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  • Mutation  (6)
  • Computer Simulation  (5)
  • American Association for the Advancement of Science (AAAS)  (11)
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  • American Association for the Advancement of Science (AAAS)  (11)
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  • 1
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    Activation of Drosophila Toll during fungal infection by a blood serine protease (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-06
    Description: Drosophila host defense to fungal and Gram-positive bacterial infection is mediated by the Spaetzle/Toll/cactus gene cassette. It has been proposed that Toll does not function as a pattern recognition receptor per se but is activated through a cleaved form of the cytokine Spaetzle. The upstream events linking infection to the cleavage of Spaetzle have long remained elusive. Here we report the identification of a central component of the fungal activation of Toll. We show that ethylmethane sulfonate-induced mutations in the persephone gene, which encodes a previously unknown serine protease, block induction of the Toll pathway by fungi and resistance to this type of infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ligoxygakis, Petros -- Pelte, Nadege -- Hoffmann, Jules A -- Reichhart, Jean-Marc -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):114-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Biologie Moleculaire et Cellulaire, UPR 9022 du CNRS, 15 rue R. Descartes, F67084 Strasbourg Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12098703" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Chromosome Mapping ; Drosophila/genetics/immunology/*metabolism/*microbiology ; Drosophila Proteins/*blood/chemistry/*genetics/*metabolism ; Escherichia coli/physiology ; Female ; Gene Expression Regulation ; Genes, Insect ; Gram-Positive Cocci/physiology ; Hemolymph/immunology/metabolism ; Hypocreales/*physiology ; Insect Proteins/genetics/metabolism ; Male ; Molecular Sequence Data ; Mutation ; Protein Sorting Signals ; Protein Structure, Tertiary ; Receptors, Cell Surface/genetics/*metabolism ; Serine Endopeptidases/*blood/chemistry/*genetics ; Toll-Like Receptors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    A kinetic framework for a mammalian RNA polymerase in vivo (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-26
    Description: We have analyzed the kinetics of assembly and elongation of the mammalian RNA polymerase I complex on endogenous ribosomal genes in the nuclei of living cells with the use of in vivo microscopy. We show that components of the RNA polymerase I machinery are brought to ribosomal genes as distinct subunits and that assembly occurs via metastable intermediates. With the use of computational modeling of imaging data, we have determined the in vivo elongation time of the polymerase, and measurements of recruitment and incorporation frequencies show that incorporation of components into the assembling polymerase is inefficient. Our data provide a kinetic and mechanistic framework for the function of a mammalian RNA polymerase in living cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dundr, Miroslav -- Hoffmann-Rohrer, Urs -- Hu, Qiyue -- Grummt, Ingrid -- Rothblum, Lawrence I -- Phair, Robert D -- Misteli, Tom -- New York, N.Y. -- Science. 2002 Nov 22;298(5598):1623-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12446911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalytic Domain ; Cell Line ; Cell Nucleolus/metabolism ; Cell Nucleus/*metabolism ; Computer Simulation ; DNA, Ribosomal/genetics ; Fluorescence ; Fluorescence Recovery After Photobleaching ; Fluorescent Dyes ; Green Fluorescent Proteins ; Haplorhini ; Humans ; In Situ Hybridization, Fluorescence ; Kinetics ; Least-Squares Analysis ; Luminescent Proteins ; Microscopy ; Pol1 Transcription Initiation Complex Proteins/metabolism ; Probability ; Promoter Regions, Genetic ; Protein Subunits ; RNA Polymerase I/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Large-scale sequence analysis of avian influenza isolates (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-28
    Description: The spread of H5N1 avian influenza viruses (AIVs) from China to Europe has raised global concern about their potential to infect humans and cause a pandemic. In spite of their substantial threat to human health, remarkably little AIV whole-genome information is available. We report here a preliminary analysis of the first large-scale sequencing of AIVs, including 2196 AIV genes and 169 complete genomes. We combine this new information with public AIV data to identify new gene alleles, persistent genotypes, compensatory mutations, and a potential virulence determinant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Obenauer, John C -- Denson, Jackie -- Mehta, Perdeep K -- Su, Xiaoping -- Mukatira, Suraj -- Finkelstein, David B -- Xu, Xiequn -- Wang, Jinhua -- Ma, Jing -- Fan, Yiping -- Rakestraw, Karen M -- Webster, Robert G -- Hoffmann, Erich -- Krauss, Scott -- Zheng, Jie -- Zhang, Ziwei -- Naeve, Clayton W -- AI95357/AI/NIAID NIH HHS/ -- CA 21765/CA/NCI NIH HHS/ -- R01 GM061739/GM/NIGMS NIH HHS/ -- R01 