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  • 1
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    Edge-based sensitivity analysis of signaling networks by using Boolean dynamics (2016)
    Oxford University Press
    Details
    Publication Date: 2016-09-02
    Description: Motivation: Biological networks are composed of molecular components and their interactions represented by nodes and edges, respectively, in a graph model. Based on this model, there were many studies with respect to effects of node-based mutations on the network dynamics, whereas little attention was paid to edgetic mutations so far. Results: In this paper, we defined an edgetic sensitivity measure that quantifies how likely a converging attractor is changed by edge-removal mutations in a Boolean network model. Through extensive simulations based on that measure, we found interesting properties of highly sensitive edges in both random and real signaling networks. First, the sensitive edges in random networks tend to link two end nodes both of which are susceptible to node-knockout mutations. Interestingly, it was analogous to an observation that the sensitive edges in human signaling networks are likely to connect drug-target genes. We further observed that the edgetic sensitivity predicted drug-targets better than the node-based sensitivity. In addition, the sensitive edges showed distinguished structural characteristics such as a lower connectivity, more involving feedback loops and a higher betweenness. Moreover, their gene-ontology enrichments were clearly different from the other edges. We also observed that genes incident to the highly sensitive interactions are more central by forming a considerably large connected component in human signaling networks. Finally, we validated our approach by showing that most sensitive interactions are promising edgetic drug-targets in p53 cancer and T-cell apoptosis networks. Taken together, the edgetic sensitivity is valuable to understand the complex dynamics of signaling networks. Contact: kwonyk@ulsan.ac.kr Supplementary information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 2
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    Reverse signaling through the costimulatory ligand CD137L in epithelial cells is essential for natural killer cell-mediated acute tissue inflammation [Immunology] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-01-05
    Description: Renal ischemia-reperfusion injury (IRI) after kidney transplantation is a major cause of delayed graft function. Even though IRI is recognized as a highly coordinated and specific process, the pathways and mechanisms through which the innate response is activated are poorly understood. In this study, we used a mouse model of acute kidney IRI to examine whether the interactions of costimulatory receptor CD137 and its ligand (CD137L) are involved in the early phase of acute kidney inflammation caused by IRI. We report here that the specific expressions of CD137 on natural killer cells and of CD137L on tubular epithelial cells (TECs) are required for acute kidney IRI. Reverse signaling through CD137L in TECs results in their production of the chemokine (C-X-C motif) receptor 2 ligands CXCL1 and CXCL2 and the subsequent induction of neutrophil recruitment, resulting in a cascade of proinflammatory events during kidney IRI. Our findings identify an innate pathogenic pathway for renal IRI involving the natural killer cell–TEC–neutrophil axis, whereby CD137–CD137L interactions provide the causal contribution of epithelial cell dysregulation to renal IRI. The CD137L reverse signaling pathway in epithelial cells therefore may represent a good target for blocking the initial stage of inflammatory diseases, including renal IRI.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 3
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    Co-option of a default secretory pathway for plant immune responses (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-02-15
    Description: Cell-autonomous immunity is widespread in plant-fungus interactions and terminates fungal pathogenesis either at the cell surface or after pathogen entry. Although post-invasive resistance responses typically coincide with a self-contained cell death of plant cells undergoing attack by parasites, these cells survive pre-invasive defence. Mutational analysis in Arabidopsis identified PEN1 syntaxin as one component of two pre-invasive resistance pathways against ascomycete powdery mildew fungi. Here we show that plasma-membrane-resident PEN1 promiscuously forms SDS-resistant soluble N-ethylmaleimide sensitive factor attachment protein receptor (SNARE) complexes together with the SNAP33 adaptor and a subset of vesicle-associated membrane proteins (VAMPs). PEN1-dependent disease resistance acts in vivo mainly through two functionally redundant VAMP72 subfamily members, VAMP721 and VAMP722. Unexpectedly, the same two VAMP proteins also operate redundantly in a default secretory pathway, suggesting dual functions in separate biological processes owing to evolutionary co-option of the default pathway for plant immunity. The disease resistance function of the secretory PEN1-SNAP33-VAMP721/722 complex and the pathogen-induced subcellular dynamics of its components are mechanistically reminiscent of immunological synapse formation in vertebrates, enabling execution of immune responses through focal secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwon, Chian -- Neu, Christina -- Pajonk, Simone -- Yun, Hye Sup -- Lipka, Ulrike -- Humphry, Matt -- Bau, Stefan -- Straus, Marco -- Kwaaitaal, Mark -- Rampelt, Heike -- El Kasmi, Farid -- Jurgens, Gerd -- Parker, Jane -- Panstruga, Ralph -- Lipka, Volker -- Schulze-Lefert, Paul -- England -- Nature. 2008 Feb 14;451(7180):835-40. doi: 10.1038/nature06545.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Microbe Interactions, Max-Planck-Institut fur Zuchtungsforschung, Carl-von-Linne-Weg 10, D-50829 Koln, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18273019" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/genetics/metabolism ; Arabidopsis/genetics/*immunology/*microbiology ; Arabidopsis Proteins/genetics/*metabolism ; Ascomycota/physiology ; N-Glycosyl Hydrolases/genetics/metabolism ; Qa-SNARE Proteins/genetics/metabolism ; SNARE Proteins/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Phosphodiesterase 9A controls nitric-oxide-independent cGMP and hypertrophic heart disease (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-03-25
