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Titolo:
Regulation of Ca2+-release-activated Ca2+ current (I-crac) by ryanodine receptors in inositol 1,4,5-trisphosphate-receptor-deficient DT40 cells
Autore:
Kiselyov, K; Shin, DM; Shcheynikov, N; Kurosaki, T; Muallem, S;
Indirizzi:
Univ Texas, SW Med Ctr, Dept Physiol, Dallas, TX 75390 USA Univ Texas Dallas TX USA 75390 ed Ctr, Dept Physiol, Dallas, TX 75390 USA Kansai Med Univ, Inst Liver Res, Dept Mol Genet, Moriguchi, Osaka 5708506,Japan Kansai Med Univ Moriguchi Osaka Japan 5708506 iguchi, Osaka 5708506,Japan
Titolo Testata:
BIOCHEMICAL JOURNAL
, volume: 360, anno: 2001,
parte:, 1
pagine: 17 - 22
SICI:
0264-6021(20011115)360:<17:ROCCC(>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
OPERATED HTRP3 CHANNELS; INTRACELLULAR CA2+; T-LYMPHOCYTES; DEPLETION; STORES; TRISPHOSPHATE; ACTIVATION; MECHANISM; MESSENGER; INFLUX;
Keywords:
calcium influx; patch-clamp; ryanodine receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Kiselyov, K Univ Texas, SW Med Ctr, Dept Physiol, 5323 Harry Hines Blvd, Dallas, TX 75390 USA Univ Texas 5323 Harry Hines Blvd Dallas TX USA 75390 75390 USA
Citazione:
K. Kiselyov et al., "Regulation of Ca2+-release-activated Ca2+ current (I-crac) by ryanodine receptors in inositol 1,4,5-trisphosphate-receptor-deficient DT40 cells", BIOCHEM J, 360, 2001, pp. 17-22

Abstract

Persistence of capacitative Ca2+ influx in inositol 1,4,5-trisphosphate (IP3) receptor (IP3R)-deficient DT40 cells (DT40(IP3R-/-)) raises the question of whether gating of Ca2+ release activated Ca2+ current (I-crae) by conformational coupling to Ca2+-release channels is a general mechanism of gating of these channels. In the present work we examined the properties and mechanism of activation of Ca2+ current in wild-type and DT40(IP3R-/-) cells. In both cell types passive depletion of internal Ca2+ stores by infusion of EGTA activated a Ca2+ current with similar characteristics and time course. The current was highly Ca2+-selective and showed strong inward rectification, all typical of The activator of I-crae ryanodine receptor (RyR), cADP-ribose (cADPR), facilitated activation of I-crae, and the inhibitors of the RyRs, 8-N-cADPR, ryanodine and Ruthenium Red, all inhibited I-crae, activation in DT40(IP3R-/-) cells, even after complete depletion of intracellular Ca2+ stores by ionomycin. Wild-type and DT40(IP3R-/-) cells express RyR isoforms I and 3. RyR levels were adapted in DT40(IP3R-/-) cells to a lower RyR3/RyR1 ratio than in wild-type cells. These results suggest that IP(3)Rsand RyRs can efficiently gate I-crae in DT40 cells and explain the persistence of I-crae gating by internal stores in the absence of IP(3)Rs.

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Documento generato il 25/11/20 alle ore 18:43:56