ライフサイエンスコーパス: Ca2 induced

1 of NSF produced dose-dependent inhibition of Ca2+-induced 3H-NA release.

2 -perforated rat brain cortical synaptosomes, Ca2+-induced [3H]noradrenaline (3H-NA) release began wit

3 Removal of external Ca2+ induced a membrane conductance that differed from M

4 ory process, whereas buffering intracellular Ca2+ induced aberrant migration onto inappropriate pathw

5 nses to raised cytoplasmic Ca2+, we examined Ca2+-induced actin reorganization in normal and HHD kera

6 further increase in RET, which was due to a Ca2+-induced activating conformational change, as verifi

7 ations can be driven by a coupled process of Ca2+-induced activation and obligatory intrinsic inactiv

8 embranes of Scott cells were unresponsive to Ca2+-induced activation of PL scramblase at neutral pH,

9 ed desensitization of TRPV1, indicating that Ca2+-induced activation of PLC contributes to desensitiz

10 sis rate per unit of isometric force) during Ca2+-induced activation of Triton X-100-permeabilized ca

11 nel function due to increased sensitivity to Ca2+-induced activation.

12 t these residues directly participate in the Ca2+-induced active conformation of the polypeptide.

13 An antibody to syntaxin 4 also inhibited Ca2+-induced alpha-granule release by approximately 75%

14 ciated membrane protein completely inhibited Ca2+-induced alpha-granule release.

15 le-associated membrane protein and inhibited Ca2+-induced alpha-granule secretion from streptolysin O

16 mpal slices, briefly elevating extracellular Ca2+ induced an activity-dependent, transient potentiati

17 This study investigates the mechanism of Ca2+-induced binding of PKC betaII to anionic membranes

18 mal titration calorimetry analysis reveals a Ca2+-induced binding of the CaBP1 C-domain to the N-term

19 -flow fluorescence spectroscopy reveals that Ca2+-induced binding of the isolated C2 domain to anioni

20 Studies with PKC betaII reveal that Ca2+-induced binding to membranes by the full-length pro

21 is mutation causes a delay and a decrease in Ca2+-induced but not in hypertonic sucrose-induced relea

22 in which GTP- and GDP-bound Rab11b inhibited Ca2+-induced, but not constitutive, exocytosis, in non-n

23 Hypoxia depresses the increase in Ca2+ induced by anti-CD3/CD28 antibodies in approximatel

24 Strikingly similar entry of Ca2+ induced by cell permeant alkylators indicated that

25 poride on increases in intracellular Na+ and Ca2+ induced by oxidative stress.

26 nhibits the transient elevation of cytosolic Ca2+ induced by thapsigargin (TG), a selective inhibitor

27 urrents activated by a rise in intracellular Ca2+, induced by either Ca(2+)-induced Ca2+ release or b

28 that a sustained elevation of intracellular Ca2+, induced by membrane potential depolarization and m

29 (CICR) was triggered by a rapid increase in [Ca2+] induced by flash photolysis of Nitr-5 (0.08 mM), r

30 In contrast, an increase in intracellular [Ca2+] induced by ionomycin activated Cl- currents with v

31 synaptic responses, and a transition between Ca2+ -induced Ca2+ release and inositol trisphosphate wa

32 tage-dependent Ca2+ channels and followed by Ca2+ -induced Ca2+ release from the endoplasmic reticulu

33 xtracellular Ca2+ or on the classic model of Ca2+ -induced Ca2+ release in cardiac myocytes.

34 se ventricular myocytes and are activated on Ca2+ -induced Ca2+ release.

35 this model are compared with those based on Ca2+(-)induced Ca2+ release alone in the bullfrog sympat

36 has been developed and its significance for Ca2+(-)induced Ca2+ release and Ca2+ oscillations invest

37 Calcium (Ca2+)-induced Ca2+ release (CICR) in cardiac myocytes ex

38 To minimize Ca2+-induced Ca2+ inactivation, Ba2+ current (I(Ba)) was

39 ction pathway responsible for cAMP-dependent Ca2+-induced Ca2+ release (CICR) from endoplasmic reticu

40 Ca2+-induced Ca2+ release (CICR) from intracellular stor

41 se-fire" model that mimics the properties of Ca2+-induced Ca2+ release (CICR) from isolated sites is

42 ition, we tested the hypothesis that altered Ca2+-induced Ca2+ release (CICR) from ryanodine receptor

43 ed ryanodine receptor type 2 (RyR2)-mediated Ca2+-induced Ca2+ release (CICR) from SR membranes (IC50

44 r the graded nature and early termination of Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic r

45 nous cADPR increases the Ca2+ sensitivity of Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic r

46 e-mode Na+-Ca2+ exchange (NCX) in activating Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic r

47 -adrenergic receptor (betaAR) stimulation of Ca2+-induced Ca2+ release (CICR) in cardiac myocytes.

