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  • 1
    Publication Date: 2014-10-18
    Description: T cells that mediate autoimmune diseases such as rheumatoid arthritis (RA) are difficult to characterize because they are likely to be deleted or inactivated in the thymus if the self antigens they recognize are ubiquitously expressed. One way to obtain and analyze these autoimmune T cells is to alter T cell receptor (TCR) signaling in developing T cells to change their sensitivity to thymic negative selection, thereby allowing their thymic production. From mice thus engineered to generate T cells mediating autoimmune arthritis, we isolated arthritogenic TCRs and characterized the self antigens they recognized. One of them was the ubiquitously expressed 60S ribosomal protein L23a (RPL23A), with which T cells and autoantibodies from RA patients reacted. This strategy may improve our understanding of the underlying drivers of autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Yoshinaga -- Hashimoto, Motomu -- Hirota, Keiji -- Ohkura, Naganari -- Morikawa, Hiromasa -- Nishikawa, Hiroyoshi -- Tanaka, Atsushi -- Furu, Moritoshi -- Ito, Hiromu -- Fujii, Takao -- Nomura, Takashi -- Yamazaki, Sayuri -- Morita, Akimichi -- Vignali, Dario A A -- Kappler, John W -- Matsuda, Shuichi -- Mimori, Tsuneyo -- Sakaguchi, Noriko -- Sakaguchi, Shimon -- R01 DK089125/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):363-8. doi: 10.1126/science.1259077.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. ; Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. Department of the Control for Rheumatic Diseases, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. ; Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. ; Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. Department of Frontier Research in Tumor Immunology, Center of Medical Innovation and Translational Research, Osaka University, Osaka 565-0871, Japan. ; Department of the Control for Rheumatic Diseases, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. Department of Orthopaedic Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. ; Department of the Control for Rheumatic Diseases, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. ; Department of Geriatric and Environmental Dermatology, Graduate School of Medical Sciences, Nagoya City University, Nagoya 467-8601, Japan. ; Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA. ; Integrated Department of Immunology, National Jewish Health, Denver, CO 80206, USA. Howard Hughes Medical Institute, National Jewish Health, Denver, CO 80206, USA. ; Department of Orthopaedic Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. ; Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan. ; Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita 565-0871, Japan. Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Tokyo 102-0075, Japan. shimon@ifrec.osaka-u.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324392" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/genetics/*immunology ; Autoantigens/*immunology ; Autoimmunity/*immunology ; DNA-Binding Proteins/genetics ; Gene Expression Regulation ; Genes, T-Cell Receptor beta ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Mutant Strains ; Receptors, Antigen, T-Cell/*immunology ; Ribosomal Proteins/genetics/*immunology ; T-Lymphocytes/*immunology
    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
    Publication Date: 2000-02-26
    Description: Because of a critical shortage in suitable organs, many patients with terminal liver disease die each year before liver transplantation can be performed. Transplantation of isolated hepatocytes has been proposed for the temporary metabolic support of patients awaiting liver transplantation or spontaneous reversion of their liver disease. A major limitation of this form of therapy is the present inability to isolate an adequate number of transplantable hepatocytes. A highly differentiated cell line, NKNT-3, was generated by retroviral transfer in normal primary adult human hepatocytes of an immortalizing gene that can be subsequently and completely excised by Cre/Lox site-specific recombination. When transplanted into the spleen of rats under transient immunosuppression, reversibly