GM069916/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1576-80. Epub 2006 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hartwell Center for Bioinformatics and Biotechnology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439620" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/virology ; Computational Biology ; *Genes, Viral ; Genome, Viral ; Humans ; Influenza A Virus, H1N1 Subtype/genetics ; Influenza A Virus, H2N2 Subtype/genetics ; Influenza A Virus, H3N2 Subtype/genetics ; Influenza A Virus, H3N8 Subtype/genetics ; Influenza A Virus, H5N1 Subtype/chemistry/*genetics/pathogenicity ; Influenza A Virus, H5N2 Subtype/genetics ; Influenza A Virus, H7N7 Subtype/genetics ; Influenza A Virus, H9N2 Subtype/genetics ; Influenza A virus/chemistry/*genetics/isolation & purification/pathogenicity ; Influenza in Birds/virology ; Influenza, Human/virology ; Molecular Sequence Data ; Mutation ; Phylogeny ; RNA, Viral/genetics ; Reassortant Viruses/genetics ; Sequence Analysis, DNA ; Viral Nonstructural Proteins/*chemistry/genetics ; Viral Proteins/chemistry/genetics ; Virulence Factors/*chemistry/genetics
    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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    Positive feedback within a kinase signaling complex functions as a switch mechanism for NF-kappaB activation (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-05-17
    Description: A switchlike response in nuclear factor-kappaB (NF-kappaB) activity implies the existence of a threshold in the NF-kappaB signaling module. We show that the CARD-containing MAGUK protein 1 (CARMA1, also called CARD11)-TAK1 (MAP3K7)-inhibitor of NF-kappaB (IkappaB) kinase-beta (IKKbeta) module is a switch mechanism for NF-kappaB activation in B cell receptor (BCR) signaling. Experimental and mathematical modeling analyses showed that IKK activity is regulated by positive feedback from IKKbeta to TAK1, generating a steep dose response to BCR stimulation. Mutation of the scaffolding protein CARMA1 at serine-578, an IKKbeta target, abrogated not only late TAK1 activity, but also the switchlike activation of NF-kappaB in single cells, suggesting that phosphorylation of this residue accounts for the feedback.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shinohara, Hisaaki -- Behar, Marcelo -- Inoue, Kentaro -- Hiroshima, Michio -- Yasuda, Tomoharu -- Nagashima, Takeshi -- Kimura, Shuhei -- Sanjo, Hideki -- Maeda, Shiori -- Yumoto, Noriko -- Ki, Sewon -- Akira, Shizuo -- Sako, Yasushi -- Hoffmann, Alexander -- Kurosaki, Tomohiro -- Okada-Hatakeyama, Mariko -- 5R01CA141722/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2014 May 16;344(6185):760-4. doi: 10.1126/science.1250020.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Integrated Cellular Systems, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. ; Signaling Systems Laboratory, Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093, USA. Institute for Quantitative and Computational Biosciences (QC Bio) and Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90025, USA. ; Laboratory for Cell Signaling Dynamics, RIKEN Quantitative Biology Center (QBiC), 6-2-3, Furuedai, Suita, Osaka 565-0874, Japan. Cellular Informatics Laboratory, RIKEN, 2-1 Hirosawa, Wako 351-0198, Japan. ; Laboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. ; Graduate School of Engineering, Tottori University 4-101, Koyama-minami, Tottori 680-8552, Japan. ; Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan. ; Cellular Informatics Laboratory, RIKEN, 2-1 Hirosawa, Wako 351-0198, Japan. ; Signaling Systems Laboratory, Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093, USA. Institute for Quantitative and Computational Biosciences (QC Bio) and Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90025, USA. ahoffmann@ucla.edu kurosaki@rcai.riken.jp marikoh@rcai.riken.jp. ; Laboratory for Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. Laboratory for Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan. ahoffmann@ucla.edu kurosaki@rcai.riken.jp marikoh@rcai.riken.jp. ; Laboratory for Integrated Cellular Systems, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. ahoffmann@ucla.edu kurosaki@rcai.riken.jp marikoh@rcai.riken.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24833394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; CARD Signaling Adaptor Proteins/genetics/*metabolism ; Cell Line ; Chickens ; Feedback, Physiological ; Guanylate Cyclase/genetics/*metabolism ; I-kappa B Kinase/*metabolism ; MAP Kinase Kinase Kinases/genetics/*metabolism ; Mice ; Mice, Knockout ; Mutation ; NF-kappa B/*agonists ; Phosphorylation ; Receptors, Antigen, B-Cell/genetics/*metabolism ; Serine/genetics/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 5
