ライフサイエンスコーパス: calcium release from

1 Increasing HP causes calcium release from a ryanodine-sensitive cytoplasmic s

2 that sphingosine is a positive regulator of calcium release from acidic stores and that understandin

3 er hypothesis for NAADP action proposes that calcium release from acidic stores subsequently acts to

4 ne Dinucleotide Phosphate (NAADP) stimulates calcium release from acidic stores such as lysosomes and

5 ged Sph leads to a significant and transient calcium release from acidic stores that is independent o

6 provide further evidence that NAADP mediates calcium release from acidic stores through activation of

7 ells loaded with indo-1 provided evidence of calcium release from an intracellular calcium store sens

8 ium storage, 1,25(OH)(2)D not only increases calcium release from bone, but also inhibits calcium inc

9 d treatment with dantrolene, an inhibitor of calcium release from caffeine-ryanodine-sensitive stores

10 nity and the ability to invoke intracellular calcium release from CHO cells transfected with the MIP-

11 inositol 1,4,5-trisphosphate (IP3)-dependent calcium release from endoplasmic reticulum by inducing d

12 lation activates ryanodine receptor-mediated calcium release from endoplasmic reticulum stores, leadi

13 cium chelator BAPTA AM and agents that block calcium release from ER and influx through voltage-depen

14 ways leading to apoptotic cell death require calcium release from inositol 1,4,5-trisphosphate recept

15 hrough voltage-gated calcium channels and by calcium release from internal cellular stores.

16 imulated calcium response consisting of both calcium release from internal stores and influx from the

17 orescence changes in all platelets indicated calcium release from internal stores and influx of exter

18 by other nicotinic receptors and depends on calcium release from internal stores and probably influx

19 This indicates that both calcium influx and calcium release from internal stores are required for th

20 showed that the potentiation of RyR-mediated calcium release from internal stores by caffeine was abs

21 lcineurin to its substrates and may regulate calcium release from internal stores during neuronal isc

22 e solution and has been attributed either to calcium release from internal stores or to a direct effe

23 ibition of voltage-gated calcium channels or calcium release from internal stores reduces regenerativ

24 own, demonstrating further a requirement for calcium release from internal stores.

25 ux through voltage-gated channels and not to calcium release from internal stores.

26 ists include a significant contribution from calcium release from internal stores.

27 receptors, and suppression of InsP3-induced calcium release from internal stores.

28 sphate (NAADP) is a messenger that regulates calcium release from intracellular acidic stores.

29 Cholinergic inhibitory responses depend on calcium release from intracellular calcium stores, and r

30 ar calcium influx and subsequently affecting calcium release from intracellular calcium stores.

31 sphingosine 1-phosphate (S1P) can stimulate calcium release from intracellular organelles, resulting

32 endent increase in platelet shape change, in calcium release from intracellular stores [Ca2+]iand in

33 o block or enhance CICR to determine whether calcium release from intracellular stores affected actio

34 s in signal transduction, as cADPR regulates calcium release from intracellular stores and ADPR contr

35 effects on the efferent arteriole are due to calcium release from intracellular stores and calcium en

36 Interestingly, BMP-2 induced calcium release from intracellular stores and increased

37 s regulating two processes essential for LTD-calcium release from intracellular stores and phosphatas

38 stimulation of these receptors leads both to calcium release from intracellular stores and to dendrit

39 ular communication through gap junctions and calcium release from intracellular stores as mediators o

40 Nonetheless, a strong calcium release from intracellular stores can be elicite

41 Calmodulin (CaM) regulates calcium release from intracellular stores in skeletal mu

42 ropagation in the cell body, indicating that calcium release from intracellular stores is necessary.

43 Spontaneous calcium release from intracellular stores occurs during

44 Calcium release from intracellular stores occurs in a gr

45 lso produces vasomotor responses by inducing calcium release from intracellular stores through its pr

46 It has been proposed that calcium release from intracellular stores via InsP3 rece

47 protein coupled receptors (GPCRs) that cause calcium release from intracellular stores while other st

48 luR-mediated phosphoinositide hydrolysis and calcium release from intracellular stores, bridge the in

49 ) activates signaling cascades, resulting in calcium release from intracellular stores, ERK1/2 activa

50 ults demonstrate that, in addition to gating calcium release from intracellular stores, mAChR activat

51 concentrations by activating calcium-induced calcium release from intracellular stores, triggered by

52 oxide stimulates a tyrosine kinase-dependent calcium release from intracellular stores, which is assu

53 mechanism downstream from or independent of calcium release from intracellular stores.

54 ability of extracellular calcium to trigger calcium release from intracellular stores.

55 ibition of N- or P/Q-type VDCCs, or block of calcium release from intracellular stores.

56 e to an effect on calcium influx rather than calcium release from intracellular stores.

57 ospholipase C gamma(1), critical signals for calcium release from intracellular stores.

58 cium channels and ryanodine receptor-induced calcium release from intracellular stores.

59 ds Wnt proteins and can signal by activating calcium release from intracellular stores.

60 receptors, stimulated IP3 receptor-regulated calcium release from intracellular stores.

61 ingerprinting suggest that a third source of calcium, release from intracellular stores through the r

62 These findings indicate that calcium-induced calcium released from intraneuronal stores plays an impo

63 Agents that block calcium release from IP(3)- and ryanodine-sensitive stor

64 Although calcium release from IP(3)-sensitive stores was not requ

65 q), G(12), RhoA, actin, phospholipase C, and calcium release from IP(3)R-gated stores.