immortalized NKNT-3 cells provided life-saving metabolic support during acute liver failure induced by 90% hepatectomy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, N -- Fujiwara, T -- Westerman, K A -- Inoue, Y -- Sakaguchi, M -- Noguchi, H -- Miyazaki, M -- Cai, J -- Tanaka, N -- Fox, I J -- Leboulch, P -- DK48794/DK/NIDDK NIH HHS/ -- HL55435/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Feb 18;287(5456):1258-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉First Department of Surgery and Department of Cell Biology, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10678831" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Antigens, Polyomavirus Transforming/genetics ; Cell Culture Techniques/*methods ; Cell Differentiation ; Cell Line ; *Cell Transplantation ; Gene Expression ; Genetic Vectors ; Hepatectomy ; Humans ; Integrases/metabolism ; Liver/*cytology/metabolism/pathology ; Liver Failure, Acute/metabolism/pathology/*prevention & control/therapy ; Liver Regeneration ; Mice ; Mice, SCID ; Rats ; Retroviridae/genetics ; Spleen/cytology ; Transfection ; *Viral Proteins
    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
    Publication Date: 1992-09-25
    Description: Observation of filamentous actin (F-actin) in living cells is currently limited to the resolution of the light microscope. Higher resolution procedures require sample fixation and preclude dynamic studies. The atomic force microscope (AFM) can image and manipulate samples at very high, sometimes atomic resolution by scanning a fine tip over the surface of interest and detecting physical interactions between the tip and sample. This study demonstrates that F-actin can be readily resolved in living cells with the AFM and that the dynamic properties of F-actin are easily observed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henderson, E -- Haydon, P G -- Sakaguchi, D S -- New York, N.Y. -- Science. 1992 Sep 25;257(5078):1944-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology and Genetics, Iowa State University, Ames 50011.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411511" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*ultrastructure ; Actins/*physiology ; Animals ; *Cell Movement ; Cells, Cultured ; In Vitro Techniques ; Membrane Fluidity ; Microscopy/*methods ; Neuroglia/*ultrastructure ; Xenopus laevis
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2007-08-04
    Description: Much progress has been made in understanding how the immune system is regulated, with a great deal of recent interest in naturally occurring CD4+ regulatory T cells that actively engage in the maintenance of immunological self-tolerance and immune homeostasis. The challenge ahead for immunologists is the further elucidation of the molecular and cellular processes that govern the development and function of these cells. From this, exciting possibilities are emerging for the manipulation of regulatory T cell pathways in treating immunological diseases and suppressing or augmenting physiological immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sakaguchi, Shimon -- Powrie, Fiona -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):627-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17673654" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens/immunology ; Autoimmune Diseases/immunology ; Forkhead Transcription Factors/metabolism ; Homeostasis ; Humans ; Immune Tolerance ; Infection/immunology ; Inflammation/immunology ; Lymphocyte Activation ; Mice ; Self Tolerance ; T-Lymphocytes/immunology ; T-Lymphocytes, Regulatory/*immunology/physiology
    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
    Publication Date: 2008-10-11
