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  • Humans  (6)
  • American Association for the Advancement of Science (AAAS)  (6)
  • Elsevier
  • Oxford University Press
  • Springer
  • 2005-2009  (3)
  • 1990-1994  (3)
  • 2005  (3)
  • 1991  (3)
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Verlag/Herausgeber
  • American Association for the Advancement of Science (AAAS)  (6)
  • Elsevier
  • Oxford University Press
  • Springer
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  • 2005-2009  (3)
  • 1990-1994  (3)
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  • 1
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1991-03-29
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nunn, P B -- Davis, A J -- O'Brien, P -- New York, N.Y. -- Science. 1991 Mar 29;251(5001):1619-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1859531" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acids/chemistry/*toxicity ; Animals ; *Carbamates ; Cysteine/chemistry ; Humans ; Kinetics ; Molecular Conformation ; N-Methylaspartate/chemistry ; *Neurotoxins
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 1991-02-15
    Beschreibung: The myoD gene converts many differentiated cell types into muscle. MyoD is a member of the basic-helix-loop-helix family of proteins; this 68-amino acid domain in MyoD is necessary and sufficient for myogenesis. MyoD binds cooperatively to muscle-specific enhancers and activates transcription. The helix-loop-helix motif is responsible for dimerization, and, depending on its dimerization partner, MyoD activity can be controlled. MyoD senses and integrates many facets of cell state. MyoD is expressed only in skeletal muscle and its precursors; in nonmuscle cells myoD is repressed by specific genes. MyoD activates its own transcription; this may stabilize commitment to myogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weintraub, H -- Davis, R -- Tapscott, S -- Thayer, M -- Krause, M -- Benezra, R -- Blackwell, T K -- Turner, D -- Rupp, R -- Hollenberg, S -- New York, N.Y. -- Science. 1991 Feb 15;251(4995):761-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1846704" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Differentiation/genetics ; DNA-Binding Proteins/*genetics/physiology ; Gene Expression Regulation ; *Genes, Regulator ; Humans ; Multigene Family ; Muscle Proteins/*genetics/physiology ; Muscles/*cytology/embryology ; MyoD Protein
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Publikationsdatum: 1991-07-05
    Beschreibung: Although neurotrophic factors were originally isolated on the basis of their ability to support the survival of neurons, these molecules are now thought to influence many aspects of the development and maintenance of the nervous system. Identifying the receptors for these neurotrophic factors should aid in identifying the cells on which these factors act and in understanding their precise mechanisms of action. A "tagged-ligand panning" procedure was used to clone a receptor for ciliary neurotrophic factor (CNTF). This receptor is expressed exclusively within the nervous system and skeletal muscle. The CNTF receptor has a structure unrelated to the receptors utilized by the nerve growth factor family of neurotrophic molecules, but instead is most homologous to the receptor for a cytokine, interleukin-6. This similarity suggestes that the CNTF receptor, like the interleukin-6 receptor, requires a second, signal-transducing component. In contrast to all known receptors, the CNTF receptor is anchored to cell membranes by a glycosyl-phosphatidylinositol linkage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S -- Aldrich, T H -- Valenzuela, D M -- Wong, V V -- Furth, M E -- Squinto, S P -- Yancopoulos, G D -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):59-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals, Inc., Tarrytown, NY 10591.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1648265" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Base Sequence ; Blotting, Northern ; Cell Line ; Cloning, Molecular ; Electrophoresis, Agar Gel ; Gene Expression ; Humans ; In Vitro Techniques ; Molecular Sequence Data ; Muscles/metabolism ; Nervous System/metabolism ; Neuroblastoma/metabolism ; Rats ; Receptor, Ciliary Neurotrophic Factor ; Receptors, Cell Surface/blood/*genetics ; Sequence Homology, Nucleic Acid ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    Publikationsdatum: 2005-09-06
