ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Animals  (298)
  • American Association for the Advancement of Science (AAAS)  (298)
Collection
Publisher
  • 1
    Publication Date: 2012-06-16
    Description: Seagrasses evolved from terrestrial plants into marine foundation species around 100 million years ago. Their ecological success, however, remains a mystery because natural organic matter accumulation within the beds should result in toxic sediment sulfide levels. Using a meta-analysis, a field study, and a laboratory experiment, we reveal how an ancient three-stage symbiosis between seagrass, lucinid bivalves, and their sulfide-oxidizing gill bacteria reduces sulfide stress for seagrasses. We found that the bivalve-sulfide-oxidizer symbiosis reduced sulfide levels and enhanced seagrass production as measured in biomass. In turn, the bivalves and their endosymbionts profit from organic matter accumulation and radial oxygen release from the seagrass roots. These findings elucidate the long-term success of seagrasses in warm waters and offer new prospects for seagrass ecosystem conservation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van der Heide, Tjisse -- Govers, Laura L -- de Fouw, Jimmy -- Olff, Han -- van der Geest, Matthijs -- van Katwijk, Marieke M -- Piersma, Theunis -- van de Koppel, Johan -- Silliman, Brian R -- Smolders, Alfons J P -- van Gils, Jan A -- New York, N.Y. -- Science. 2012 Jun 15;336(6087):1432-4. doi: 10.1126/science.1219973.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Community and Conservation Ecology Group, Centre for Ecological and Evolutionary Studies, University of Groningen, Post Office Box 11103, 9700 CC Groningen, Netherlands. t.van.der.heide@rug.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22700927" target="_blank"〉PubMed〈/a〉
    Keywords: Angiosperms/growth & development/*physiology ; Animals ; Bacteria/growth & development/*metabolism ; Biomass ; Bivalvia/metabolism/microbiology/*physiology ; Chemoautotrophic Growth ; *Ecosystem ; Geologic Sediments/chemistry ; Gills/microbiology ; Oxidation-Reduction ; Oxygen/metabolism ; Plant Roots/metabolism ; *Seawater/chemistry ; Sulfides/analysis/metabolism ; *Symbiosis ; Zosteraceae/growth & development/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2002-11-26
    Description: The DJ-1 gene encodes a ubiquitous, highly conserved protein. Here, we show that DJ-1 mutations are associated with PARK7, a monogenic form of human parkinsonism. The function of the DJ-1 protein remains unknown, but evidence suggests its involvement in the oxidative stress response. Our findings indicate that loss of DJ-1 function leads to neurodegeneration. Elucidating the physiological role of DJ-1 protein may promote understanding of the mechanisms of brain neuronal maintenance and pathogenesis of Parkinson's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonifati, Vincenzo -- Rizzu, Patrizia -- van Baren, Marijke J -- Schaap, Onno -- Breedveld, Guido J -- Krieger, Elmar -- Dekker, Marieke C J -- Squitieri, Ferdinando -- Ibanez, Pablo -- Joosse, Marijke -- van Dongen, Jeroen W -- Vanacore, Nicola -- van Swieten, John C -- Brice, Alexis -- Meco, Giuseppe -- van Duijn, Cornelia M -- Oostra, Ben A -- Heutink, Peter -- New York, N.Y. -- Science. 2003 Jan 10;299(5604):256-9. Epub 2002 Nov 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetic-Epidemiologic Unit, Department of Clinical Genetics, Department of Epidemiology and Biostatistics, Erasmus Medical Center Rotterdam, Post Office Box 1738, 3000 DR Rotterdam, Netherlands. bonifati@kgen.fgg.eur.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12446870" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Base Sequence ; Brain/metabolism ; COS Cells ; Cell Nucleus/metabolism ; Chromosomes, Human, Pair 1 ; Cloning, Molecular ; Cytoplasm/metabolism ; DNA, Complementary ; Exons ; Genes, Recessive ; Humans ; Intracellular Signaling Peptides and Proteins ; Molecular Sequence Data ; *Mutation ; Oncogene Proteins/chemistry/*genetics/metabolism ; Oxidative Stress ; PC12 Cells ; Parkinsonian Disorders/*genetics/metabolism ; Pedigree ; Physical Chromosome Mapping ; Point Mutation ; Protein Structure, Secondary ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; Sequence Deletion ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2002-04-16
