Co-expression of mCysLT1 receptors and IK channels in Xenopus laevis oocytes elicits LTD4-stimulated IK current, independent of an increase in [Ca2+]i.
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Co-expression of mCysLT1 receptors and IK channels in Xenopus laevis oocytes elicits LTD4-stimulated IK current, independent of an increase in [Ca2+]i. / Wulff, Tune; Hougaard, Charlotte; Klaerke, Dan A; Hoffmann, Else K.
I: BBA General Subjects, Bind 1660, Nr. 1-2, 2004, s. 75-9.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Co-expression of mCysLT1 receptors and IK channels in Xenopus laevis oocytes elicits LTD4-stimulated IK current, independent of an increase in [Ca2+]i.
AU - Wulff, Tune
AU - Hougaard, Charlotte
AU - Klaerke, Dan A
AU - Hoffmann, Else K
N1 - Keywords: Animals; Calcium; Cations, Divalent; Cell Line; Cytokines; Egtazic Acid; Humans; Hydrogen-Ion Concentration; Large-Conductance Calcium-Activated Potassium Channels; Leukotriene D4; Membrane Proteins; Oocytes; Potassium Channels; Potassium Channels, Calcium-Activated; Potassium Channels, Tandem Pore Domain; RNA, Complementary; Receptors, Leukotriene; Transfection; Xenopus laevis
PY - 2004
Y1 - 2004
N2 - Addition of LTD4 (10 nM) to Xenopus laevis oocytes expressing the mCysLT1 receptor together with hBK or hIK channels resulted in the activation of both channels secondary to an LTD4-induced increase in [Ca2+]i. In addition, the hIK channel is activated by low concentrations of LTD4 (<0.1 nM), which did not result in any increase in [Ca2+]i. Even though activation of hIK by low concentrations of LTD4 was independent of an increase in [Ca2+]i, a certain "permissive" level of [Ca2+]i was required for its activation, since buffering of intracellular Ca2+ by EGTA completely abolished the response to LTD4. Neither hTBAK1 nor hTASK2 was activated following stimulations with LTD4 (0.1 and 100 nM).
AB - Addition of LTD4 (10 nM) to Xenopus laevis oocytes expressing the mCysLT1 receptor together with hBK or hIK channels resulted in the activation of both channels secondary to an LTD4-induced increase in [Ca2+]i. In addition, the hIK channel is activated by low concentrations of LTD4 (<0.1 nM), which did not result in any increase in [Ca2+]i. Even though activation of hIK by low concentrations of LTD4 was independent of an increase in [Ca2+]i, a certain "permissive" level of [Ca2+]i was required for its activation, since buffering of intracellular Ca2+ by EGTA completely abolished the response to LTD4. Neither hTBAK1 nor hTASK2 was activated following stimulations with LTD4 (0.1 and 100 nM).
U2 - 10.1016/j.bbamem.2003.11.001
DO - 10.1016/j.bbamem.2003.11.001
M3 - Journal article
C2 - 14757222
VL - 1660
SP - 75
EP - 79
JO - B B A - General Subjects
JF - B B A - General Subjects
SN - 0304-4165
IS - 1-2
ER -
ID: 6768716