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  • Patch clamp  (2)
  • Cell Aging/*immunology  (1)
  • Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics/metabolism  (1)
  • Interferon-gamma/immunology  (1)
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  • 1
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    T-helper-1-cell cytokines drive cancer into senescence (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-02-05
    Description: Cancer control by adaptive immunity involves a number of defined death and clearance mechanisms. However, efficient inhibition of exponential cancer growth by T cells and interferon-gamma (IFN-gamma) requires additional undefined mechanisms that arrest cancer cell proliferation. Here we show that the combined action of the T-helper-1-cell cytokines IFN-gamma and tumour necrosis factor (TNF) directly induces permanent growth arrest in cancers. To safely separate senescence induced by tumour immunity from oncogene-induced senescence, we used a mouse model in which the Simian virus 40 large T antigen (Tag) expressed under the control of the rat insulin promoter creates tumours by attenuating p53- and Rb-mediated cell cycle control. When combined, IFN-gamma and TNF drive Tag-expressing cancers into senescence by inducing permanent growth arrest in G1/G0, activation of p16INK4a (also known as CDKN2A), and downstream Rb hypophosphorylation at serine 795. This cytokine-induced senescence strictly requires STAT1 and TNFR1 (also known as TNFRSF1A) signalling in addition to p16INK4a. In vivo, Tag-specific T-helper 1 cells permanently arrest Tag-expressing cancers by inducing IFN-gamma- and TNFR1-dependent senescence. Conversely, Tnfr1(-/-)Tag-expressing cancers resist cytokine-induced senescence and grow aggressively, even in TNFR1-expressing hosts. Finally, as IFN-gamma and TNF induce senescence in numerous murine and human cancers, this may be a general mechanism for arresting cancer progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Braumuller, Heidi -- Wieder, Thomas -- Brenner, Ellen -- Assmann, Sonja -- Hahn, Matthias -- Alkhaled, Mohammed -- Schilbach, Karin -- Essmann, Frank -- Kneilling, Manfred -- Griessinger, Christoph -- Ranta, Felicia -- Ullrich, Susanne -- Mocikat, Ralph -- Braungart, Kilian -- Mehra, Tarun -- Fehrenbacher, Birgit -- Berdel, Julia -- Niessner, Heike -- Meier, Friedegund -- van den Broek, Maries -- Haring, Hans-Ulrich -- Handgretinger, Rupert -- Quintanilla-Martinez, Leticia -- Fend, Falko -- Pesic, Marina -- Bauer, Jurgen -- Zender, Lars -- Schaller, Martin -- Schulze-Osthoff, Klaus -- Rocken, Martin -- England -- Nature. 2013 Feb 21;494(7437):361-5. doi: 10.1038/nature11824. Epub 2013 Feb 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, Eberhard Karls University, Liebermeister Strasse 25, 72076 Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23376950" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/genetics/metabolism ; Cell Aging/*immunology ; Cell Cycle ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics/metabolism ; Cytokines/*immunology ; Disease Models, Animal ; Disease Progression ; Female ; Humans ; Interferon-gamma/immunology ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Neoplasms/*immunology/*pathology ; Oncogenes/genetics ; Phosphoserine/metabolism ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Retinoblastoma Protein/chemistry/metabolism ; STAT1 Transcription Factor/metabolism ; Th1 Cells/*immunology ; Time Factors ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/immunology ; Tumor Suppressor Protein p53/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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  • 2
    Electronic Resource
    Electronic Resource
    Comparison of K+-channel activation and deactivation in guard cells from a dicotyledon (Vicia faba L.) and a graminaceous monocotyledon (Zea mays) (1993)
    Springer
    Planta 189 (1993), S. 410-419 
    Details
    ISSN: 1432-2048
    Keywords: Guard cell ; Patch clamp ; Potassium channel (kinetics) ; Stomate ; Vicia ; Zea
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract We describe and compare inward and outward whole-cell K+ currents across the plasma membrane surrounding guard-cell protoplasts from the dicotyledon, Vicia faba, and the graminaceous monocotyledon, Zea mays. Macrosopic whole-cell current is considered in terms of microscopic single-channel activity, which involves discrete steps between conducting (open) and nonconducting (closed) states of the channel protein. Kinetic equations are used to model the number of open and closed states for channels conducting K+ influx (K(in)) and K+ efflux (K(out)) in the two species, and to calculate the rate at which open-closed transitions occur. The opening and closure of K(in) channels in both Vicia and Zea follow single-exponential timecourses, indicating that K(in)-channel proteins in each species simply fluctuate between one open and one closed state. In both species, opening of K(in) channels is voltage-independent, but closure of K(in) channels is faster at more positive membrane potentials. In response to identical voltage stimuli, K(in) channels in Zea open and close approximately three times as fast as in Vicia. In contrast to K(in), K(out) channels in Zea open and close more slowly than in Vicia. The closure of K(out) channels follows a single-exponential timecourse in each species, indicating one open state. The kinetics of K(out)-channel opening are more complicated and indicate the presence of at least two (Vicia) or three (Zea) closed states.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00194439
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  • 3
    Electronic Resource
    Electronic Resource
    Whole-cell K+ current across the plasma membrane of guard cells from a grass: Zea mays (1992)
    Springer
    Planta 186 (1992), S. 282-293 
    Details
    ISSN: 1432-2048
    Keywords: Guard cell ; Patch clamp ; Plasma membrane ; Potassium channels ; Zea (K+ currents)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Knowledge of ion fluxes in the dumbell-shaped guard cells of grass species has been limited by the difficulty of obtaining isolated epidermes or guard-cell protoplasts for use in radioactive-tracer or electrophysiological studies. We describe here a method for isolating guard-cell protoplasts from Zea mays L. Whole-cell patch clamp has been used to measure K+-channel current across the plasma membrane surrounding these protoplasts. Two populations of K+-permeable channels have been identified. Hyperpolarization of the membrane to potentials (Vm) more negative than -100 mV results in inward K+ current through one population of channels. Inward current activation is faster than in the dicotyledon, Vicia faba L. (mean activation half-time 26 ms (Z. mays) versus 123 ms (V. faba) at Vm=-180 mV). Steady-state current density is less than in V. faba (-22 μA · cm−2 (Z. mays) versus -40 μA · cm−2 (V. faba) at Vm=- 180 mV in 12 mM external K+). Depolarization of the membrane to potentials more positive than -20 mV results in outward K+ current through a second population of channels; these channels activate and (upon repolarization of the membrane) deactivate more slowly than in V. faba (mean activation half-time 375 ms (Z. mays) versus 187 ms (V. faba) at Vm=+ 80 mV) but result in a similar steady-state current density (23.8 μA · cm−2 (Z. mays) versus 28.7 μA · cm−2 (V. faba) at Vm= + 80 mV with 105 mM internal K+). Omission of K+ eliminates the current. The K+ current is sensitive to both internal and external Ca2+ concentration: increasing internal Ca2+ from 2 nM to 0.2 μM or increasing external Ca2+ from 1 mM to 8.5 mM reduces the magnitude of both inward and outward current.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00196258
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