    Description: One of the factors postulated to drive the aging process is the accumulation of DNA damage. Here, we provide strong support for this hypothesis by describing studies of mice with a mutation in XPD, a gene encoding a DNA helicase that functions in both repair and transcription and that is mutated in the human disorder trichothiodystrophy (TTD). TTD mice were found to exhibit many symptoms of premature aging, including osteoporosis and kyphosis, osteosclerosis, early greying, cachexia, infertility, and reduced life-span. TTD mice carrying an additional mutation in XPA, which enhances the DNA repair defect, showed a greatly accelerated aging phenotype, which correlated with an increased cellular sensitivity to oxidative DNA damage. We hypothesize that aging in TTD mice is caused by unrepaired DNA damage that compromises transcription, leading to functional inactivation of critical genes and enhanced apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Boer, Jan -- Andressoo, Jaan Olle -- de Wit, Jan -- Huijmans, Jan -- Beems, Rudolph B -- van Steeg, Harry -- Weeda, Geert -- van der Horst, Gijsbertus T J -- van Leeuwen, Wibeke -- Themmen, Axel P N -- Meradji, Morteza -- Hoeijmakers, Jan H J -- AG 17242-02/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2002 May 17;296(5571):1276-9. Epub 2002 Apr 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Genetics Center, Department of Cell Biology and Genetics, Center for Biomedical Genetics, Erasmus University, 3000 DR Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11950998" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Aging, Premature/*etiology ; Animals ; Apoptosis ; Bone Density ; Cachexia/etiology ; Crosses, Genetic ; *DNA Damage ; DNA Helicases/genetics/*physiology ; *DNA Repair ; DNA-Binding Proteins/genetics/physiology ; Female ; Fertility ; Gene Targeting ; Growth Disorders/etiology/genetics ; Hair Diseases/genetics ; Kyphosis/etiology/genetics/pathology ; Male ; Mice ; Mutation ; Oxidative Stress ; Phenotype ; Point Mutation ; Proteins/genetics/*physiology ; RNA-Binding Proteins/genetics/physiology ; *Transcription Factors ; Transcription, Genetic ; Xeroderma Pigmentosum Group A Protein ; Xeroderma Pigmentosum Group D Protein
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2012-10-23
    Description: Tipping points in complex systems may imply risks of unwanted collapse, but also opportunities for positive change. Our capacity to navigate such risks and opportunities can be boosted by combining emerging insights from two unconnected fields of research. One line of work is revealing fundamental architectural features that may cause ecological networks, financial markets, and other complex systems to have tipping points. Another field of research is uncovering generic empirical indicators of the proximity to such critical thresholds. Although sudden shifts in complex systems will inevitably continue to surprise us, work at the crossroads of these emerging fields offers new approaches for anticipating critical transitions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheffer, Marten -- Carpenter, Stephen R -- Lenton, Timothy M -- Bascompte, Jordi -- Brock, William -- Dakos, Vasilis -- van de Koppel, Johan -- van de Leemput, Ingrid A -- Levin, Simon A -- van Nes, Egbert H -- Pascual, Mercedes -- Vandermeer, John -- 268732/European Research Council/International -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):344-8. doi: 10.1126/science.1225244.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Environmental Sciences, Wageningen University, Post Office Box 47, NL-6700 AA Wageningen, Netherlands. marten.scheffer@wur.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23087241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Forecasting ; Humans ; Risk Assessment/*statistics & numerical data
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    Publication Date: 2014-11-02