    Description: Naturally occurring Foxp3+CD4+ regulatory T cells (Tregs) are essential for maintaining immunological self-tolerance and immune homeostasis. Here, we show that a specific deficiency of cytotoxic T lymphocyte antigen 4 (CTLA-4) in Tregs results in spontaneous development of systemic lymphoproliferation, fatal T cell-mediated autoimmune disease, and hyperproduction of immunoglobulin E in mice, and it also produces potent tumor immunity. Treg-specific CTLA-4 deficiency impairs in vivo and in vitro suppressive function of Tregs-in particular, Treg-mediated down-regulation of CD80 and CD86 expression on dendritic cells. Thus, natural Tregs may critically require CTLA-4 to suppress immune responses by affecting the potency of antigen-presenting cells to activate other T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wing, Kajsa -- Onishi, Yasushi -- Prieto-Martin, Paz -- Yamaguchi, Tomoyuki -- Miyara, Makoto -- Fehervari, Zoltan -- Nomura, Takashi -- Sakaguchi, Shimon -- New York, N.Y. -- Science. 2008 Oct 10;322(5899):271-5. doi: 10.1126/science.1160062.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18845758" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Antigens, CD/genetics/immunology/*metabolism ; Antigens, CD80/metabolism ; Antigens, CD86/metabolism ; Autoimmune Diseases/immunology ; *Autoimmunity ; CD8-Positive T-Lymphocytes/immunology ; CTLA-4 Antigen ; Dendritic Cells/immunology ; Down-Regulation ; Female ; Forkhead Transcription Factors/genetics/metabolism ; *Immune Tolerance ; Immunoglobulin E/blood ; Immunoglobulin G/blood ; Leukemia/immunology ; Lymphocyte Activation ; Lymphocytes/immunology ; Male ; Mice ; Mice, Inbred BALB C ; T-Lymphocytes, Regulatory/*immunology
    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
    Publication Date: 2003-01-11
    Description: Regulatory T cells engage in the maintenance of immunological self-tolerance by actively suppressing self-reactive lymphocytes. Little is known, however, about the molecular mechanism of their development. Here we show that Foxp3, which encodes a transcription factor that is genetically defective in an autoimmune and inflammatory syndrome in humans and mice, is specifically expressed in naturally arising CD4+ regulatory T cells. Furthermore, retroviral gene transfer of Foxp3 converts naive T cells toward a regulatory T cell phenotype similar to that of naturally occurring CD4+ regulatory T cells. Thus, Foxp3 is a key regulatory gene for the development of regulatory T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hori, Shohei -- Nomura, Takashi -- Sakaguchi, Shimon -- New York, N.Y. -- Science. 2003 Feb 14;299(5609):1057-61. Epub 2003 Jan 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunopathology, Research Center for Allergy and Immunology, Institute for Physical and Chemical Research, Yokohama 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/analysis ; Autoimmune Diseases/immunology/prevention & control ; CD4-Positive T-Lymphocytes/immunology ; Cytokines/biosynthesis ; DNA-Binding Proteins/genetics/*metabolism ; Forkhead Transcription Factors ; Gastritis/immunology/prevention & control ; *Immune Tolerance ; Inflammatory Bowel Diseases/immunology/prevention & control ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Mice, Transgenic ; Mutation ; Receptors, Antigen, T-Cell/immunology ; Receptors, Interleukin-2/analysis ; Recombinant Fusion Proteins/metabolism ; Self Tolerance ; T-Lymphocyte Subsets/cytology/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes, Regulatory/*immunology/*metabolism ; Thymus Gland/cytology/metabolism ; Transduction, Genetic
    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
    Publication Date: 2013-07-12
    Description: Manipulation of the gut microbiota holds great promise for the treatment of inflammatory and allergic diseases. Although numerous probiotic microorganisms have been identified, there remains a compelling need to discover organisms that elicit more robust therapeutic responses, are compatible with the host, and can affect a specific arm of the host immune system in a well-controlled, physiological manner. Here we use a rational approach to isolate CD4(+)FOXP3(+) regulatory T (Treg)-cell-inducing bacterial strains from the human indigenous microbiota. Starting with a healthy human faecal sample, a sequence of selection steps was applied to obtain mice colonized with human microbiota enriched in Treg-cell-inducing species. From these mice, we isolated and selected 17 strains of bacteria on the basis of their high potency in enhancing Treg cell abundance and inducing important anti-inflammatory molecules--including interleukin-10 (IL-) and inducible T-cell co-stimulator (ICOS)--in Treg cells upon inoculation into germ-free