaiser, William J -- Strasser, Andreas -- Degterev, Alexei -- Silke, John -- P30 CA021765/CA/NCI NIH HHS/ -- R01 AI044828/AI/NIAID NIH HHS/ -- R01 CA169291/CA/NCI NIH HHS/ -- England -- Nature. 2014 Feb 27;506(7489):E4-6. doi: 10.1038/nature13024.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech, Inc., South San Francisco, California 94080, USA. ; 1] The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia [2] Department of Medical Biology, University of Melbourne, Parkville, Victoria 3050, Australia. ; National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China. ; Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Department of Biochemistry, Tufts University, Boston, Massachusetts 02111, USA. ; Department of Microbiology and Immunology, Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia 30322, USA. ; Laboratory of Integrative and Systems Physiology, EPFL, CH-1015 Lausanne, Switzerland. ; 1] Molecular Signaling and Cell Death Unit, Inflammation Research Center, VIB, 9052 Gent, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, 9052 Gent, Belgium [3] Methusalem BOF09/01M00709, Ghent University, 9052 Gent, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24572428" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Humans ; Male ; Necrosis/*enzymology ; Sirtuin 2/*genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    CEACAM1 regulates TIM-3-mediated tolerance and exhaustion (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-11-05
    Description: T-cell immunoglobulin domain and mucin domain-3 (TIM-3, also known as HAVCR2) is an activation-induced inhibitory molecule involved in tolerance and shown to induce T-cell exhaustion in chronic viral infection and cancers. Under some conditions, TIM-3 expression has also been shown to be stimulatory. Considering that TIM-3, like cytotoxic T lymphocyte antigen 4 (CTLA-4) and programmed death 1 (PD-1), is being targeted for cancer immunotherapy, it is important to identify the circumstances under which TIM-3 can inhibit and activate T-cell responses. Here we show that TIM-3 is co-expressed and forms a heterodimer with carcinoembryonic antigen cell adhesion molecule 1 (CEACAM1), another well-known molecule expressed on activated T cells and involved in T-cell inhibition. Biochemical, biophysical and X-ray crystallography studies show that the membrane-distal immunoglobulin-variable (IgV)-like amino-terminal domain of each is crucial to these interactions. The presence of CEACAM1 endows TIM-3 with inhibitory function. CEACAM1 facilitates the maturation and cell surface expression of TIM-3 by forming a heterodimeric interaction in cis through the highly related membrane-distal N-terminal domains of each molecule. CEACAM1 and TIM-3 also bind in trans through their N-terminal domains. Both cis and trans interactions between CEACAM1 and TIM-3 determine the tolerance-inducing function of TIM-3. In a mouse adoptive transfer colitis model, CEACAM1-deficient T cells are hyper-inflammatory with reduced cell surface expression of TIM-3 and regulatory cytokines, and this is restored by T-cell-specific CEACAM1 expression. During chronic viral infection and in a tumour environment, CEACAM1 and TIM-3 mark exhausted T cells. Co-blockade of CEACAM1 and TIM-3 leads to enhancement of anti-tumour immune responses with improved elimination of tumours in mouse colorectal cancer models. Thus, CEACAM1 serves as a heterophilic ligand for TIM-3 that is required for its ability to mediate T-cell inhibition, and this interaction has a crucial role in regulating autoimmunity and anti-tumour immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297519/" 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/PMC4297519/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Yu-Hwa -- Zhu, Chen -- Kondo, Yasuyuki -- Anderson, Ana C -- Gandhi, Amit -- Russell, Andrew -- Dougan, Stephanie K -- Petersen, Britt-Sabina -- Melum, Espen -- Pertel, Thomas -- Clayton, Kiera L -- Raab, Monika -- Chen, Qiang -- Beauchemin, Nicole -- Yazaki, Paul J -- Pyzik, Michal -- Ostrowski, Mario A -- Glickman, Jonathan N -- Rudd, Christopher E -- Ploegh, Hidde L -- Franke, Andre -- Petsko, Gregory A -- Kuchroo, Vijay K -- Blumberg, Richard S -- AI039671/AI/NIAID NIH HHS/ -- AI056299/AI/NIAID NIH HHS/ -- AI073748/AI/NIAID NIH HHS/ -- DK0034854/DK/NIDDK NIH HHS/ -- DK044319/DK/NIDDK NIH HHS/ -- DK051362/DK/NIDDK NIH HHS/ -- DK053056/DK/NIDDK NIH HHS/ -- DK088199/DK/NIDDK NIH HHS/ -- GM32415/GM/NIGMS NIH HHS/ -- MOP-93787/Canadian Institutes of Health Research/Canada -- NS045937/NS/NINDS NIH HHS/ -- P01 AI039671/AI/NIAID NIH HHS/ -- P01 AI056299/AI/NIAID NIH HHS/ -- P01 AI073748/AI/NIAID NIH HHS/ -- P30 DK034854/DK/NIDDK NIH HHS/ -- P41 GM111244/GM/NIGMS NIH HHS/ -- R01 DK051362/DK/NIDDK NIH HHS/ -- R01 GM026788/GM/NIGMS NIH HHS/ -- R01 NS045937/NS/NINDS NIH HHS/ -- T32 GM007122/GM/NIGMS NIH HHS/ -- UL1 TR001102/TR/NCATS NIH HHS/ -- England -- Nature. 