    Description: Cyclic guanosine monophosphate (cGMP) is a second messenger molecule that transduces nitric-oxide- and natriuretic-peptide-coupled signalling, stimulating phosphorylation changes by protein kinase G. Enhancing cGMP synthesis or blocking its degradation by phosphodiesterase type 5A (PDE5A) protects against cardiovascular disease. However, cGMP stimulation alone is limited by counter-adaptions including PDE upregulation. Furthermore, although PDE5A regulates nitric-oxide-generated cGMP, nitric oxide signalling is often depressed by heart disease. PDEs controlling natriuretic-peptide-coupled cGMP remain uncertain. Here we show that cGMP-selective PDE9A (refs 7, 8) is expressed in the mammalian heart, including humans, and is upregulated by hypertrophy and cardiac failure. PDE9A regulates natriuretic-peptide- rather than nitric-oxide-stimulated cGMP in heart myocytes and muscle, and its genetic or selective pharmacological inhibition protects against pathological responses to neurohormones, and sustained pressure-overload stress. PDE9A inhibition reverses pre-established heart disease independent of nitric oxide synthase (NOS) activity, whereas PDE5A inhibition requires active NOS. Transcription factor activation and phosphoproteome analyses of myocytes with each PDE selectively inhibited reveals substantial differential targeting, with phosphorylation changes from PDE5A inhibition being more sensitive to NOS activation. Thus, unlike PDE5A, PDE9A can regulate cGMP signalling independent of the nitric oxide pathway, and its role in stress-induced heart disease suggests potential as a therapeutic target.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376609/" 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/PMC4376609/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Dong I -- Zhu, Guangshuo -- Sasaki, Takashi -- Cho, Gun-Sik -- Hamdani, Nazha -- Holewinski, Ronald -- Jo, Su-Hyun -- Danner, Thomas -- Zhang, Manling -- Rainer, Peter P -- Bedja, Djahida -- Kirk, Jonathan A -- Ranek, Mark J -- Dostmann, Wolfgang R -- Kwon, Chulan -- Margulies, Kenneth B -- Van Eyk, Jennifer E -- Paulus, Walter J -- Takimoto, Eiki -- Kass, David A -- HHSN268201000032C/HL/NHLBI NIH HHS/ -- HL-07227/HL/NHLBI NIH HHS/ -- HL-089297/HL/NHLBI NIH HHS/ -- HL-093432/HL/NHLBI NIH HHS/ -- HL-119012/HL/NHLBI NIH HHS/ -- HL089847/HL/NHLBI NIH HHS/ -- HL105993/HL/NHLBI NIH HHS/ -- HL68891/HL/NHLBI NIH HHS/ -- N01HV28180/HL/NHLBI NIH HHS/ -- P01 HL107153/HL/NHLBI NIH HHS/ -- R01 HL089297/HL/NHLBI NIH HHS/ -- R01 HL089847/HL/NHLBI NIH HHS/ -- R01 HL093432/HL/NHLBI NIH HHS/ -- R01 HL105993/HL/NHLBI NIH HHS/ -- R01 HL111198/HL/NHLBI NIH HHS/ -- R01 HL119012/HL/NHLBI NIH HHS/ -- T32 HL007227/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Mar 26;519(7544):472-6. doi: 10.1038/nature14332. Epub 2015 Mar 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cardiology, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA. ; Advanced Medical Research Laboratories, Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Kanagawa 227-0033, Japan. ; Department of Physiology, Institute for Cardiovascular Research, VU University Medical Center, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands. ; 1] Division of Cardiology, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA [2] Heart Institute and Advanced Clinical Biosystems Research Institute, Cedar Sinai Medical Center, 8700 Beverly Blvd, AHSP A9229 Los Angeles, California 90048, USA. ; Department of Physiology, Institute of Bioscience and Biotechnology, BK21 plus Graduate Program, Kangwon National University College of Medicine, Chuncheon 200-701, Korea. ; Department of Pharmacology, University of Vermont, Burlington, Vermont 05405, USA. ; Department of Medicine, Division of Cardiovascular Medicine, Cardiovascular Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25799991" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-AMP Phosphodiesterases/antagonists & ; inhibitors/deficiency/genetics/*metabolism ; Animals ; Aortic Valve Stenosis/complications ; Cardiomegaly/drug therapy/*enzymology/etiology/*metabolism ; Cyclic GMP/*metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Muscle Cells/enzymology ; Myocardium/enzymology ; Natriuretic Peptides/metabolism ; *Nitric Oxide/metabolism ; Nitric Oxide Synthase ; Phosphodiesterase Inhibitors/pharmacology/therapeutic use ; Pressure ; Signal Transduction/drug effects ; Stress, Physiological ; Up-Regulation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    {beta}-Arrestin2 in myeloid leukemia [Cell Biology] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-08-01
