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  • Harvey-ras  (1)
  • Intracellular calcium oscillations  (1)
  • Na+/H+ Exchanger  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 291 (1991), S. 113-116 
    ISSN: 0014-5793
    Keywords: Bombesin ; Calcium ; Harvey-ras ; Inositolphosphate ; NIH3T3 fibroblast
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2013
    Keywords: Ras oncogene ; Bradykinin ; NIH fibroblasts ; Intracellular calcium oscillations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In NIH fibroblasts expressing the ras oncogene bradykinin leads to sustained, calcium-dependent oscillations of cell membrane potential by oscillating activity of calcium sensitive potassium channels. The present study has been performed to further analyse the underlying mechanisms. In cells expressing the oncogene, but not in NIH fibroblasts not expressing the oncogene, bradykinin elicits calcium oscillations, which are detected by fura-2 fluorescence and amplified by a decrease of extracellular sodium activity. These calcium oscillations are dependent on the presence of extracellular calcium and are inhibited by lanthanum ions. It is concluded that in cells expressing the ras oncogene, bradykinin activates lanthanum sensitive calcium entry from the extracellular space. Ras oncogene expression leads to enhanced bradykinin-induced formation of both, 1, 4, 5 inositoltrisphosphate and 1, 3, 4, 5 inositoltetrakisphosphate, an effect probably accounting for the oscillations of intracellular calcium activity.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2013
    Keywords: Cell volume regulation ; Ras oncogene ; Na+/H+ Exchanger ; Na+, K+,2Cl− Cotransporter ; Dimethylamiloride ; Furosemide ; Quinidine ; Bumetanide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Expression of the Ha-ras oncogene has been reported to stimulate the dimethylamiloride sensitive Na+/H+ exchanger and Na+, K+, 2Cl− cotransport, both transport systems which are involved in cell volume regulation. The present study has been performed to test for an influence of ras oncogene expression on cell volume regulation in NIH 3T3 fibroblasts expressing the Ha-ras oncogene (+ ras). As controls served NIH 3T3 fibroblasts not expressing the ras oncogene (− ras). In isotonic extracellular fluid, the cell volume of + ras cells (2.70±0.08 pl) is significantly greater than the cell volume of −ras cells (2.04±0.10 pl). Both, + ras and − ras cells exhibit a regulatory cell volume increase in hypertonic extracellular fluid and a regulatory cell volume decrease in hypotonic extracellular fluid. The regulatory cell volume decrease is inhibited by 1 mmol/l quinidine and barium, the regulatory cell volume increase is inhibited in − ras and + ras cells by dimethyl-amiloride (100 μmol/l) and, only in + ras cells, by furosemide (100 μmol/l) and bumetanide (10 μmol/l). In conclusion, expression of the ras oncogene leads to a shift of the set point for cell volume regulation to greater cell volumes, which may contribute to the activation of the Na+/H+ exchanger and Na+, K+, 2Cl− cotransport.
    Type of Medium: Electronic Resource
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