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  1. Article: Heterogeneous expression of the triggering receptor expressed on myeloid cells-2 on adult murine microglia.

    Schmid, Christoph D / Sautkulis, Lauren N / Danielson, Patria E / Cooper, Judith / Hasel, Karl W / Hilbush, Brian S / Sutcliffe, J Gregor / Carson, Monica J

    Journal of neurochemistry

    2002  Volume 83, Issue 6, Page(s) 1309–1320

    Abstract: Microglial activation is an early and common feature of almost all neuropathologies, including multiple sclerosis, Alzheimer's disease and mechanical injury. To better understand the relative contributions microglia make toward neurodegeneration and ... ...

    Abstract Microglial activation is an early and common feature of almost all neuropathologies, including multiple sclerosis, Alzheimer's disease and mechanical injury. To better understand the relative contributions microglia make toward neurodegeneration and neuroprotection, we used TOGA(R) to identify molecules expressed by microglia and regulated by inflammatory signals. Triggering receptor expressed on myeloid cells-2 (TREM-2) was among the mRNAs identified as being expressed by unactivated microglia, but down-regulated by lipopolysaccharide/interferon gamma. In the healthy CNS, not all microglia expressed TREM-2. Microglial expression of TREM-2 varied not only between brain regions but also within each brain region. Brain regions with an incomplete blood-brain barrier had the lowest percentages of TREM-2- expressing microglia, whereas the lateral entorhinal and cingulate cortex had the highest percentages. A novel form of TREM-2b that lacked a transmembrane domain was detected, perhaps indicating a soluble form of the protein. Taken together, these data suggest that (1) subsets of microglia are specialized to respond to defined extracellular signals; and (2) regional variations in TREM-2 expression may contribute to the varying sensitivities of different brain regions to similar pathological signals.
    MeSH term(s) Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Brain/cytology ; Brain/drug effects ; Brain/metabolism ; Cell Count ; Cells, Cultured ; Cloning, Molecular ; Down-Regulation/drug effects ; Down-Regulation/physiology ; Interferon-gamma/pharmacology ; Lipopolysaccharides/pharmacology ; Macrophages, Peritoneal/cytology ; Macrophages, Peritoneal/drug effects ; Macrophages, Peritoneal/metabolism ; Membrane Glycoproteins ; Mice ; Mice, Inbred C57BL ; Microglia/cytology ; Microglia/metabolism ; Molecular Sequence Data ; Protein Isoforms/biosynthesis ; Protein Isoforms/genetics ; Protein Structure, Tertiary/genetics ; Receptors, Immunologic/biosynthesis ; Receptors, Immunologic/genetics
    Chemical Substances Lipopolysaccharides ; Membrane Glycoproteins ; Protein Isoforms ; Receptors, Immunologic ; Trem2 protein, mouse ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2002-08-23
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1046/j.1471-4159.2002.01243.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Aberrant recombination involving the granzyme locus occurs in Atm-/- T-cell lymphomas.

    Winrow, Christopher J / Pankratz, Daniel G / Vibat, Cecile Rose T / Bowen, T J / Callahan, Marie A / Warren, Amy J / Hilbush, Brian S / Wynshaw-Boris, Anthony / Hasel, Karl W / Weaver, Zoë / Lockhart, David J / Barlow, Carrolee

    Human molecular genetics

    2005  Volume 14, Issue 18, Page(s) 2671–2684

    Abstract: Ataxia telangiectasia (A-T) is an autosomal recessive disease caused by loss of function of the serine/threonine protein kinase ATM (ataxia telangiectasia mutated). A-T patients have a 250-700-fold increased risk of developing lymphomas and leukemias ... ...