mice. Genome sequencing revealed that the 17 strains fall within clusters IV, XIVa and XVIII of Clostridia, which lack prominent toxins and virulence factors. The 17 strains act as a community to provide bacterial antigens and a TGF-beta-rich environment to help expansion and differentiation of Treg cells. Oral administration of the combination of 17 strains to adult mice attenuated disease in models of colitis and allergic diarrhoea. Use of the isolated strains may allow for tailored therapeutic manipulation of human immune disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atarashi, Koji -- Tanoue, Takeshi -- Oshima, Kenshiro -- Suda, Wataru -- Nagano, Yuji -- Nishikawa, Hiroyoshi -- Fukuda, Shinji -- Saito, Takuro -- Narushima, Seiko -- Hase, Koji -- Kim, Sangwan -- Fritz, Joelle V -- Wilmes, Paul -- Ueha, Satoshi -- Matsushima, Kouji -- Ohno, Hiroshi -- Olle, Bernat -- Sakaguchi, Shimon -- Taniguchi, Tadatsugu -- Morita, Hidetoshi -- Hattori, Masahira -- Honda, Kenya -- England -- Nature. 2013 Aug 8;500(7461):232-6. doi: 10.1038/nature12331. Epub 2013 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN Center for Integrative Medical Sciences (IMS-RCAI), 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23842501" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cell Proliferation ; Clostridium/classification/genetics/*immunology ; Colitis/microbiology/pathology ; Colon/immunology/microbiology ; Disease Models, Animal ; Feces/microbiology ; Germ-Free Life ; Humans ; Inducible T-Cell Co-Stimulator Protein/metabolism ; Interleukin-10/metabolism ; Male ; Metagenome/genetics/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, SCID ; RNA, Ribosomal, 16S/genetics ; Rats ; Rats, Inbred F344 ; T-Lymphocytes, Regulatory/cytology/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2014-03-29
    Description: Regulated transcription controls the diversity, developmental pathways and spatial organization of the hundreds of cell types that make up a mammal. Using single-molecule cDNA sequencing, we mapped transcription start sites (TSSs) and their usage in human and mouse primary cells, cell lines and tissues to produce a comprehensive overview of mammalian gene expression across the human body. We find that few genes are truly 'housekeeping', whereas many mammalian promoters are composite entities composed of several closely separated TSSs, with independent cell-type-specific expression profiles. TSSs specific to different cell types evolve at different rates, whereas promoters of broadly expressed genes are the most conserved. Promoter-based expression analysis reveals key transcription factors defining cell states and links them to binding-site motifs. The functions of identified novel transcripts can be predicted by coexpression and sample ontology enrichment analyses. The functional annotation of the mammalian genome 5 (FANTOM5) project provides comprehensive expression profiles and functional annotation of mammalian cell-type-specific transcriptomes with wide applications in biomedical research.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4529748/" 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/PMC4529748/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉FANTOM Consortium and the RIKEN PMI and CLST (DGT) -- Forrest, Alistair R R -- Kawaji, Hideya -- Rehli, Michael -- Baillie, J Kenneth -- de Hoon, Michiel J L -- Haberle, Vanja -- Lassmann, Timo -- Kulakovskiy, Ivan V -- Lizio, Marina -- Itoh, Masayoshi -- Andersson, Robin -- Mungall, Christopher J -- Meehan, Terrence F -- Schmeier, Sebastian -- Bertin, Nicolas -- Jorgensen, Mette -- Dimont, Emmanuel -- Arner, Erik -- Schmidl, Christian -- Schaefer, Ulf -- Medvedeva, Yulia A -- Plessy, Charles -- Vitezic, Morana -- Severin, Jessica -- Semple, Colin A -- Ishizu, Yuri -- Young, Robert S -- Francescatto, Margherita -- Alam, Intikhab -- Albanese, Davide -- Altschuler, Gabriel M -- Arakawa, Takahiro -- Archer, John A C -- Arner, Peter -- Babina, Magda -- Rennie, Sarah -- Balwierz, Piotr J -- Beckhouse, Anthony G -- Pradhan-Bhatt, Swati -- Blake, Judith A -- Blumenthal, Antje -- Bodega, Beatrice -- Bonetti, Alessandro -- Briggs, James -- Brombacher, Frank -- Burroughs, A Maxwell -- Califano, Andrea -- Cannistraci, Carlo V -- Carbajo, Daniel -- Chen, Yun -- Chierici, Marco -- Ciani, Yari -- Clevers, Hans C -- Dalla, Emiliano -- Davis, Carrie A -- Detmar, Michael -- Diehl, Alexander D -- Dohi, Taeko -- Drablos, Finn -- Edge, Albert S B -- Edinger, Matthias -- Ekwall, Karl -- Endoh, Mitsuhiro -- Enomoto, Hideki -- Fagiolini, Michela -- Fairbairn, Lynsey -- Fang, Hai -- Farach-Carson, Mary C -- Faulkner, Geoffrey J -- Favorov, Alexander V -- Fisher, Malcolm E -- Frith, Martin C -- Fujita, Rie -- Fukuda, Shiro -- Furlanello, Cesare -- Furino, Masaaki -- Furusawa, Jun-ichi -- Geijtenbeek, Teunis B -- Gibson, Andrew P -- Gingeras, Thomas -- Goldowitz, Daniel -- Gough, Julian -- Guhl, Sven -- Guler, Reto -- Gustincich, Stefano -- Ha, Thomas J -- Hamaguchi, Masahide -- Hara, Mitsuko -- Harbers, Matthias -- Harshbarger, Jayson -- Hasegawa, Akira -- Hasegawa, Yuki -- Hashimoto, Takehiro -- Herlyn, Meenhard -- Hitchens, Kelly J -- Ho Sui, Shannan J -- Hofmann, Oliver M -- Hoof, Ilka -- Hori, Furni -- Huminiecki, Lukasz -- Iida, Kei -- Ikawa, Tomokatsu -- Jankovic, Boris R -- Jia, Hui -- Joshi, Anagha -- Jurman, Giuseppe -- Kaczkowski, Bogumil -- Kai, Chieko -- Kaida, Kaoru -- Kaiho, Ai -- Kajiyama, Kazuhiro -- Kanamori-Katayama, Mutsumi -- Kasianov, Artem S -- Kasukawa, Takeya -- Katayama, Shintaro -- Kato, Sachi -- Kawaguchi, Shuji -- Kawamoto, Hiroshi -- Kawamura, Yuki I -- Kawashima, Tsugumi -- Kempfle, Judith S -- Kenna, Tony J -- Kere, Juha -- Khachigian, Levon M -- Kitamura, Toshio -- Klinken, S Peter -- Knox, Alan J -- Kojima, Miki -- Kojima, Soichi -- Kondo, Naoto -- Koseki, Haruhiko -- Koyasu, Shigeo -- Krampitz, Sarah -- Kubosaki, Atsutaka -- Kwon, Andrew T -- Laros, Jeroen F J -- Lee, Weonju -- Lennartsson, Andreas -- Li, Kang -- Lilje, Berit -- Lipovich, Leonard -- Mackay-Sim, Alan -- Manabe, Ri-ichiroh -- Mar, Jessica C -- Marchand, Benoit -- Mathelier, Anthony -- Mejhert, Niklas -- Meynert, Alison -- Mizuno, Yosuke -- de Lima Morais, David A -- Morikawa, Hiromasa -- Morimoto, Mitsuru -- Moro, Kazuyo -- Motakis, Efthymios -- Motohashi, Hozumi -- Mummery, Christine L -- Murata, Mitsuyoshi -- Nagao-Sato, Sayaka -- Nakachi, Yutaka -- Nakahara, Fumio -- Nakamura, Toshiyuki -- Nakamura, Yukio -- Nakazato, Kenichi -- van Nimwegen, Erik -- Ninomiya, Noriko -- Nishiyori, Hiromi -- Noma, Shohei -- Noazaki, Tadasuke -- Ogishima, Soichi -- Ohkura, Naganari -- Ohimiya, Hiroko -- Ohno, Hiroshi -- Ohshima, Mitsuhiro -- Okada-Hatakeyama, Mariko -- Okazaki, Yasushi -- Orlando, Valerio -- Ovchinnikov, Dmitry A -- Pain, Arnab -- Passier, Robert -- Patrikakis, Margaret -- Persson, Helena -- Piazza, Silvano -- Prendergast, James G D -- Rackham, Owen J L -- Ramilowski, Jordan A -- Rashid, Mamoon -- Ravasi, Timothy -- Rizzu, Patrizia -- Roncador, Marco -- Roy, Sugata -- Rye, Morten B -- Saijyo, Eri -- Sajantila, Antti -- Saka, Akiko -- Sakaguchi, Shimon -- Sakai, Mizuho -- Sato, Hiroki -- Savvi, Suzana -- Saxena, Alka -- Schneider, Claudio -- Schultes, Erik A -- Schulze-Tanzil, Gundula G -- Schwegmann, Anita -- Sengstag, Thierry -- Sheng, Guojun -- Shimoji, Hisashi -- Shimoni, Yishai -- Shin, Jay W -- Simon, Christophe -- Sugiyama, Daisuke -- Sugiyama, Takaai -- Suzuki, Masanori -- Suzuki, Naoko -- Swoboda, Rolf K -- 't Hoen, Peter A C -- Tagami, Michihira -- Takahashi, Naoko -- Takai, Jun -- Tanaka, Hiroshi -- Tatsukawa, Hideki -- Tatum, Zuotian -- Thompson, Mark -- Toyodo, Hiroo -- Toyoda, Tetsuro -- Valen, Elvind -- van de Wetering, Marc -- van den Berg, Linda M -- Verado, Roberto -- Vijayan, Dipti -- Vorontsov, Ilya E -- Wasserman, Wyeth W -- Watanabe, Shoko -- Wells, Christine A -- Winteringham, Louise N -- Wolvetang, Ernst -- Wood, Emily J -- Yamaguchi, Yoko -- Yamamoto, Masayuki -- Yoneda, Misako -- Yonekura, Yohei -- Yoshida, Shigehiro -- Zabierowski, Susan E -- Zhang, Peter G -- Zhao, Xiaobei -- Zucchelli, Silvia -- Summers, Kim M -- Suzuki, Harukazu -- Daub, Carsten O -- Kawai, Jun -- Heutink, Peter -- Hide, Winston -- Freeman, Tom C -- Lenhard, Boris -- Bajic, Vladimir B -- Taylor, Martin S -- Makeev, Vsevolod J -- Sandelin, Albin -- Hume, David A -- Carninci, Piero -- Hayashizaki, Yoshihide -- BB/F003722/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G022771/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/I001107/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- MC_PC_U127597124/Medical Research Council/United Kingdom -- MC_UP_1102/1/Medical Research Council/United Kingdom -- R01 DE022969/DE/NIDCR NIH HHS/ -- R01 GM084875/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Mar 27;507(7493):462-70. doi: 10.1038/nature13182.