    Description: Emerging infectious diseases are reducing biodiversity on a global scale. Recently, the emergence of the chytrid fungus Batrachochytrium salamandrivorans resulted in rapid declines in populations of European fire salamanders. Here, we screened more than 5000 amphibians from across four continents and combined experimental assessment of pathogenicity with phylogenetic methods to estimate the threat that this infection poses to amphibian diversity. Results show that B. salamandrivorans is restricted to, but highly pathogenic for, salamanders and newts (Urodela). The pathogen likely originated and remained in coexistence with a clade of salamander hosts for millions of years in Asia. As a result of globalization and lack of biosecurity, it has recently been introduced into naive European amphibian populations, where it is currently causing biodiversity loss.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martel, A -- Blooi, M -- Adriaensen, C -- Van Rooij, P -- Beukema, W -- Fisher, M C -- Farrer, R A -- Schmidt, B R -- Tobler, U -- Goka, K -- Lips, K R -- Muletz, C -- Zamudio, K R -- Bosch, J -- Lotters, S -- Wombwell, E -- Garner, T W J -- Cunningham, A A -- Spitzen-van der Sluijs, A -- Salvidio, S -- Ducatelle, R -- Nishikawa, K -- Nguyen, T T -- Kolby, J E -- Van Bocxlaer, I -- Bossuyt, F -- Pasmans, F -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 Oct 31;346(6209):630-1. doi: 10.1126/science.1258268.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, B-9820 Merelbeke, Belgium. an.martel@ugent.be. ; Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, B-9820 Merelbeke, Belgium. Centre for Research and Conservation, Royal Zoological Society of Antwerp, Koningin Astridplein 26, Antwerp, Belgium. ; Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, B-9820 Merelbeke, Belgium. ; CIBIO/InBIO, Centro de Investigacao em Biodiversidade e Recursos Geneticos da Universidade do Porto, Instituto de Ciencias Agrarias de Vairao, Rua Padre Armando Quintas, Vairao, Portugal. ; Department of Infectious Disease Epidemiology, Imperial College London, Norfolk Place, London W2 1PG, UK. ; Genome Sequencing and Analysis Program, The Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Koordinationsstelle fur amphibien- und reptilienschutz in der Schweiz (KARCH), Passage Maximilien-de-Meuron 6, 2000 Neuchatel, Switzerland. Institut fur Evolutionsbiologie und Umweltwissenschaften, Universitat Zurich. Winterthurerstrasse 190, 8057 Zurich, Switzerland. ; Invasive Alien Species Research Team, National Institute for Environment Studies, 16-2 Onogawa, Tsukuba, Ibaraki 305-8506, Japan. ; Department of Biology, University of Maryland, College Park, MD 20742, USA. ; Department of Ecology and Evolutionary Biology, Cornell University, Ithaca, NY 14853, USA. ; Museo Nacional de Ciencias Naturales, Consejo Superior de Investigaciones cientificas (CSIC), Jose Gutierrez Abascal 2, 28006 Madrid, Spain. ; Biogeography Department, Trier University, 54286 Trier, Germany. ; Durrell Institute of Conservation and Ecology, University of Kent, Kent CT2 7NR, UK. Institute of Zoology, Zoological Society of London, London NW1 4RY, UK. ; Institute of Zoology, Zoological Society of London, London NW1 4RY, UK. ; Reptile, Amphibian and Fish Conservation the Netherlands (RAVON), Post Office Box 1413, 6501 BK Nijmegen, Netherlands. ; Department of Earth Science, Environmental and Life (Di.S.T.A.V.), University of Genova, Corso Europa 26, I-16132 Genova, Italy. ; Graduate School of Human and Environmental Studies, Kyoto University, Yoshida Nihonmatsu-cho, Sakyo-ku, Kyoto 606-8501, Japan. ; Vietnam National Museum of Nature, Vietnam Academy of Science and Technology, 18 Hoang Quoc Viet, Cau Giay, Hanoi, Vietnam. ; James Cook University, One Health Research Group, School of Public Health, Tropical Medicine and Rehabilitation Sciences, Townsville, Queensland, Australia. ; Amphibian Evolution Lab, Biology Department, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussels, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25359973" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; *Chytridiomycota ; Communicable Diseases, Emerging/microbiology/*veterinary ; *Endangered Species ; Mycoses/microbiology/*veterinary ; Phylogeny ; Urodela/classification/*microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 6
    Publication Date: 2014-09-27