48 ed [Ca2+]i increases, providing evidence for Ca2+-induced Ca2+ release (CICR) in rods and cones.

49 The effects of modulating Ca2+-induced Ca2+ release (CICR) in single cardiac myocy

50 Ca2+-induced Ca2+ release (CICR) is a well characterized

51 confocal microscopy to provide evidence that Ca2+-induced Ca2+ release (CICR) may contribute to the m

52 Ca2+-induced Ca2+ release (CICR) plays an important role

53 art, to Ca2+ discharge from an intracellular Ca2+-induced Ca2+ release (CICR) pool.

54 ctionally related: they reflect a process of Ca2+-induced Ca2+ release (CICR) that requires activatio

55 The contribution of Ca2+-induced Ca2+ release (CICR) to trigger muscle contr

56 e cytosolic [Ca2+] reached the threshold for Ca2+-induced Ca2+ release (CICR) was able to simulate ea

57 Alternatively, Ca2+-induced Ca2+ release (CICR) was triggered by a rapi

58 IP3Rs display Ca2+-induced Ca2+ release (CICR), but are grouped in clu

59 the inward Ca2+ current (ICa) gives rise to Ca2+-induced Ca2+ release (CICR), the amplifying Ca2+ si

60 n beta-cells indicate that GLP-1 facilitates Ca2+-induced Ca2+ release (CICR), whereby mobilization o

61 depends on the positive feedback process of Ca2+-induced Ca2+ release (CICR).

62 ryanodine receptors (RyRs) in the process of Ca2+-induced Ca2+ release (CICR).

63 The Ca2+-induced Ca2+ release amplification factor or gain (

64 Our results suggest that Ca2+-induced Ca2+ release contributes little to the elev

65 closure approach to study the restitution of Ca2+-induced Ca2+ release during simulated two-pulse vol

66 gh plasma membrane Ca2+ channels, as well as Ca2+-induced Ca2+ release from cytoplasmic stores.

67 Activation of Ca2+-induced Ca2+ release from internal stores with a gr

68 ors, voltage-dependent calcium channels, and Ca2+-induced Ca2+ release from internal stores.

69 Ca2+-induced Ca2+ release from presynaptic endoplasmic r

70 reverse Na+-Ca2+ exchange, and the resulting Ca2+-induced Ca2+ release from SR.

71 phosphorylation as a homeostatic response by Ca2+-induced Ca2+ release from the ER.

72 m is required to counteract the regenerative Ca2+-induced Ca2+ release from the sarcoplasmic reticulu

73 action and that the contractions depended on Ca2+-induced Ca2+ release from the sarcoplasmic reticulu

74 s that accurately represent local control of Ca2+-induced Ca2+ release in cardiac myocytes can reprod

75 ensity approach to modeling local control of Ca2+-induced Ca2+ release in cardiac myocytes, where we

76 ort that 2-aminoethoxydiphenyl borate blocks Ca2+-induced Ca2+ release in isolated, non-synaptosomal

77 hyperpolarization and arterial dilation via Ca2+-induced Ca2+ release in response to an endothelial-

78 ing enhances SR release channel activity and Ca2+-induced Ca2+ release in TG4 cardiac myocytes, and t

79 dence validating the local control theory of Ca2+-induced Ca2+ release in the heart.

80 ulator of ryanodine receptors also amplified Ca2+-induced Ca2+ release in these neurons.

81 d the model is inconsistent with the data if Ca2+-induced Ca2+ release is a dominating factor.

82 Ca2+-induced Ca2+ release is a general mechanism that mo

83 We find that Ca2+-induced Ca2+ release is not necessary to explain th

84 try across the plasma membrane (50%) whereas Ca2+-induced Ca2+ release is the major contributor to Ca

85 g and release functions and destabilizes the Ca2+-induced Ca2+ release mechanism by reducing the effe

86 zed Ca2+ influx via L-type Ca2+ channels and Ca2+-induced Ca2+ release mediated by clusters of ryanod

87 Waves of Ca2+-induced Ca2+ release occur in various cell types an

88 hat depolarization-induced Ca2+ entry evoked Ca2+-induced Ca2+ release only from the ryanodine-sensit

89 cycles of Ca2+ uptake into and release from Ca2+-induced Ca2+ release stores (pool 2).

