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  • Cell Line  (2)
  • American Association for the Advancement of Science (AAAS)  (2)
  • Springer Nature
  • 2005-2009  (2)
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  • 1
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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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    The orphan G protein-coupled receptor 3 modulates amyloid-beta peptide generation in neurons (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-14
    Description: Deposition of the amyloid-beta peptide is a pathological hallmark of Alzheimer's disease. A high-throughput functional genomics screen identified G protein-coupled receptor 3 (GPR3), a constitutively active orphan G protein-coupled receptor, as a modulator of amyloid-beta production. Overexpression of GPR3 stimulated amyloid-beta production, whereas genetic ablation of GPR3 prevented accumulation of the amyloid-beta peptide in vitro and in an Alzheimer's disease mouse model. GPR3 expression led to increased formation and cell-surface localization of the mature gamma-secretase complex in the absence of an effect on Notch processing. GPR3 is highly expressed in areas of the normal human brain implicated in Alzheimer's disease and is elevated in the sporadic Alzheimer's disease brain. Thus, GPR3 represents a potential therapeutic target for the treatment of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thathiah, Amantha -- Spittaels, Kurt -- Hoffmann, Marcel -- Staes, Mik -- Cohen, Adrian -- Horre, Katrien -- Vanbrabant, Mieke -- Coun, Frea -- Baekelandt, Veerle -- Delacourte, Andre -- Fischer, David F -- Pollet, Dirk -- De Strooper, Bart -- Merchiers, Pascal -- New York, N.Y. -- Science. 2009 Feb 13;323(5916):946-51. doi: 10.1126/science.1160649.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Developmental Genetics, Vlaams Institute for Biotechnology, Center for Human Genetics, Catholic University of Leuven, Herestraat 49, 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19213921" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/*biosynthesis ; Animals ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Female ; Humans ; Male ; Mice ; Middle Aged ; Neurons/*metabolism ; Protein Structure, Tertiary ; Receptors, G-Protein-Coupled/*metabolism ; Receptors, Notch/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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    PAPER CURRENT
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