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  • Computer Simulation  (3)
  • American Association for the Advancement of Science (AAAS)  (3)
  • Springer Nature
  • 2010-2014  (1)
  • 2005-2009  (2)
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  • American Association for the Advancement of Science (AAAS)  (3)
  • Springer Nature
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  • 1
    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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  • 2
    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-12-17
    Description: Stochasticity inherent to biochemical reactions (intrinsic noise) and variability in cellular states (extrinsic noise) degrade information transmitted through signaling networks. We analyzed the ability of temporal signal modulation--that is, dynamics--to reduce noise-induced information loss. In the extracellular signal-regulated kinase (ERK), calcium (Ca(2+)), and nuclear factor kappa-B (NF-kappaB) pathways, response dynamics resulted in significantly greater information transmission capacities compared to nondynamic responses. Theoretical analysis demonstrated that signaling dynamics has a key role in overcoming extrinsic noise. Experimental measurements of information transmission in the ERK network under varying signal-to-noise levels confirmed our predictions and showed that signaling dynamics mitigate, and can potentially eliminate, extrinsic noise-induced information loss. By curbing the information-degrading effects of cell-to-cell variability, dynamic responses substantially increase the accuracy of biochemical signaling networks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selimkhanov, Jangir -- Taylor, Brooks -- Yao, Jason -- Pilko, Anna -- Albeck, John -- Hoffmann, Alexander -- Tsimring, Lev -- Wollman, Roy -- P50 GM085764/GM/NIGMS NIH HHS/ -- P50-GM085764/GM/NIGMS NIH HHS/ -- R01 GM089976/GM/NIGMS NIH HHS/ -- R01-GM071573/GM/NIGMS NIH HHS/ -- R01-GM089976/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1370-3. doi: 10.1126/science.1254933.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, University of California-San Diego, La Jolla, CA 92093, USA. ; Department of Chemistry and Biochemistry, University of California-San Diego, La Jolla, CA 92093, USA. ; Department of Molecular and Cellular Biology, University of California-Davis, Davis 95616, USA. ; San Diego Center for Systems Biology, La Jolla, CA 92093, USA. Institute for Quantitative and Computational Biosciences and Department of Microbiology, Immunology, and Molecular Genetics, University of California-Los Angeles, Los Angeles, CA 90025, USA. ; San Diego Center for Systems Biology, La Jolla, CA 92093, USA. BioCircuits Institute, University of California-San Diego, La Jolla, CA 92093, USA. ; Department of Chemistry and Biochemistry, University of California-San Diego, La Jolla, CA 92093, USA. San Diego Center for Systems Biology, La Jolla, CA 92093, USA. Cell and Developmental Biology Section, Division of Biological Sciences, University of California-San Diego, La Jolla, CA 92093, USA. rwollman@ucsd.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504722" target="_blank"〉PubMed〈/a〉
    Keywords: *Calcium Signaling ; Cell Line ; Computer Simulation ; Extracellular Signal-Regulated MAP Kinases/*metabolism ; Humans ; *MAP Kinase Signaling System ; NF-kappa B/*metabolism ; *Signal Transduction ; Signal-To-Noise Ratio ; Single-Cell Analysis ; Systems Biology
    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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