66 aling pathway that involves phospholipase C, calcium release from IP3-sensitive internal stores, and

67 r 1 and purinergic receptors and mediated by calcium release from IP3-sensitive internal stores.

68 Calcium released from IP3-sensitive calcium stores also

69 ctive pharmacological targeting of apoptotic calcium release from IP3R may enhance tumor cell immunog

70 ificantly, a specific inhibitor of apoptotic calcium release from IP3R strongly blocked lymphocyte ap

71 a cells by SW620 colon cancer cells requires calcium release from IP3R.

72 1a-mediated inositol phosphate formation and calcium release from mouse neurons in a PKC-dependent ma

73 erved function of AIP proteins is to inhibit calcium release from ryanodine receptors.

74 n catfish cone horizontal cells is linked to calcium release from ryanodine-sensitive intracellular c

75 Abnormal calcium release from sarcoplasmic reticulum (SR) is cons

76 Studies have shown that evoked calcium release from sarcoplasmic reticulum is compromis

77 Luminal calcium released from secretory organelles has been sugg

78 aled a unique receptor-mediated mechanism of calcium release from SGs that involves SG store-operated

79 ening on SG membranes as a potential mode of calcium release from SGs that may serve to raise local c

80 alcium, we also propose that caffeine-evoked calcium release from stores activates a calcium transpor

81 r, whereas increased axon outgrowth involves calcium release from stores through IP3 receptors as wel

82 e, and on I(Ca) in rods can be attributed to calcium release from stores: (1) caffeine's actions on [

83 Calcium release from the agonist-sensitive pool was also

84 Here we show that calcium release from the axonal endoplasmic reticulum (E

85 Investigating how calcium release from the endoplasmic reticulum (ER) is t

86 helial hyperplasia via apoptosis mediated by calcium release from the endoplasmic reticulum (ER), but

87 ptors (InsP3Rs) are channels responsible for calcium release from the endoplasmic reticulum (ER).

88 Induction of calcium release from the endoplasmic reticulum also lead

89 yR2-R4496C mutant HEK-293 cell line in which calcium release from the endoplasmic reticulum through t

90 We find here that localized calcium release from the endoplasmic reticulum via ryano

91 ed CD36 function in FA uptake and FA-induced calcium release from the endoplasmic reticulum, supporti

92 caused an increase in the InsP(3)-dependent calcium release from the endoplasmic reticulum.

93 inositol-1,4,5-trisphosphate (IP3)-meditated calcium release from the endoplasmic reticulum.

94 r factor of activated T cells (NFAT) through calcium release from the endoplasmic reticulum.

95 as indicated by reduced RyR agonist-induced calcium release from the ER and RyR-mediated synaptic re

96 n induces endoplasmic reticulum (ER) stress, calcium release from the ER and subsequent uptake of cal

97 m overload in SOD1G93A astrocytes and excess calcium release from the ER during ATP stimulation.

98 Bcl-2 inhibited the extent of calcium release from the ER of permeabilized WEHI7.2 cel

99 d that purinergic stimulation induces excess calcium release from the ER stores in SOD1G93A astrocyte

100 FasL stimulation and found that LFG inhibits calcium release from the ER, a process that correlates w

101 R calcium-ATPase pump inhibitor that induces calcium release from the ER, to investigate the possible

102 e receptor antagonist that inhibits abnormal calcium release from the ER.

103 tivation and thereby regulates InsP3-induced calcium release from the ER.

104 ies, we hypothesize that p12(I) may modulate calcium release from the ER.

105 Once liberated, ACh acts to trigger calcium release from the internal store in endothelial c

106 Calcium release from the intracellular stores plays an i

107 between plasma membrane and SR, resulting in calcium release from the latter.

108 o serve as a countercurrent mechanism during calcium release from the nuclear envelope.

109 Calcium release from the S-ER in neurons couples electri

110 TA are based on a steep relationship between calcium release from the sarcoplasmic reticulum (SR) and

111 ma membrane calcium current (ICa) and evoked calcium release from the sarcoplasmic reticulum (SR), wh

112 It activates calcium release from the sarcoplasmic reticulum via prot

113 In skeletal and cardiac muscle, calcium release from the sarcoplasmic reticulum, leading

114 ) activated ryanodine binding to and induced calcium release from the sarcoplasmic reticulum.

115 e sensor coupling t-tubule depolarization to calcium release from the sarcoplasmic reticulum.

116 macromolecular complex devoted to control of calcium release from the sarcoplasmic reticulum.

117 um-dependent relaxation is mediated by local calcium release from the sarcoplasmic reticulum.

118 lcium sparks." The ability of ICa to trigger calcium release from the SR in both hypertrophied and fa

119 m acidic stores subsequently acts to enhance calcium release from the SR.

120 expressed in the junctional SR, the site of calcium release from the SR.

121 obtained were consistent with a significant calcium release from the vacuole contributing to the ove

122 either TMTC1 or TMTC2 caused a reduction of calcium released from the ER following stimulation, wher

123 menon is a steep nonlinear dependence of the calcium released from the SR on the diastolic SR calcium

124 tudy we examined the causal role of abnormal calcium releases from the sarcoplasmic reticulum in prod

125 The ectopic calcium released from these receptors induces pro-hypert

126 oponin complex, CK-2017357 slows the rate of calcium release from troponin C and sensitizes muscle to

127 ner mechanistically dependent upon apoptotic calcium release from voltage-gated calcium channels.