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    Regulation of cell cycle synchronization by decapentaplegic during Drosophila eye development (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: In the developing Drosophila eye, differentiation is coordinated with synchronized progression through the cell cycle. Signaling mediated by the transforming growth factor-beta-related gene decapentaplegic (dpp) was required for the synchronization of the cell cycle but not for cell fate specification. DPP may affect cell cycle synchronization by promoting cell cycle progression through the G2-M phases. This synchronization is critical for the precise assembly of the eye.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Penton, A -- Selleck, S B -- Hoffmann, F M -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):203-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McArdle Laboratory for Cancer Research and Laboratory of Genetics, University of Wisconsin Medical School, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Patterning ; *Cell Cycle ; Cell Differentiation ; Cell Nucleus/ultrastructure ; Cyclins/metabolism ; Drosophila/*genetics/physiology ; *Drosophila Proteins ; Eye/cytology ; Female ; G1 Phase ; G2 Phase ; *Genes, Insect ; Insect Proteins/*genetics/physiology ; Male ; Membrane Glycoproteins/genetics/physiology ; Mitosis ; Mutation ; Photoreceptor Cells, Invertebrate/*cytology ; Proteoglycans/genetics/physiology ; Signal Transduction
    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
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    Stimulus specificity of gene expression programs determined by temporal control of IKK activity (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-17
    Description: A small number of mammalian signaling pathways mediate a myriad of distinct physiological responses to diverse cellular stimuli. Temporal control of the signaling module that contains IkappaB kinase (IKK), its substrate inhibitor of NF-kappaB (IkappaB), and the key inflammatory transcription factor NF-kappaB can allow for selective gene activation. We have demonstrated that different inflammatory stimuli induce distinct IKK profiles, and we examined the underlying molecular mechanisms. Although tumor necrosis factor-alpha (TNFalpha)-induced IKK activity was rapidly attenuated by negative feedback, lipopolysaccharide (LPS) signaling and LPS-specific gene expression programs were dependent on a cytokine-mediated positive feedback mechanism. Thus, the distinct biological responses to LPS and TNFalpha depend on signaling pathway-specific mechanisms that regulate the temporal profile of IKK activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Werner, Shannon L -- Barken, Derren -- Hoffmann, Alexander -- GM071573/GM/NIGMS NIH HHS/ -- GM72024/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1857-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signaling Systems Laboratory, Department of Chemistry and Biochemistry, 9500 Gilman Drive, Mailcode 0375, La Jolla, CA 92093-0375, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166517" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Autocrine Communication ; Cell Line ; Cells, Cultured ; Computer Simulation ; Cytokines/genetics ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation ; I-kappa B Kinase ; I-kappa B Proteins/metabolism ; Lipopolysaccharides/immunology/metabolism/pharmacology ; Mice ; Models, Biological ; NF-kappa B/deficiency/metabolism ; Oligonucleotide Array Sequence Analysis ; Protein-Serine-Threonine Kinases/*metabolism ; Receptors, Immunologic/metabolism ; Signal Transduction ; Toll-Like Receptor 4 ; Transcriptional Activation ; Tumor Necrosis Factor-alpha/deficiency/immunology/metabolism/pharmacology
    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
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    Dual activation of the Drosophila toll pathway by two pattern recognition receptors (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: The Toll-dependent defense against Gram-positive bacterial infections in Drosophila is mediated through the peptidoglycan recognition protein SA (PGRP-SA). A mutation termed osiris disrupts the Gram-negative binding protein 1 (GNBP1) gene and leads to compromised survival of mutant flies after Gram-positive infections, but not after fungal or Gram-negative bacterial challenge. Our results demonstrate that GNBP1 and PGRP-SA can jointly activate the Toll pathway. The potential for a combination of distinct proteins to mediate detection of infectious nonself in the fly will refine the concept of pattern recognition in insects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gobert, Vanessa -- Gottar, Marie -- Matskevich, Alexey A -- Rutschmann, Sophie -- Royet, Julien -- Belvin, Marcia -- Hoffmann, Jules A -- Ferrandon, Dominique -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2126-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite Propre de Recherche 9022 du CNRS, Institut de Biologie Moleculaire et Cellulaire, 15 rue Rene Descartes, F67084 Strasbourg Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/*metabolism ; DNA Transposable Elements ; Drosophila/genetics/immunology/*metabolism/*microbiology ; Drosophila Proteins/genetics/*metabolism ; Gene Expression ; Genes, Insect ; Gram-Negative Bacteria/*physiology ; Gram-Positive Bacteria/*physiology ; Hemolymph/metabolism ; Hypocreales/physiology ; Insect Proteins/genetics/metabolism ; Mutation ; Phenotype ; Receptors, Cell Surface/genetics/*metabolism ; Serine Endopeptidases/genetics/metabolism ; Toll-Like Receptors
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Comment on "Oscillations in NF-kappaB signaling control the dynamics of gene expression" (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-02