    Beschreibung: This study describes comprehensive polling of transcription start and termination sites and analysis of previously unidentified full-length complementary DNAs derived from the mouse genome. We identify the 5' and 3' boundaries of 181,047 transcripts with extensive variation in transcripts arising from alternative promoter usage, splicing, and polyadenylation. There are 16,247 new mouse protein-coding transcripts, including 5154 encoding previously unidentified proteins. Genomic mapping of the transcriptome reveals transcriptional forests, with overlapping transcription on both strands, separated by deserts in which few transcripts are observed. The data provide a comprehensive platform for the comparative analysis of mammalian transcriptional regulation in differentiation and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carninci, P -- Kasukawa, T -- Katayama, S -- Gough, J -- Frith, M C -- Maeda, N -- Oyama, R -- Ravasi, T -- Lenhard, B -- Wells, C -- Kodzius, R -- Shimokawa, K -- Bajic, V B -- Brenner, S E -- Batalov, S -- Forrest, A R R -- Zavolan, M -- Davis, M J -- Wilming, L G -- Aidinis, V -- Allen, J E -- Ambesi-Impiombato, A -- Apweiler, R -- Aturaliya, R N -- Bailey, T L -- Bansal, M -- Baxter, L -- Beisel, K W -- Bersano, T -- Bono, H -- Chalk, A M -- Chiu, K P -- Choudhary, V -- Christoffels, A -- Clutterbuck, D R -- Crowe, M L -- Dalla, E -- Dalrymple, B P -- de Bono, B -- Della Gatta, G -- di Bernardo, D -- Down, T -- Engstrom, P -- Fagiolini, M -- Faulkner, G -- Fletcher, C F -- Fukushima, T -- Furuno, M -- Futaki, S -- Gariboldi, M -- Georgii-Hemming, P -- Gingeras, T R -- Gojobori, T -- Green, R E -- Gustincich, S -- Harbers, M -- Hayashi, Y -- Hensch, T K -- Hirokawa, N -- Hill, D -- Huminiecki, L -- Iacono, M -- Ikeo, K -- Iwama, A -- Ishikawa, T -- Jakt, M -- Kanapin, A -- Katoh, M -- Kawasawa, Y -- Kelso, J -- Kitamura, H -- Kitano, H -- Kollias, G -- Krishnan, S P T -- Kruger, A -- Kummerfeld, S K -- Kurochkin, I V -- Lareau, L F -- Lazarevic, D -- Lipovich, L -- Liu, J -- Liuni, S -- McWilliam, S -- Madan Babu, M -- Madera, M -- Marchionni, L -- Matsuda, H -- Matsuzawa, S -- Miki, H -- Mignone, F -- Miyake, S -- Morris, K -- Mottagui-Tabar, S -- Mulder, N -- Nakano, N -- Nakauchi, H -- Ng, P -- Nilsson, R -- Nishiguchi, S -- Nishikawa, S -- Nori, F -- Ohara, O -- Okazaki, Y -- Orlando, V -- Pang, K C -- Pavan, W J -- Pavesi, G -- Pesole, G -- Petrovsky, N -- Piazza, S -- Reed, J -- Reid, J F -- Ring, B Z -- Ringwald, M -- Rost, B -- Ruan, Y -- Salzberg, S L -- Sandelin, A -- Schneider, C -- Schonbach, C -- Sekiguchi, K -- Semple, C A M -- Seno, S -- Sessa, L -- Sheng, Y -- Shibata, Y -- Shimada, H -- Shimada, K -- Silva, D -- Sinclair, B -- Sperling, S -- Stupka, E -- Sugiura, K -- Sultana, R -- Takenaka, Y -- Taki, K -- Tammoja, K -- Tan, S L -- Tang, S -- Taylor, M S -- Tegner, J -- Teichmann, S A -- Ueda, H R -- van Nimwegen, E -- Verardo, R -- Wei, C L -- Yagi, K -- Yamanishi, H -- Zabarovsky, E -- Zhu, S -- Zimmer, A -- Hide, W -- Bult, C -- Grimmond, S M -- Teasdale, R D -- Liu, E T -- Brusic, V -- Quackenbush, J -- Wahlestedt, C -- Mattick, J S -- Hume, D A -- Kai, C -- Sasaki, D -- Tomaru, Y -- Fukuda, S -- Kanamori-Katayama, M -- Suzuki, M -- Aoki, J -- Arakawa, T -- Iida, J -- Imamura, K -- Itoh, M -- Kato, T -- Kawaji, H -- Kawagashira, N -- Kawashima, T -- Kojima, M -- Kondo, S -- Konno, H -- Nakano, K -- Ninomiya, N -- Nishio, T -- Okada, M -- Plessy, C -- Shibata, K -- Shiraki, T -- Suzuki, S -- Tagami, M -- Waki, K -- Watahiki, A -- Okamura-Oho, Y -- Suzuki, H -- Kawai, J -- Hayashizaki, Y -- FANTOM Consortium -- RIKEN Genome Exploration Research Group and Genome Science Group (Genome Network Project Core Group) -- TGM03P17/Telethon/Italy -- TGM06S01/Telethon/Italy -- New York, N.Y. -- Science. 2005 Sep 2;309(5740):1559-63.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16141072" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3' Untranslated Regions ; Animals ; Base Sequence ; Conserved Sequence ; DNA, Complementary/chemistry ; *Genome ; Genome, Human ; Genomics ; Humans ; Mice/*genetics ; Promoter Regions, Genetic ; Proteins/genetics ; RNA/chemistry/classification ; RNA Splicing ; RNA, Untranslated/chemistry ; Regulatory Sequences, Ribonucleic Acid ; *Terminator Regions, Genetic ; *Transcription Initiation Site ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Publikationsdatum: 2005-01-18
