Capacitative calcium entry

Berridge, Michael J.

doi:10.1042/bj3120001

Cited by 1,047 publications

(885 citation statements)

References 132 publications

(213 reference statements)

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“…Recently, a lot of interest has focused on the question whether the trp (transient receptor potential) channel from Drosophila photoreceptors or one of its mammalian homologues is similar or identical to the CRAC channel [1,2,7]. It has been suggested that trp is a store-operated Ca 2+ channel and it has been shown that trp channels expressed in Sf9 cells or Xenopus oocytes could be activated by thapsigargin [24,27,29].…”

Section: Discussionmentioning

confidence: 99%

Depletion of intracellular calcium stores activates an outward potassium current in mast and RBL‐1 cells that is correlated with CRAC channel activation

Hoth

1996

FEBS Letters

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Highly Ca 2+ selective Ca 2+ channels activated by store depletion have been recently described in several cell types and have been termed CRAC channels (for calcium releaseactivated calcium). The present study shows that following store depletion in mast and RBL-I cells, monovalent outward currents could be recorded if the internal solution contained K + but not Cs +. The activation of the outward K + current correlated with the activation of ICRAC, in both time and amplitude, suggesting that the K + current might be carried by CRAC channels. The amplitude of the outward current was increased if external Ca z+ was reduced or replaced by external Ba 2+. The outward K + conductance might have a physiological role in maintaining the driving force for Ca 2+ entry during the activation of CRAC channels.

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Section: Discussionmentioning

confidence: 99%

Depletion of intracellular calcium stores activates an outward potassium current in mast and RBL‐1 cells that is correlated with CRAC channel activation

Hoth

1996

FEBS Letters

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“…Small G proteins may be implicated in SOC channel modulation [4], while CIF and cGMP might be analogous, since this cyclic nucleotide appears to potentiate Ca 2+ influx activated in response to Ca 2+ store depletion in a variety of cells [6][7][8][9]. It is noteworthy that the first SOC to be identified, the Ca 2+ releaseactivated Ca 2+ (CRAC) channel, has been proposed to be a mammalian homologue of the transient receptor potential (trp) gene product of Drosophila photoreceptors [4], which shares significant amino acid sequence homology to voltagegated Ca 2+ channels (VGCs) [10]. This may indicate structural and functional similarities between SOCs and VGCs, whilst also pointing to the possibility that specific drug modulators of VGCs might also be effective against SOCs.…”

Section: Introductionmentioning

confidence: 99%

Functional importance of the dihydropyridine‐sensitive, yet voltage‐insensitive store‐operated Ca²⁺ influx of U937 cells

1996

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The Ca 2+ current activated by Ca 2+ store depletion in non-excitable cells is classically regarded as being dihydropyridine-insensitive, suggesting that store-operated Ca 2+ channels (SOCs) are dissimilar to voltage-gated Ca 2+ channels (VGCs) of excitable-cells. Here, we demonstrate dihydropyridine-sensitivity for the store-operated Ca 2+ influx induced by ATP and thapsigargin (Tg) in the non-excitable U937 cell-line. Ca 2+ store depletion by prior treatment of cells with either Tg or ATP, stimulated a 2+ Ca entry mechanism that was inhibited by nicardipine, nifedipine, and the specific L-type Ca 2+ channel blocker, calciseptine. A functional requirement for this Ca 2+ influx mechanism in agonist-induced mitogenesis seemed likely, since nicardipine, a particularly potent inhibitor of storeoperated Ca 2+ influx in these cells, suppressed ATP-and Tgstimulated cell proliferation. Depolarisation of cells with KCI, or gramicidin failed to elicit an increase in cytosolic Ca 2÷, suggesting that while the store-operated Ca 2+ influx channel of U937 cells shares pharmacologic properties with the L-type Ca 2+ channel, it is voltage-insensitive and therefore may resemble an L-type Ca 2+ channel lacking a voltage sensor.