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821939/" 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/PMC2821939/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barken, Derren -- Wang, Chiaochun Joanne -- Kearns, Jeff -- Cheong, Raymond -- Hoffmann, Alexander -- Levchenko, Andre -- GM072024-01/GM/NIGMS NIH HHS/ -- P01 GM071862/GM/NIGMS NIH HHS/ -- P01 GM071862-01A20005/GM/NIGMS NIH HHS/ -- R01 GM071573/GM/NIGMS NIH HHS/ -- R01 GM071573-01A1/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Apr 1;308(5718):52; author reply 52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signaling Systems Laboratory, Department of Chemistry and Biochemistry and Bioinformatics Graduate Program, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0375, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15802586" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Cell Nucleus/metabolism ; Computer Simulation ; Cytoplasm/metabolism ; Feedback, Physiological ; *Gene Expression Regulation ; HeLa Cells ; Humans ; I-kappa B Proteins/metabolism ; Immunohistochemistry ; Models, Biological ; NF-kappa B/*metabolism ; Recombinant Fusion Proteins ; *Signal Transduction ; Transcription Factor RelA ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    The IkappaB-NF-kappaB signaling module: temporal control and selective gene activation (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-09
    Description: Nuclear localization of the transcriptional activator NF-kappaB (nuclear factor kappaB) is controlled in mammalian cells by three isoforms of NF-kappaB inhibitor protein: IkappaBalpha, -beta, and - epsilon. Based on simplifying reductions of the IkappaB-NF-kappaB signaling module in knockout cell lines, we present a computational model that describes the temporal control of NF-kappaB activation by the coordinated degradation and synthesis of IkappaB proteins. The model demonstrates that IkappaBalpha is responsible for strong negative feedback that allows for a fast turn-off of the NF-kappaB response, whereas IkappaBbeta and - epsilon function to reduce the system's oscillatory potential and stabilize NF-kappaB responses during longer stimulations. Bimodal signal-processing characteristics with respect to stimulus duration are revealed by the model and are shown to generate specificity in gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmann, Alexander -- Levchenko, Andre -- Scott, Martin L -- Baltimore, David -- New York, N.Y. -- Science. 2002 Nov 8;298(5596):1241-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12424381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Nucleus/metabolism ; Chemokine CCL5/genetics ; Chemokine CXCL10 ; Chemokines, CXC/genetics ; Computer Simulation ; Cytoplasm ; DNA-Binding Proteins/genetics/*metabolism ; Electrophoretic Mobility Shift Assay ; Feedback, Physiological ; *Gene Expression Regulation ; Humans ; I-kappa B Proteins/genetics/*metabolism ; Mice ; Mice, Knockout ; Models, Biological ; NF-kappa B/*metabolism ; Proto-Oncogene Proteins/genetics/*metabolism ; *Signal Transduction ; Transcriptional Activation ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/metabolism/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    An ancient mechanism controls the development of cells with a rooting function in land plants (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-09
    Description: Root hairs and rhizoids are cells with rooting functions in land plants. We describe two basic helix-loop-helix transcription factors that control root hair development in the sporophyte (2n) of the angiosperm Arabidopsis thaliana and rhizoid development in the gametophytes (n) of the bryophyte Physcomitrella patens. The phylogeny of land plants supports the hypothesis that early land plants were bryophyte-like and possessed a dominant gametophyte and later the sporophyte rose to dominance. If this hypothesis is correct, our data suggest that the increase in morphological complexity of the sporophyte body in the Paleozoic resulted at least in part from the recruitment of regulatory genes from gametophyte to sporophyte.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Menand, Benoit -- Yi, Keke -- Jouannic, Stefan -- Hoffmann, Laurent -- Ryan, Eoin -- Linstead, Paul -- Schaefer, Didier G -- Dolan, Liam -- BBS/E/J/0000A218/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Jun 8;316(5830):1477-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, John Innes Centre, Norwich NR47UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17556585" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/cytology/genetics/growth & development/*physiology ; Arabidopsis Proteins/genetics/*physiology ; Basic Helix-Loop-Helix Transcription Factors/genetics/*physiology ; Biological Evolution ; Bryopsida/cytology/genetics/growth & development/*physiology ; Diploidy ; Genes, Plant ; Haploidy ; Molecular Sequence Data ; Mutation ; Phylogeny ; Plant Epidermis/cytology/physiology ; Plant Proteins/genetics/physiology ; Plant Roots/*cytology/growth & development ; Plants, Genetically Modified
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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