    Description: Monocyte differentiation into macrophages represents a cornerstone process for host defense. Concomitantly, immunological imprinting of either tolerance or trained immunity determines the functional fate of macrophages and susceptibility to secondary infections. We characterized the transcriptomes and epigenomes in four primary cell types: monocytes and in vitro-differentiated naive, tolerized, and trained macrophages. Inflammatory and metabolic pathways were modulated in macrophages, including decreased inflammasome activation, and we identified pathways functionally implicated in trained immunity. beta-glucan training elicits an exclusive epigenetic signature, revealing a complex network of enhancers and promoters. Analysis of transcription factor motifs in deoxyribonuclease I hypersensitive sites at cell-type-specific epigenetic loci unveiled differentiation and treatment-specific repertoires. Altogether, we provide a resource to understand the epigenetic changes that underlie innate immunity in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242194/" 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/PMC4242194/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saeed, Sadia -- Quintin, Jessica -- Kerstens, Hindrik H D -- Rao, Nagesha A -- Aghajanirefah, Ali -- Matarese, Filomena -- Cheng, Shih-Chin -- Ratter, Jacqueline -- Berentsen, Kim -- van der Ent, Martijn A -- Sharifi, Nilofar -- Janssen-Megens, Eva M -- Ter Huurne, Menno -- Mandoli, Amit -- van Schaik, Tom -- Ng, Aylwin -- Burden, Frances -- Downes, Kate -- Frontini, Mattia -- Kumar, Vinod -- Giamarellos-Bourboulis, Evangelos J -- Ouwehand, Willem H -- van der Meer, Jos W M -- Joosten, Leo A B -- Wijmenga, Cisca -- Martens, Joost H A -- Xavier, Ramnik J -- Logie, Colin -- Netea, Mihai G -- Stunnenberg, Hendrik G -- P30 DK043351/DK/NIDDK NIH HHS/ -- RG/09/012/28096/British Heart Foundation/United Kingdom -- New York, N.Y. -- Science. 2014 Sep 26;345(6204):1251086. doi: 10.1126/science.1251086.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Faculties of Science and Medicine, Radboud Institute for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. ; Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. ; Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard School of Medicine, Boston, MA 02114, USA. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA. ; Department of Haematology, University of Cambridge, Cambridge, UK. National Health Service, Blood and Transplant Cambridge Centre, Cambridge Biomedical Campus, Cambridge CB0 2PT, UK. ; University of Groningen, University Medical Center Groningen, Department of Genetics, Groningen, Netherlands. ; Fourth Department of Internal Medicine, University of Athens, Medical School, 1 Rimini Street, 12462 Athens, Greece. ; Department of Molecular Biology, Faculties of Science and Medicine, Radboud Institute for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. h.stunnenberg@ncmls.ru.nl mihai.netea@radboudumc.nl c.logie@ncmls.ru.nl. ; Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. h.stunnenberg@ncmls.ru.nl mihai.netea@radboudumc.nl c.logie@ncmls.ru.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25258085" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites/genetics ; Cell Differentiation/*genetics ; Deoxyribonuclease I/chemistry ; *Epigenesis, Genetic ; Genomic Imprinting ; Humans ; Immunity, Innate/*genetics ; Immunologic Memory ; Inflammasomes/genetics/immunology ; Macrophages/*cytology/immunology ; Mice ; Monocytes/*cytology/immunology ; Transcription Factors/metabolism ; beta-Glucans/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 7
    Publication Date: 2010-03-13
    Description: Mammalian epidermis consists of three self-renewing compartments: the hair follicle, the sebaceous gland, and the interfollicular epidermis. We generated knock-in alleles of murine Lgr6, a close relative of the Lgr5 stem cell gene. Lgr6 was expressed in the earliest embryonic hair placodes. In adult hair follicles, Lgr6+ cells resided in a previously uncharacterized region directly above the follicle bulge. They expressed none of the known bulge stem cell markers. Prenatal Lgr6+ cells established the hair follicle, sebaceous gland, and interfollicular epidermis. Postnatally, Lgr6+ cells generated sebaceous gland and interfollicular epidermis, whereas contribution to hair lineages gradually diminished with age. Adult Lgr6+ cells executed long-term wound repair, including the formation of new hair follicles. We conclude that Lgr6 marks the most primitive epidermal stem cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snippert, Hugo J -- Haegebarth, Andrea -- Kasper, Maria -- Jaks, Viljar -- van Es, Johan H -- Barker, Nick -- van de Wetering, Marc -- van den Born, Maaike -- Begthel, Harry -- Vries, Robert G -- Stange, Daniel E -- Toftgard, Rune -- Clevers, Hans -- New York, N.Y. -- Science. 2010 Mar 12;327(5971):1385-9. doi: 10.1126/science.1184733.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences) and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20223988" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Lineage ; Epidermis/cytology ; Gene Expression Profiling ; Gene Knock-In Techniques ; Hair/cytology/embryology/growth & development ; Hair Follicle/*cytology/embryology/growth & development ; Mice ; Mice, Nude ; Receptors, G-Protein-Coupled/*genetics/*metabolism ; Sebaceous Glands/cytology ; Signal Transduction ; Skin/*cytology ; Stem Cell Transplantation ; Stem Cells/*cytology/metabolism ; Wound Healing
