Activation of T cell calcium influx by the second messenger ADP-ribose.
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Activation of T cell calcium influx by the second messenger ADP-ribose. / Gasser, Andreas; Glassmeier, Günter; Fliegert, Ralf; Langhorst, Matthias F; Meinke, Stephan; Hein, Dörte; Krüger, Sylvia; Weber, Karin; Heiner, Inka; Oppenheimer, Norman; Schwarz, Jürgen R; Guse, Andreas H.
In: J BIOL CHEM, Vol. 281, No. 5, 5, 2006, p. 2489-2496.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Activation of T cell calcium influx by the second messenger ADP-ribose.
AU - Gasser, Andreas
AU - Glassmeier, Günter
AU - Fliegert, Ralf
AU - Langhorst, Matthias F
AU - Meinke, Stephan
AU - Hein, Dörte
AU - Krüger, Sylvia
AU - Weber, Karin
AU - Heiner, Inka
AU - Oppenheimer, Norman
AU - Schwarz, Jürgen R
AU - Guse, Andreas H
PY - 2006
Y1 - 2006
N2 - Stimulation of Jurkat T cells by high concentrations of concanavalin A (ConA) induced an elevation of the endogenous adenosine diphosphoribose (ADPR) concentration and an inward current significantly different from the Ca2+ release-activated Ca2+ current (I(CRAC)). Electrophysiological characterization and activation of a similar current by infusion of ADPR indicated that the ConA-induced current is carried by TRPM2. Expression of TRPM2 in the plasma membrane of Jurkat T cells was demonstrated by reverse transcription-PCR, Western blot, and immunofluorescence. Inhibition of ADPR formation reduced ConA-mediated, but not store-operated, Ca2+ entry and prevented ConA-induced cell death of Jurkat cells. Moreover, gene silencing of TRPM2 abolished the ADPR- and ConA-mediated inward current. Thus, ADPR is a novel second messenger significantly involved in ConA-mediated cell death in T cells.
AB - Stimulation of Jurkat T cells by high concentrations of concanavalin A (ConA) induced an elevation of the endogenous adenosine diphosphoribose (ADPR) concentration and an inward current significantly different from the Ca2+ release-activated Ca2+ current (I(CRAC)). Electrophysiological characterization and activation of a similar current by infusion of ADPR indicated that the ConA-induced current is carried by TRPM2. Expression of TRPM2 in the plasma membrane of Jurkat T cells was demonstrated by reverse transcription-PCR, Western blot, and immunofluorescence. Inhibition of ADPR formation reduced ConA-mediated, but not store-operated, Ca2+ entry and prevented ConA-induced cell death of Jurkat cells. Moreover, gene silencing of TRPM2 abolished the ADPR- and ConA-mediated inward current. Thus, ADPR is a novel second messenger significantly involved in ConA-mediated cell death in T cells.
M3 - SCORING: Zeitschriftenaufsatz
VL - 281
SP - 2489
EP - 2496
JO - J BIOL CHEM
JF - J BIOL CHEM
SN - 0021-9258
IS - 5
M1 - 5
ER -