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  • 1
    Publication Date: 2011-08-10
    Description: During immune responses, neutrophils must integrate survival and death signals from multiple sources to regulate their lifespan. Signals that activate either the Bcl-2- or death receptor-regulated apoptosis pathways can provide powerful stimuli for neutrophils to undergo cell death, but whether they act cooperatively in parallel or directly cross-talk in neutrophils is not known. Previous studies suggested that Bcl-2 family proteins are not required for Fas-induced cell death in neutrophils, but did not examine whether they could modulate its rapid onset. By monitoring the rate of change in neutrophil viability associated with activation of the Fas-triggered death receptor pathway using real-time cell imaging, we show that the Bcl-2-related proteins Bid, Bax, and Bak accelerate neutrophil apoptosis but are not essential for cell death. Increased Bcl-2 or Mcl-1 expression prevents efficient induction of apoptosis by Fas stimulation indicating that the Bcl-2-regulated apoptosis pathway can directly interfere with Fas-triggered apoptosis. Fas has been shown to initiate NFκB activation and gene transcription in cell lines, however gene transcription is not altered in Fas-activated Bid−/− neutrophils, indicating that apoptosis occurs independently of gene transcription in neutrophils. The specification of kinetics of neutrophil apoptosis by Bid impacts on the magnitude of neutrophil IL-1β production, implicating a functional role for the Bcl-2-regulated pathway in controlling neutrophil responses to FasL. These data demonstrate that the intrinsic apoptosis pathway directly controls the kinetics of Fas-triggered apoptosis in neutrophils.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 2
    Publication Date: 2015-06-18
    Description: Synapse formation is a process tightly controlled in space and time. How gene regulatory mechanisms specify spatial and temporal aspects of synapse formation is not well understood. In the nematode Caenorhabditis elegans, two subtypes of the D-type inhibitory motor neuron (MN) classes, the dorsal D (DD) and ventral D (VD) neurons, extend axons along both the dorsal and ventral nerve cords. The embryonically generated DD motor neurons initially innervate ventral muscles in the first (L1) larval stage and receive their synaptic input from cholinergic motor neurons in the dorsal cord. They rewire by the end of the L1 moult to innervate dorsal muscles and to be innervated by newly formed ventral cholinergic motor neurons. VD motor neurons develop after the L1 moult; they take over the innervation of ventral muscles and receive their synaptic input from dorsal cholinergic motor neurons. We show here that the spatiotemporal control of synaptic wiring of the D-type neurons is controlled by an intersectional transcriptional strategy in which the UNC-30 Pitx-type homeodomain transcription factor acts together, in embryonic and early larval stages, with the temporally controlled LIN-14 transcription factor to prevent premature synapse rewiring of the DD motor neurons and, together with the UNC-55 nuclear hormone receptor, to prevent aberrant VD synaptic wiring in later larval and adult stages. A key effector of this intersectional transcription factor combination is a novel synaptic organizer molecule, the single immunoglobulin domain protein OIG-1. OIG-1 is perisynaptically localized along the synaptic outputs of the D-type motor neurons in a temporally controlled manner and is required for appropriate selection of both pre- and post-synaptic partners.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howell, Kelly -- White, John G -- Hobert, Oliver -- R01 NS039996/NS/NINDS NIH HHS/ -- R01 NS050266/NS/NINDS NIH HHS/ -- R01NS039996-05/NS/NINDS NIH HHS/ -- R01NS050266-03/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- Medical Research Council/United Kingdom -- England -- Nature. 2015 Jul 2;523(7558):83-7. doi: 10.1038/nature14545. Epub 2015 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, Columbia University Medical Center, New York, New York 10032, USA. ; MRC Laboratory of Molecular Biology, Cambridge CB2 2QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26083757" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/embryology/genetics/growth & development/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Gene Expression Regulation ; Homeodomain Proteins/genetics/metabolism ; Motor Neurons/*physiology ; Mutation ; Nerve Tissue Proteins/genetics/*metabolism ; Nuclear Proteins/genetics/metabolism ; Receptors, Cell Surface/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Synapses/genetics/pathology/physiology ; Transcription Factors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1995-10-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chalfie, M -- Eddy, S -- Hengartner, M O -- Hodgkin, J -- Kohara, Y -- Plasterk, R H -- Waterston, R H -- White, J G -- New York, N.Y. -- Science. 1995 Oct 20;270(5235):415-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Columbia University, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569996" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Caenorhabditis elegans/*genetics ; *Chromosome Mapping ; Gene Expression ; *Genes, Helminth ; *Genome ; Molecular Sequence Data
    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
    Publication Date: 1982-01-01
    Description: Alpha-adrenergic agonists that promote platelet aggregation were found to reduce ferric heme to ferrous heme. Agents that bind iron in heme inhibited epinephrine-induced platelet aggregation. It is proposed that epinephrine first binds to its receptor and then reduces an adjacent heme group to transmit its agonist stimulus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peterson, D A -- Gerrard, J M -- Glover, S M -- Rao, G H -- White, J G -- HL 11880/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1982 Jan 1;215(4528):71-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6274020" target="_blank"〉PubMed〈/a〉
    Keywords: *Epinephrine/pharmacology ; *Heme ; Oxidation-Reduction ; Platelet Aggregation/*drug effects ; Receptors, Adrenergic, alpha/drug effects
    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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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-02-19
    Description: A concerted flow of actin filaments associated with the inner face of the plasma membrane may provide the basis for many animal cell movements. The flow is driven by gradients of tension in the cell cortex, which pull cortical components from regions of relaxation to regions of contraction. In some cases cortical components return through the cytoplasm to establish a continuous cycle. This cortically located motor may drive cell locomotion, growth cone migration, the capping of antigens on a lymphocyte surface, and cytokinesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bray, D -- White, J G -- New York, N.Y. -- Science. 1988 Feb 19;239(4842):883-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Cell Biophysics Unit, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3277283" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*physiology ; Amoeba/physiology ; Animals ; Cell Division ; Cell Membrane/ultrastructure ; Cell Movement ; *Cell Physiological Phenomena ; Cells/ultrastructure ; Fibroblasts/physiology ; Lymphocytes/immunology/ultrastructure ; Neurons/physiology/ultrastructure ; Neutrophils/physiology/ultrastructure
    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
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Inorganic chemistry 3 (1964), S. 1220-1228 
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
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  • 7
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Inorganic chemistry 4 (1965), S. 970-973 
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Inorganic chemistry 4 (1965), S. 1760-1763 
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Inorganic chemistry 10 (1971), S. 1934-1935 
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 100 (1978), S. 7994-7997 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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