    Description: β-Arrestins were initially discovered as negative regulators of G protein-coupled receptor signaling. Although β-arrestins have more recently been implicated as scaffold proteins that interact with various mitogenic and developmental signals, the genetic role of β-arrestins in driving oncogenesis is not known. Here we have investigated the role of β-arrestin in hematologic malignancies and have found that although both β-arrestin1 and -2 are expressed in the hematopoietic system, loss of β-arrestin2 preferentially leads to a severe impairment in the establishment and propagation of the chronic and blast crisis phases of chronic myelogenous leukemia (CML). These defects are linked to a reduced frequency, as well as defective self-renewal capacity of the cancer stem-cell population, in mouse models and in human CML patient samples. At a molecular level, the loss of β-arrestin2 leads to a significant inhibition of β-catenin stabilization, and ectopic activation of Wnt signaling reverses the defects observed in the β-arrestin2 mutant cells. These data cumulatively show that β-arrestin2 is essential for CML disease propagation and indicate that β-arrestins and the Wnt/β-catenin pathway lie in a signaling hierarchy in the context of CML cancer stem cell maintenance.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    Synaptic stabilization of NMDARs by neuroligin-1 [Neuroscience] (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-01-09
    Description: Despite the pivotal functions of the NMDA receptor (NMDAR) for neural circuit development and synaptic plasticity, the molecular mechanisms underlying the dynamics of NMDAR trafficking are poorly understood. The cell adhesion molecule neuroligin-1 (NL1) modifies NMDAR-dependent synaptic transmission and synaptic plasticity, but it is unclear whether NL1 controls synaptic accumulation...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 7
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    Genome-wide reorganization of histone H2AX toward particular fragile sites on cell activation (2014)
    Oxford University Press
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    Publication Date: 2014-01-28
    Description: H2AX formation by phosphorylation of the histone variant H2AX is the key process in the repair of DNA lesions including those arising at fragile sites under replication stress. Here we demonstrate that H2AX is dynamically reorganized to preoccupy H2AX hotspots on increased replication stress by activated cell proliferation and that H2AX is enriched in aphidicolin-induced replisome stalling sites in cycling cells. Interestingly, H2AX enrichment was particularly found in genomic regions that replicate in early S phase. High transcription activity, a hallmark of early replicating fragile sites, was a determinant of H2AX localization. Subtelomeric H2AX enrichment was also attributable to early replication and high gene density. In contrast, late replicating and infrequently transcribed regions, including common fragile sites and heterochromatin, lacked H2AX enrichment. In particular, heterochromatin was inaccessible to H2AX incorporation, maybe partly explaining the cause of mutation accumulation in cancer heterochromatin. Meanwhile, H2AX in actively dividing cells was intimately colocalized with INO80. INO80 silencing reduced H2AX levels, particularly at the INO80-enriched sites. Our findings suggest that active DNA replication is accompanied with the specific localization of H2AX and INO80 for efficient damage repair or replication-fork stabilization in actively transcribed regions.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 8
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    RIP1 inhibition blocks inflammatory diseases but not tumor growth or metastases (2019)
    Springer Nature
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    Publication Date: 2019
    Print ISSN: 1350-9047
    Electronic ISSN: 1476-5403
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 9
    Electronic Resource
    Electronic Resource
    Ferromagnetic antiresonance in La0.7Ba0.3MnO3 traced out by temperature variation : The 41st annual conference on magnetism and magnetic materials (1997)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 81 (1997), S. 5157-5158 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Using the phenomenon of ferromagnetic antiresonance (FMAR) in ceramic samples of La0.67Ba0.33MnO3 at 10 GHz, we report a large magneto-impedance MI=Rs(H(parallel))−Rs(H⊥)]/Rs(H(parallel)), where Rs is the microwave surface resistance and H the applied field. The MI reaches 30% at a field of 30 mT near room temperature. The FMAR also lets us measure M(T) by following Rs as a function of T and H. ©1997 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.365154
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  • 10
    Electronic Resource
    Electronic Resource
    Characterization of epitaxial La0.7Ba0.3MnO3 structures using ferromagnetic resonance (1996)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 80 (1996), S. 2334-2338 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: We have compared a single layer of La0.7Ba0.3MnO3 and a trilayer structure of SrTiO3/La0.7Ba0.3MnO3/SrTiO3, both grown epitaxially on a LaAlO3 substrate, using information obtained by ferromagnetic resonance (FMR). The trilayer samples have a more uniform magnetization and are not susceptible to environmental degradation. This may be due to the strain relief that the buffer SrTiO3 layer provides for the La0.7Ba0.3MnO3 layer. We have also studied the magnetic homogeneity of the trilayer structure as a function of the deposition temperature. The perpendicular FMR linewidth, Γ⊥, shows a clear window in the deposition temperature where the linewidth is 〈50 Oe. However, the parallel linewidth, Γ(parallel), is nearly ten times larger than Γ⊥ with only a weak dependence on the deposition temperature. This broadening of the parallel linewidth compared to the perpendicular linewidth can be explained by invoking a local unidirectional anisotropy in the plane of the film. © 1996 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.363066
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