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 8
    Publication Date: 2012-08-03
    Description: The concept that tumors are maintained by dedicated stem cells, the so-called cancer stem cell hypothesis, has attracted great interest but remains controversial. Studying mouse models, we provide direct, functional evidence for the presence of stem cell activity within primary intestinal adenomas, a precursor to intestinal cancer. By "lineage retracing" using the multicolor Cre-reporter R26R-Confetti, we demonstrate that the crypt stem cell marker Lgr5 (leucine-rich repeat-containing heterotrimeric guanine nucleotide-binding protein-coupled receptor 5) also marks a subpopulation of adenoma cells that fuel the growth of established intestinal adenomas. These Lgr5(+) cells, which represent about 5 to 10% of the cells in the adenomas, generate additional Lgr5(+) cells as well as all other adenoma cell types. The Lgr5(+) cells are intermingled with Paneth cells near the adenoma base, a pattern reminiscent of the architecture of the normal crypt niche.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schepers, Arnout G -- Snippert, Hugo J -- Stange, Daniel E -- van den Born, Maaike -- van Es, Johan H -- van de Wetering, Marc -- Clevers, Hans -- New York, N.Y. -- Science. 2012 Aug 10;337(6095):730-5. doi: 10.1126/science.1224676. Epub 2012 Aug 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hubrecht Institute, Koninklijke Nederlandse Akademie van Wetenschappen, and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22855427" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/genetics/metabolism/*pathology ; Animals ; Biomarkers/analysis ; Cell Lineage ; Cell Transformation, Neoplastic ; Gene Expression Profiling ; Gene Knock-In Techniques ; Genes, Reporter ; Intestinal Mucosa/metabolism/pathology ; Intestinal Neoplasms/genetics/*pathology ; Mice ; Multipotent Stem Cells/pathology/physiology ; Neoplastic Stem Cells/*pathology/*physiology ; Paneth Cells/pathology ; Receptors, G-Protein-Coupled/*analysis ; Stem Cell Niche ; Tamoxifen/pharmacology ; Tumor Stem Cell Assay
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 9
    Publication Date: 2014-09-27
    Description: Epigenetic reprogramming of myeloid cells, also known as trained immunity, confers nonspecific protection from secondary infections. Using histone modification profiles of human monocytes trained with the Candida albicans cell wall constituent beta-glucan, together with a genome-wide transcriptome, we identified the induced expression of genes involved in glucose metabolism. Trained monocytes display high glucose consumption, high lactate production, and a high ratio of nicotinamide adenine dinucleotide (NAD(+)) to its reduced form (NADH), reflecting a shift in metabolism with an increase in glycolysis dependent on the activation of mammalian target of rapamycin (mTOR) through a dectin-1-Akt-HIF-1alpha (hypoxia-inducible factor-1alpha) pathway. Inhibition of Akt, mTOR, or HIF-1alpha blocked monocyte induction of trained immunity, whereas the adenosine monophosphate-activated protein kinase activator metformin inhibited the innate immune response to fungal infection. Mice with a myeloid cell-specific defect in HIF-1alpha were unable to mount trained immunity against bacterial sepsis. Our results indicate that induction of aerobic glycolysis through an Akt-mTOR-HIF-1alpha pathway represents the metabolic basis of trained immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4226238/" 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/PMC4226238/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Shih-Chin -- Quintin, Jessica -- Cramer, Robert A -- Shepardson, Kelly M -- Saeed, Sadia -- Kumar, Vinod -- Giamarellos-Bourboulis, Evangelos J -- Martens, Joost H A -- Rao, Nagesha Appukudige -- Aghajanirefah, Ali -- Manjeri, Ganesh R -- Li, Yang -- Ifrim, Daniela C -- Arts, Rob J W -- van der Veer, Brian M J W -- Deen, Peter M T -- Logie, Colin -- O'Neill, Luke A -- Willems, Peter -- van de Veerdonk, Frank L -- van der Meer, Jos W M -- Ng, Aylwin -- Joosten, Leo A B -- Wijmenga, Cisca -- Stunnenberg, Hendrik G -- Xavier, Ramnik J -- Netea, Mihai G -- 1P30GM106394-01/GM/NIGMS NIH HHS/ -- 5P30GM103415-03/GM/NIGMS NIH HHS/ -- DK097485/DK/NIDDK NIH HHS/ -- DK43351/DK/NIDDK NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P30 GM103415/GM/NIGMS NIH HHS/ -- P30 GM106394/GM/NIGMS NIH HHS/ -- R01 AI081838/AI/NIAID NIH HHS/ -- R01 DK097485/DK/NIDDK NIH HHS/ -- R01AI81838/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 26;345(6204):1250684. doi: 10.1126/science.1250684.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. ; Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA. ; Department of Molecular Biology, Faculties of Science and Medicine, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. ; Department of Genetics, University of Groningen, University Medical Center Groningen, Groningen, Netherlands. ; 4th Department of Internal Medicine, University of Athens Medical School, 12462 Athens, Greece. ; Department of Biochemistry, Faculties of Science and Medicine, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. ; Department of Physiology, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. ; School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland. ; Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard School of Medicine, Boston, MA 02114, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. mihai.netea@radboudumc.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25258083" target="_blank"〉PubMed〈/a〉
    Keywords: Aerobiosis/immunology ; Animals ; Candida albicans/immunology ; Candidiasis/immunology/metabolism ; Disease Models, Animal ; *Epigenesis, Genetic ; Female ; Glucose/metabolism ; Glycolysis/*immunology ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics/*metabolism ; Immunity, Innate/*genetics ; Immunologic Memory/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Monocytes/*immunology/metabolism ; Sepsis/genetics/immunology/metabolism ; Staphylococcal Infections/immunology/metabolism ; Staphylococcus aureus ; TOR Serine-Threonine Kinases/genetics/*metabolism ; Transcriptome ; beta-Glucans/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 10
    Publication Date: 1999-09-18
    Description: Mutations in APC or beta-catenin inappropriately activate the transcription factor Tcf4, thereby transforming intestinal epithelial cells. Here it is shown that one of the target genes of Tcf4 in epithelial cells is Tcf1. The most abundant Tcf1 isoforms lack a beta-catenin interaction domain. Tcf1(-/-) mice develop adenomas in the gut and mammary glands. Introduction of a mutant APC allele into these mice substantially increases the number of these adenomas. Tcf1 may act as a feedback repressor of beta-catenin-Tcf4 target genes and thus may cooperate with APC to suppress malignant transformation of epithelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roose, J -- Huls, G -- van Beest, M -- Moerer, P -- van der Horn, K -- Goldschmeding, R -- Logtenberg, T -- Clevers, H -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1923-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Center for Biomedical Genetics, Department of Pathology, University Medical Center Utrecht, Post Office Box 85500, 3508 GA Utrecht, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489374" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/genetics/metabolism/pathology ; Adenomatous Polyposis Coli Protein ; Animals ; Cytoskeletal Proteins/*metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Hepatocyte Nuclear Factor 1-alpha ; Humans ; Intestinal Neoplasms/genetics/metabolism/pathology ; Lymphoid Enhancer-Binding Factor 1 ; Male ; Mammary Neoplasms, Experimental/genetics/metabolism/pathology ; Mice ; Neoplasm Proteins/metabolism ; Promoter Regions, Genetic ; T Cell Transcription Factor 1 ; TCF Transcription Factors ; *Trans-Activators ; Transcription Factor 7-Like 2 Protein ; Transcription Factors/*genetics/*metabolism ; Transfection ; Tumor Cells, Cultured ; beta Catenin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...