    Abstract Ataxia telangiectasia (A-T) is an autosomal recessive disease caused by loss of function of the serine/threonine protein kinase ATM (ataxia telangiectasia mutated). A-T patients have a 250-700-fold increased risk of developing lymphomas and leukemias which are typically highly invasive and proliferative. In addition, a subset of adult acute lymphoblastic leukemias and aggressive B-cell chronic lymphocytic leukemias that occur in the general population show loss of heterozygosity for ATM. To define the specific role of ATM in lymphomagenesis, we studied T-cell lymphomas isolated from mice with mutations in ATM and/or p53 using cytogenetic analysis and mRNA transcriptional profiling. The analyses identified genes misregulated as a consequence of the amplifications, deletions and translocation events arising as a result of ATM loss. A specific recurrent disruption of the granzyme gene family locus was identified resulting in an aberrant granzyme B/C fusion product. The combined application of cytogenetic and gene expression approaches identified specific loci and genes that define the pathway of initiation and progression of lymphoreticular malignancies in the absence of ATM.
    MeSH term(s) Animals ; Ataxia Telangiectasia Mutated Proteins ; Blotting, Northern ; Cell Cycle Proteins/genetics ; Cell Line, Tumor ; Computational Biology ; Cytogenetic Analysis ; DNA Primers ; DNA-Binding Proteins/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Granzymes ; In Situ Hybridization, Fluorescence ; Lymphoma, T-Cell/genetics ; Mice ; Mice, Knockout ; Microarray Analysis ; Models, Biological ; Mutation/genetics ; Protein-Serine-Threonine Kinases/genetics ; Recombination, Genetic/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Serine Endopeptidases/genetics ; Serine Endopeptidases/metabolism ; Tumor Suppressor Proteins/genetics
    Chemical Substances Cell Cycle Proteins ; DNA Primers ; DNA-Binding Proteins ; Tumor Suppressor Proteins ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Atm protein, mouse (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Granzymes (EC 3.4.21.-) ; Gzmb protein, mouse (EC 3.4.21.-) ; Gzmc protein, mouse (EC 3.4.21.-) ; Serine Endopeptidases (EC 3.4.21.-)
    Language English
    Publishing date 2005-09-15
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/ddi301
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3469: Show issues Location:
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  3. Article ; Online: Characterization of Cloned Measles Virus mRNAs by in vitro Transcription, Translation, and Immunoprecipitation

    Hasel, Karl W. / Day, Sharon / Millward, Stewart / Richardson, Christopher D. / Bellini, William J. / Greer, Peter A.

    Intervirology - International Journal of Basic and Medical Virology

    1987  Volume 28, Issue 1, Page(s) 26–39

    Abstract: A cDNA library was constructed from poly(A)+ RNA prepared from VERO cells infected with the Edmonston strain of measles virus. Clones corresponding to five major viral-specific transcripts were identified by northern blot hybridization analysis. Probes ... ...

    Abstract A cDNA library was constructed from poly(A)+ RNA prepared from VERO cells infected with the Edmonston strain of measles virus. Clones corresponding to five major viral-specific transcripts were identified by northern blot hybridization analysis. Probes prepared from these five clones detected an additional five minor viral RNA transcripts. The sizes and hydridization patterns of these minor RNA species are consistent with their being bicistronic transcripts arising from a viral genomic template with the gene order 3’. NP-P/C-M-F-HA-(L).. 5’. To assess the coding capacity of these cDNA clones they were inserted into pSP64, transcribed in vitro, the RNA was translated in reticulocyte lysates, and the protein was immunoprecipitated with specific antisera. From this analysis the genes for NP, P/C, M, F, and HA were identified. In vitro translation of natural mRNAs and SP6 transcripts of cDNAs consistently produced smaller polypeptides that appear to be initiated at internal AUGs. The relative abundance of these various cell-free translation products reflects the probability of translational initiation at the various in-frame AUGs. The patterns observed suggest that other factors besides sequences immediately flanking the AUGs have a significant effect on the selection of translational initiation sites. An increase in translational efficiency of the F transcript was achieved by removing 450 bases of the G-C-rich 5’ noncoding region.
    Keywords Measles virus ; cDNA clones ; In vitro transcription ; Immunoprecipitation ; Bicistronic mRNAs ; Gene order
    Language English
    Publisher S. Karger AG
    Publishing place Basel
    Publishing country Switzerland
    Document type Article ; Online
    ZDB-ID 184545-7
    ISSN 1423-0100 ; 0300-5526 ; 0300-5526
    ISSN (online) 1423-0100
    ISSN 0300-5526
    DOI 10.1159/000149994
    Database Karger publisher's database

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  4. Article ; Online: International network of cancer genome projects.

