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 ibrillar mitochondria-directly exposed to SR calcium release-from aged mice had increased calcium con

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

9 strocyte signaling is blunted by diminishing calcium release from astrocyte stores.

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

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

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

13 Both agonists induce calcium release from endoplasmic reticulum (ER) stores a

14 Many cell surface stimuli cause calcium release from endoplasmic reticulum (ER) stores t

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

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

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

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

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

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

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

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

23 ents showed that L-type calcium channels and calcium release from internal stores are both required f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 Spontaneous calcium release from intracellular stores occurs during

49 Calcium release from intracellular stores occurs in a gr

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

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

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

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

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

55 beta-cell BDNF-TrkB.T1 signaling triggers calcium release from intracellular stores, increasing gl

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

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

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

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

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

61 5 and mGluR3, which promoted IP3R2-dependent calcium release from intracellular stores.

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

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

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

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

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

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

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

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

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

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

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

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

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

75 Calcium released from IP3-sensitive calcium stores also

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

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

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

79 Calcium release from liposome-HGN can be spatially patte

80 1a-mediated inositol phosphate formation and calcium release from mouse neurons in a PKC-dependent ma

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

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

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

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

85 Luminal calcium released from secretory organelles has been sugg

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

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

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

89 either L-type calcium channel activation or calcium release from stores is sufficient to permit pote

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

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

92 Calcium release from the agonist-sensitive pool was also

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

94 Calcium release from the endoplasmic reticulum (ER) is p

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

96 gnal-induced nuclear actin responses require calcium release from the endoplasmic reticulum (ER) targ

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

98 IP(3), a secondary messenger that stimulates calcium release from the endoplasmic reticulum (ER).

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

100 Induction of calcium release from the endoplasmic reticulum also lead

101 IL-4 induces calcium release from the endoplasmic reticulum and calci

102 This profoundly limited glutamate-induced calcium release from the endoplasmic reticulum and subse

103 istically, TMEM173 binding to ITPR1 controls calcium release from the endoplasmic reticulum in macrop

104 ight on the role of an endocytosis-dependent calcium release from the endoplasmic reticulum in the co

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

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

107 where receptor activation triggers transient calcium release from the endoplasmic reticulum, followed

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

109 g, triggering phospholipase C-gamma-mediated calcium release from the endoplasmic reticulum.

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

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

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

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

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

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

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

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

118 expression of Creld2 in osteoclasts impaired calcium release from the ER which is essential for activ

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

120 ux triggered activation of GPCR/IP3-mediated calcium release from the ER, impaired mitochondrial ATP

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

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

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

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

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

126 Calcium release from the intracellular stores plays an i

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

128 Here, we identify a role for calcium release from the lumen of the endoplasmic reticu

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

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

131 odine receptors (RyRs), causing uncontrolled calcium release from the sarcoplasmic and endoplasmic re

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

133 annels (CaV1) in the plasma membrane trigger calcium release from the sarcoplasmic reticulum (SR) by

134 ias are caused by unregulated 'pathological' calcium release from the sarcoplasmic reticulum (SR), th

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

136 s by PKARIa was sufficient to prevent global calcium release from the sarcoplasmic reticulum in LV my

137 PKARIalpha was sufficient to prevent global calcium release from the sarcoplasmic reticulum in LV my

138 of Tet2 and fed a Western diet have impaired calcium release from the sarcoplasmic reticulum into the

139 It activates calcium release from the sarcoplasmic reticulum via prot

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

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

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

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

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

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

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

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

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

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

150 ion is roughly proportional to the amount of calcium released from the Sarcoplasmic Reticulum (SR) du

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

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

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

154 to the dendritic shaft, the calcium-induced calcium release from this intracellular organelle allowe

155 Our findings suggest that calcium released from TPCs is involved in Tat endolysoso

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

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