2015 Jan 15;517(7534):386-90. doi: 10.1038/nature13848. Epub 2014 Oct 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA. ; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Harvard Institutes of Medicine, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. ; Rosenstiel Basic Medical Sciences Research Center, Brandeis University, 415 South Street, Waltham, Massachusetts 02454, USA. ; Whitehead Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA. ; Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel 24105, Germany. ; 1] Division of Gastroenterology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA [2] Norwegian PSC Research Center, Division of Cancer Medicine, Surgery and Transplantation, Oslo University Hospital, Oslo 0424, Norway. ; Department of Immunology, University of Toronto, Toronto, Ontario M5S1A8, Canada. ; Cell Signalling Section, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, UK. ; State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China. ; Goodman Cancer Research Centre, McGill University, Montreal H3G 1Y6, Canada. ; Beckman Institute, City of Hope, Duarte, California 91010, USA. ; 1] Department of Immunology, University of Toronto, Toronto, Ontario M5S1A8, Canada [2] Keenan Research Centre of St. Michael's Hospital, Toronto, Ontario M5S1A8, Canada. ; GI Pathology, Miraca Life Sciences, Newton, Massachusetts 02464, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25363763" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/chemistry/immunology/*metabolism ; Autoimmunity/immunology ; Cell Adhesion Molecules/chemistry/immunology/*metabolism ; Cell Line ; Colorectal Neoplasms/immunology ; Disease Models, Animal ; Female ; Humans ; Immune Tolerance/*immunology ; Inflammation/immunology/pathology ; Ligands ; Male ; Membrane Proteins/chemistry/immunology/*metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Models, Molecular ; Mucous Membrane/immunology/pathology ; Protein Conformation ; Protein Multimerization ; Receptors, Virus/chemistry/immunology/*metabolism ; T-Lymphocytes/*immunology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Mutations in DMRT3 affect locomotion in horses and spinal circuit function in mice (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-08-31
    Description: Locomotion in mammals relies on a central pattern-generating circuitry of spinal interneurons established during development that coordinates limb movement. These networks produce left-right alternation of limbs as well as coordinated activation of flexor and extensor muscles. Here we show that a premature stop codon in the DMRT3 gene has a major effect on the pattern of locomotion in horses. The mutation is permissive for the ability to perform alternate gaits and has a favourable effect on harness racing performance. Examination of wild-type and Dmrt3-null mice demonstrates that Dmrt3 is expressed in the dI6 subdivision of spinal cord neurons, takes part in neuronal specification within this subdivision, and is critical for the normal development of a coordinated locomotor network controlling limb movements. Our discovery positions Dmrt3 in a pivotal role for configuring the spinal circuits controlling stride in vertebrates. The DMRT3 mutation has had a major effect on the diversification of the domestic horse, as the altered gait characteristics of a number of breeds apparently require this mutation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523687/" 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/PMC3523687/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andersson, Lisa S -- Larhammar, Martin -- Memic, Fatima -- Wootz, Hanna -- Schwochow, Doreen -- Rubin, Carl-Johan -- Patra, Kalicharan -- Arnason, Thorvaldur -- Wellbring, Lisbeth -- Hjalm, Goran -- Imsland, Freyja -- Petersen, Jessica L -- McCue, Molly E -- Mickelson, James R -- Cothran, Gus -- Ahituv, Nadav -- Roepstorff, Lars -- Mikko, Sofia -- Vallstedt, Anna -- Lindgren, Gabriella -- Andersson, Leif -- Kullander, Klas -- R01 HD059862/HD/NICHD NIH HHS/ -- R01HD059862/HD/NICHD NIH HHS/ -- England -- Nature. 2012 Aug 30;488(7413):642-6. doi: 10.1038/nature11399.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Breeding and Genetics, Swedish University of Agricultural Sciences, SE-75124 Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22932389" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Codon, Nonsense/genetics ; Gait/*genetics/physiology ; Gene Expression Profiling ; Gene Frequency ; Horses/classification/*genetics/*physiology ; Iceland ; Mice ; Molecular Sequence Data ; Mutation/*genetics ; Neural Pathways/physiology ; Psychomotor Performance/physiology ; Spinal Cord/cytology/*physiology ; Transcription Factors/deficiency/*genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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