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670764" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Atlases as Topic ; Cell Line ; Cells, Cultured ; Cluster Analysis ; Conserved Sequence/genetics ; Gene Expression Regulation/genetics ; Gene Regulatory Networks/genetics ; Genes, Essential/genetics ; Genome/genetics ; Humans ; Mice ; *Molecular Sequence Annotation ; Open Reading Frames/genetics ; Organ Specificity ; Promoter Regions, Genetic/*genetics ; RNA, Messenger/analysis/genetics ; Transcription Factors/metabolism ; Transcription Initiation Site ; Transcription, Genetic/genetics ; Transcriptome/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 1996-08-02
    Description: Subtype 2 of the metabotropic glutamate receptor (mGluR2) is expressed in the presynaptic elements of hippocampal mossy fiber-CA3 synapses. Knockout mice deficient in mGluR2 showed no histological changes and no alterations in basal synaptic transmission, paired-pulse facilitation, or tetanus-induced long-term potentiation (LTP) at the mossy fiber-CA3 synapses. Long-term depression (LTD) induced by low-frequency stimulation, however, was almost fully abolished. The mutant mice performed normally in water maze learning tasks. Thus, the presynaptic mGluR2 is essential for inducing LTD at the mossy fiber-CA3 synapses, but this hippocampal LTD does not seem to be required for spatial learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yokoi, M -- Kobayashi, K -- Manabe, T -- Takahashi, T -- Sakaguchi, I -- Katsuura, G -- Shigemoto, R -- Ohishi, H -- Nomura, S -- Nakamura, K -- Nakao, K -- Katsuki, M -- Nakanishi, S -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):645-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Kyoto University Faculty of Medicine, Kyoto 606, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662555" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cyclopropanes/pharmacology ; Electric Stimulation ; Gene Targeting ; Glycine/analogs & derivatives/pharmacology ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Long-Term Potentiation ; Maze Learning ; Mice ; Mice, Knockout ; *Neuronal Plasticity ; Pyramidal Cells/*physiology ; Receptors, Metabotropic Glutamate/genetics/*physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/drug effects/*physiology ; Synaptic Transmission/drug effects
    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
    Publication Date: 1992-06-26
    Description: Between 650 and 2000 different peptides are associated with the major histocompatibility complex class II molecule I-Ad. Sequences for nine of these were obtained by a combination of automated Edman degradation and tandem mass spectrometry. All of the peptides are derived from secretory or integral membrane proteins that are synthesized by the antigen-presenting cell itself. Peptides were 16 to 18 residues long, had ragged NH2-and COOH-termini, and contained a six-residue binding motif that was variably placed within the peptide chain. Binding data on truncated peptides suggest that the peptide binding groove on class II molecules can be open at both ends.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hunt, D F -- Michel, H -- Dickinson, T A -- Shabanowitz, J -- Cox, A L -- Sakaguchi, K -- Appella, E -- Grey, H M -- Sette, A -- AI18634/AI/NIAID NIH HHS/ -- GM37357/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1817-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Virginia, Charlottesville 22901.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1319610" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/chemistry ; Chromatography, High Pressure Liquid ; Histocompatibility Antigens Class II/*immunology ; Mass Spectrometry ; Membrane Proteins/*genetics ; Mice ; Molecular Sequence Data ; Sequence Homology, 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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