    Beschreibung: Cryptococcus neoformans is a basidiomycetous yeast ubiquitous in the environment, a model for fungal pathogenesis, and an opportunistic human pathogen of global importance. We have sequenced its approximately 20-megabase genome, which contains approximately 6500 intron-rich gene structures and encodes a transcriptome abundant in alternatively spliced and antisense messages. The genome is rich in transposons, many of which cluster at candidate centromeric regions. The presence of these transposons may drive karyotype instability and phenotypic variation. C. neoformans encodes unique genes that may contribute to its unusual virulence properties, and comparison of two phenotypically distinct strains reveals variation in gene content in addition to sequence polymorphisms between the genomes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3520129/" 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/PMC3520129/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loftus, Brendan J -- Fung, Eula -- Roncaglia, Paola -- Rowley, Don -- Amedeo, Paolo -- Bruno, Dan -- Vamathevan, Jessica -- Miranda, Molly -- Anderson, Iain J -- Fraser, James A -- Allen, Jonathan E -- Bosdet, Ian E -- Brent, Michael R -- Chiu, Readman -- Doering, Tamara L -- Donlin, Maureen J -- D'Souza, Cletus A -- Fox, Deborah S -- Grinberg, Viktoriya -- Fu, Jianmin -- Fukushima, Marilyn -- Haas, Brian J -- Huang, James C -- Janbon, Guilhem -- Jones, Steven J M -- Koo, Hean L -- Krzywinski, Martin I -- Kwon-Chung, June K -- Lengeler, Klaus B -- Maiti, Rama -- Marra, Marco A -- Marra, Robert E -- Mathewson, Carrie A -- Mitchell, Thomas G -- Pertea, Mihaela -- Riggs, Florenta R -- Salzberg, Steven L -- Schein, Jacqueline E -- Shvartsbeyn, Alla -- Shin, Heesun -- Shumway, Martin -- Specht, Charles A -- Suh, Bernard B -- Tenney, Aaron -- Utterback, Terry R -- Wickes, Brian L -- Wortman, Jennifer R -- Wye, Natasja H -- Kronstad, James W -- Lodge, Jennifer K -- Heitman, Joseph -- Davis, Ronald W -- Fraser, Claire M -- Hyman, Richard W -- AI47087/AI/NIAID NIH HHS/ -- AI48594/AI/NIAID NIH HHS/ -- R01 AI050184/AI/NIAID NIH HHS/ -- R01 AI050184-05/AI/NIAID NIH HHS/ -- R01 HL088905/HL/NHLBI NIH HHS/ -- R01 HL088905-04A2/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1321-4. Epub 2005 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850, USA. bjloftus@tigr.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653466" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alternative Splicing ; Cell Wall/metabolism ; Chromosomes, Fungal/genetics ; Computational Biology ; Cryptococcus neoformans/*genetics/pathogenicity/physiology ; DNA Transposable Elements ; Fungal Proteins/metabolism ; Gene Library ; Genes, Fungal ; *Genome, Fungal ; Humans ; Introns ; Molecular Sequence Data ; Phenotype ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Polysaccharides/metabolism ; RNA, Antisense ; Sequence Analysis, DNA ; Transcription, Genetic ; Virulence ; Virulence Factors/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
    Publikationsdatum: 2005-10-15
    Beschreibung: Tourette's syndrome (TS) is a genetically influenced developmental neuropsychiatric disorder characterized by chronic vocal and motor tics. We studied Slit and Trk-like 1 (SLITRK1) as a candidate gene on chromosome 13q31.1 because of its proximity to a de novo chromosomal inversion in a child with TS. Among 174 unrelated probands, we identified a frameshift mutation and two independent occurrences of the identical variant in the binding site for microRNA hsa-miR-189. These variants were absent from 3600 control chromosomes. SLITRK1 mRNA and hsa-miR-189 showed an overlapping expression pattern in brain regions previously implicated in TS. Wild-type SLITRK1, but not the frameshift mutant, enhanced dendritic growth in primary neuronal cultures. Collectively, these findings support the association of rare SLITRK1 sequence variants with TS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, Jesse F -- Kwan, Kenneth Y -- O'Roak, Brian J -- Baek, Danielle Y -- Stillman, Althea A -- Morgan, Thomas M -- Mathews, Carol A -- Pauls, David L -- Rasin, Mladen-Roko -- Gunel, Murat -- Davis, Nicole R -- Ercan-Sencicek, A Gulhan -- Guez, Danielle H -- Spertus, John A -- Leckman, James F -- Dure, Leon S 4th -- Kurlan, Roger -- Singer, Harvey S -- Gilbert, Donald L -- Farhi, Anita -- Louvi, Angeliki -- Lifton, Richard P -- Sestan, Nenad -- State, Matthew W -- K23 RR16118/RR/NCRR NIH HHS/ -- R01 NS054273/NS/NINDS NIH HHS/ -- R01 NS43520/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):317-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Child Study Center, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224024" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3' Untranslated Regions ; Adolescent ; Animals ; Attention Deficit Disorder with Hyperactivity/complications/genetics ; Brain/metabolism ; Child ; Child, Preschool ; Chromosome Inversion ; Chromosome Mapping ; *Chromosomes, Human, Pair 13 ; Dna ; DNA Mutational Analysis ; Female ; Frameshift Mutation ; Humans ; In Situ Hybridization, Fluorescence ; Male ; Membrane Proteins/*genetics ; Mice ; *Mutation ; Nerve Tissue Proteins/*genetics ; Pedigree ; Sequence Analysis, DNA ; Tourette Syndrome/complications/*genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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