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“…The rates of Ins(1,4,5)P $ F-stimulated increase in Ca# + oinduced fluo-3 fluorescence in the presence and absence of cytochalasin B and colchicine (16 µM each) were 1.85p0.18 (n l 13) and 2.15p0.16 (n l 10) fluorescence units\min respectively. Cytochalasin B plus colchicine did block the (1,4,5…”

Section: Effects Of Cytochalasin B and Colchicinementioning

confidence: 95%

“…The last-mentioned process, initially described by Putney [3], involves the release of Ca# + from a component of the smooth endoplasmic reticulum (SER), which in turn leads to activation of Ca# + inflow across the plasma membrane. This form of receptor-activated Ca# + channel is prevalent in many types of animal cell and is important in increases in intracellular Ca# + concentration promoted by extracellular signals [4].…”

Section: Introductionmentioning

confidence: 99%

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Store-activated Ca2+ inflow in Xenopus laevis oocytes: inhibition by primaquine and evaluation of the role of membrane fusion

Gregory

Barritt

1996

Biochemical Journal

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The role of membrane fusion in the activation of store-activated Ca2+ channels (SACCs) in the plasma membrane of Xenopus laevis oocytes was investigated with primaquine, an inhibitor of vesicle trafficking, reagents that disrupt the cytoskeleton, and reagents that activate or inhibit the functions of monomeric and trimeric GTP-binding regulatory proteins. Ca2+ inflow was assessed by measuring the rate of increase in the fluorescence of the intracellular Ca2+ chelator fluo-3 after the addition of extracellular Ca2+ to oocytes previously incubated in the absence of added Ca2+. Primaquine inhibited the 3-deoxy-3-fluoro-Ins(1,4,5)P3 (Ins(1,4,5)P3F)-stimulated increase in Ca2+o-induced fluo-3 fluorescence with no detectable effect on the release of Ca2+ from intracellular stores. The effect of primaquine was observed within 1.5 min, showed similarity to the inhibition induced by Gd3+, was reversible, and was observed when primaquine was added either before or after activation of the SACCs. The degree of inhibition of Ca2+ inflow by primaquine was halved when the extracellular concentration of Ca2+ was increased from 3.1 to 12.5 mM. Primaquine also inhibited Ca2+ inflow through cholera toxin-activated divalent cation channels and Drosophila Trpl channels (expressed in oocytes after injection of trpl cRNA). These results indicate that primaquine inhibits open SACCs, possibly by directly inhibiting Ca2+ flow through the channel pore. Colchicine plus cytochalasin B, Brefeldin A, the peptide Arf-1 (2–17) (introduced by microinjection), lovastatin or pertussis toxin did not inhibit the Ins(1,4,5)P3F-stimulated increase in fluo-3 fluorescence. In contrast, guanosine 5´-[γ-thio]triphosphate (GTP[S]), guanosine 5´-[β,γ-imido]triphosphate (p[NH]ppG) and AlF4-, but not guanosine 5´-[β-thio]diphosphate, inhibited the Ins(1,4,5)P3F-stimulated increase in fluo-3 fluorescence. Co-administration of GTP did not prevent the inhibition by GTP[S] or AlF4-. Staurosporine largely prevented the inhibition of store-activated Ca2+ inflow by GTP[S]. It is concluded that membrane fusion processes are unlikely to be involved in the link between the release of Ca2+ from the endoplasmic reticulum and activation of SACCs. The idea that this link is achieved by direct interaction of a protein(s) in the endoplasmic reticulum membrane with the SACC protein is briefly discussed.

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Capacitative calcium entry

Cited by 1,047 publications

References 132 publications

Depletion of intracellular calcium stores activates an outward potassium current in mast and RBL‐1 cells that is correlated with CRAC channel activation

Depletion of intracellular calcium stores activates an outward potassium current in mast and RBL‐1 cells that is correlated with CRAC channel activation

Functional importance of the dihydropyridine‐sensitive, yet voltage‐insensitive store‐operated Ca²⁺ influx of U937 cells

Store-activated Ca2+ inflow in Xenopus laevis oocytes: inhibition by primaquine and evaluation of the role of membrane fusion

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Capacitative calcium entry

Cited by 1,047 publications

References 132 publications

Depletion of intracellular calcium stores activates an outward potassium current in mast and RBL‐1 cells that is correlated with CRAC channel activation

Depletion of intracellular calcium stores activates an outward potassium current in mast and RBL‐1 cells that is correlated with CRAC channel activation

Functional importance of the dihydropyridine‐sensitive, yet voltage‐insensitive store‐operated Ca2+ influx of U937 cells

Store-activated Ca2+ inflow in Xenopus laevis oocytes: inhibition by primaquine and evaluation of the role of membrane fusion

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Functional importance of the dihydropyridine‐sensitive, yet voltage‐insensitive store‐operated Ca²⁺ influx of U937 cells