    Hudson, Thomas J / Anderson, Warwick / Artez, Axel / Barker, Anna D / Bell, Cindy / Bernabé, Rosa R / Bhan, M K / Calvo, Fabien / Eerola, Iiro / Gerhard, Daniela S / Guttmacher, Alan / Guyer, Mark / Hemsley, Fiona M / Jennings, Jennifer L / Kerr, David / Klatt, Peter / Kolar, Patrik / Kusada, Jun / Lane, David P /
    Laplace, Frank / Youyong, Lu / Nettekoven, Gerd / Ozenberger, Brad / Peterson, Jane / Rao, T S / Remacle, Jacques / Schafer, Alan J / Shibata, Tatsuhiro / Stratton, Michael R / Vockley, Joseph G / Watanabe, Koichi / Yang, Huanming / Yuen, Matthew M F / Knoppers, Bartha M / Bobrow, Martin / Cambon-Thomsen, Anne / Dressler, Lynn G / Dyke, Stephanie O M / Joly, Yann / Kato, Kazuto / Kennedy, Karen L / Nicolás, Pilar / Parker, Michael J / Rial-Sebbag, Emmanuelle / Romeo-Casabona, Carlos M / Shaw, Kenna M / Wallace, Susan / Wiesner, Georgia L / Zeps, Nikolajs / Lichter, Peter / Biankin, Andrew V / Chabannon, Christian / Chin, Lynda / Clément, Bruno / de Alava, Enrique / Degos, Françoise / Ferguson, Martin L / Geary, Peter / Hayes, D Neil / Johns, Amber L / Kasprzyk, Arek / Nakagawa, Hidewaki / Penny, Robert / Piris, Miguel A / Sarin, Rajiv / Scarpa, Aldo / van de Vijver, Marc / Futreal, P Andrew / Aburatani, Hiroyuki / Bayés, Mónica / Botwell, David D L / Campbell, Peter J / Estivill, Xavier / Grimmond, Sean M / Gut, Ivo / Hirst, Martin / López-Otín, Carlos / Majumder, Partha / Marra, Marco / McPherson, John D / Ning, Zemin / Puente, Xose S / Ruan, Yijun / Stunnenberg, Hendrik G / Swerdlow, Harold / Velculescu, Victor E / Wilson, Richard K / Xue, Hong H / Yang, Liu / Spellman, Paul T / Bader, Gary D / Boutros, Paul C / Flicek, Paul / Getz, Gad / Guigó, Roderic / Guo, Guangwu / Haussler, David / Heath, Simon / Hubbard, Tim J / Jiang, Tao / Jones, Steven M / Li, Qibin / López-Bigas, Nuria / Luo, Ruibang / Muthuswamy, Lakshmi / Ouellette, B F Francis / Pearson, John V / Quesada, Victor / Raphael, Benjamin J / Sander, Chris / Speed, Terence P / Stein, Lincoln D / Stuart, Joshua M / Teague, Jon W / Totoki, Yasushi / Tsunoda, Tatsuhiko / Valencia, Alfonso / Wheeler, David A / Wu, Honglong / Zhao, Shancen / Zhou, Guangyu / Lathrop, Mark / Thomas, Gilles / Yoshida, Teruhiko / Axton, Myles / Gunter, Chris / Miller, Linda J / Zhang, Junjun / Haider, Syed A / Wang, Jianxin / Yung, Christina K / Cros, Anthony / Cross, Anthony / Liang, Yong / Gnaneshan, Saravanamuttu / Guberman, Jonathan / Hsu, Jack / Chalmers, Don R C / Hasel, Karl W / Kaan, Terry S H / Lowrance, William W / Masui, Tohru / Rodriguez, Laura Lyman / Vergely, Catherine / Bowtell, David D L / Cloonan, Nicole / deFazio, Anna / Eshleman, James R / Etemadmoghadam, Dariush / Gardiner, Brooke B / Gardiner, Brooke A / Kench, James G / Sutherland, Robert L / Tempero, Margaret A / Waddell, Nicola J / Wilson, Peter J / Gallinger, Steve / Tsao, Ming-Sound / Shaw, Patricia A / Petersen, Gloria M / Mukhopadhyay, Debabrata / DePinho, Ronald A / Thayer, Sarah / Shazand, Kamran / Beck, Timothy / Sam, Michelle / Timms, Lee / Ballin, Vanessa / Lu, Youyong / Ji, Jiafu / Zhang, Xiuqing / Chen, Feng / Hu, Xueda / Yang, Qi / Tian, Geng / Zhang, Lianhai / Xing, Xiaofang / Li, Xianghong / Zhu, Zhenggang / Yu, Yingyan / Yu, Jun / Tost, Jörg / Brennan, Paul / Holcatova, Ivana / Zaridze, David / Brazma, Alvis / Egevard, Lars / Prokhortchouk, Egor / Banks, Rosamonde Elizabeth / Uhlén, Mathias / Viksna, Juris / Ponten, Fredrik / Skryabin, Konstantin / Birney, Ewan / Borg, Ake / Børresen-Dale, Anne-Lise / Caldas, Carlos / Foekens, John A / Martin, Sancha / Reis-Filho, Jorge S / Richardson, Andrea L / Sotiriou, Christos / Thoms, Giles / van't Veer, Laura / Birnbaum, Daniel / Blanche, Hélène / Boucher, Pascal / Boyault, Sandrine / Masson-Jacquemier, Jocelyne D / Pauporté, Iris / Pivot, Xavier / Vincent-Salomon, Anne / Tabone, Eric / Theillet, Charles / Treilleux, Isabelle / Bioulac-Sage, Paulette / Decaens, Thomas / Franco, Dominique / Gut, Marta / Samuel, Didier / Zucman-Rossi, Jessica / Eils, Roland / Brors, Benedikt / Korbel, Jan O / Korshunov, Andrey / Landgraf, Pablo / Lehrach, Hans / Pfister, Stefan / Radlwimmer, Bernhard / Reifenberger, Guido / Taylor, Michael D / von Kalle, Christof / Majumder, Partha P / Pederzoli, Paolo / Lawlor, Rita A / Delledonne, Massimo / Bardelli, Alberto / Gress, Thomas / Klimstra, David / Zamboni, Giuseppe / Nakamura, Yusuke / Miyano, Satoru / Fujimoto, Akihiro / Campo, Elias / de Sanjosé, Silvia / Montserrat, Emili / González-Díaz, Marcos / Jares, Pedro / Himmelbauer, Heinz / Himmelbaue, Heinz / Bea, Silvia / Aparicio, Samuel / Easton, Douglas F / Collins, Francis S / Compton, Carolyn C / Lander, Eric S / Burke, Wylie / Green, Anthony R / Hamilton, Stanley R / Kallioniemi, Olli P / Ley, Timothy J / Liu, Edison T / Wainwright, Brandon J

    Nature

    2010  Volume 464, Issue 7291, Page(s) 993–998

    Abstract: The International Cancer Genome Consortium (ICGC) was launched to coordinate large-scale cancer genome studies in tumours from 50 different cancer types and/or subtypes that are of clinical and societal importance across the globe. Systematic studies of ... ...

    Abstract The International Cancer Genome Consortium (ICGC) was launched to coordinate large-scale cancer genome studies in tumours from 50 different cancer types and/or subtypes that are of clinical and societal importance across the globe. Systematic studies of more than 25,000 cancer genomes at the genomic, epigenomic and transcriptomic levels will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies.
    MeSH term(s) DNA Methylation ; DNA Mutational Analysis/trends ; Databases, Genetic ; Genes, Neoplasm/genetics ; Genetics, Medical/organization & administration ; Genetics, Medical/trends ; Genome, Human/genetics ; Genomics/organization & administration ; Genomics/trends ; Humans ; Intellectual Property ; International Cooperation ; Mutation ; Neoplasms/classification ; Neoplasms/genetics ; Neoplasms/pathology ; Neoplasms/therapy
    Language English
    Publishing date 2010-02-24
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/nature08987
    Database MEDical Literature Analysis and Retrieval System OnLINE

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