90 om this Ca2+ pool, the amount of Ca2+ in the Ca2+-induced Ca2+ release stores was increased.

91 ows that the inherently positive feedback of Ca2+-induced Ca2+ release terminates, despite a large re

92 e intracellular Ca2+signals are amplified by Ca2+-induced Ca2+ release via both ryanodine and IP3 rec

93 ux through T-type Ca2+ channels, followed by Ca2+-induced Ca2+ release via RyRs, contributes to the g

94 ine receptors (RyRs) and release of Ca2+ via Ca2+-induced Ca2+ release(CICR).

95 ow propose to be an amplification mechanism (Ca2+-induced Ca2+ release).

96 (NCX) could enhance Ca2+ influx via NCX (and Ca2+-induced Ca2+ release).

97 Ca2+ from the ryanodine-sensitive store via Ca2+-induced Ca2+ release, and that depolarization-induc

98 t Ca2+ release, VDCR) and Ca2+ influx-gated (Ca2+-induced Ca2+ release, CICR) sarcoplasmic reticulum

99 odine-sensitive stores are implicated in the Ca2+-induced Ca2+ release, NO can be expected to potenti

100 This process, called Ca2+-induced Ca2+ release, relies on the properties of t

101 Ca2+-induced Ca2+ release, resulting in concerted openin

102 ess how i(Ca) and NP(o) separately influence Ca2+-induced Ca2+ release, we measured I(Ca) and junctio

103 ction coupling in cardiac myocytes occurs by Ca2+-induced Ca2+ release, where L-type Ca2+ current evo

104 with an intrinsically higher sensitivity to Ca2+-induced Ca2+ release.

105 lude IP3-dependent and voltage-dependent and Ca2+-induced Ca2+ release.

106 ase in [Ca2+]i may, however, be amplified by Ca2+-induced Ca2+ release.

107 suggest that palmitoyl-CoA may be needed for Ca2+-induced Ca2+ release.

108 ve evolved in parallel with the mechanism of Ca2+-induced Ca2+ release.

109 cement of Ca2+ signalling via the process of Ca2+-induced Ca2+ release.

110 eart rates, which may contribute to enhanced Ca2+-induced Ca2+ release.

111 trinsically unstable regenerative process of Ca2+-induced Ca2+ release.

112 discussed with respect to the properties of Ca2+-induced Ca2+-release (CICR) and the local control t

113 y serve to augment the existing regenerative Ca2+-induced Ca2+-release process; however, the sensitiv

114 Ca2+-induced, calcineurin/Crz1p-dependent activation of

115 he ATP2C1-controlled ATP metabolism mediates Ca2+-induced cell-to-cell adhesion in normal keratinocyt

116 reticulin, and ERp72 have been implicated in Ca2+-induced cellular trafficking, including the secreti

117 resence of Ca2+, failing to undergo a normal Ca2+-induced change in position.

118 In this work, measurements of Ca2+-induced changes in intrinsic tryptophan fluorescenc

119 ecular switch which is controlled by smaller Ca2+-induced changes in TnC.

120 The Ca2+-induced changes were inhibited by cyclosporin A or

121 The Ca2+-induced changes were not age dependent.

122 in binds Ca2+ at EF3 and EF4, and exhibits a Ca2+-induced closed to open transition like that of CaM.

123 binding site in a manner reminiscent of the Ca2+ -induced closure of the regulatory domain of tropon

124 nergy balance provide the fine-tuning of the Ca2+-induced conformational change in the EF-hand protei

125 n of charged ligand residues, in addition to Ca2+-induced conformational change.

126 isothermal titration calorimetry and undergo Ca2+-induced conformational changes by circular dichrois

127 g properties, its Ca2+/Mg2+-binding, and its Ca2+-induced conformational changes in comparison to the

128 mutants provide specific signals for probing Ca2+-induced conformational changes in the regulatory do

129 ted that EF-hands II and III are crucial for Ca2+-induced conformational changes in the visinin-like

130 Although much is known about the Ca2+-induced conformational changes in TnC, the Ca2+-bin

131 investigate the dynamics and kinetics of the Ca2+-induced conformational changes of the cardiac thin

132 rates of Ca2+-binding proteins dictate their Ca2+-induced conformational changes, Ca2+-induced protei

133 toylated p22, or p22 incapable of undergoing Ca2+-induced conformational changes, cannot reverse the

134 Herzberg, Moult, and James proposed that the Ca2+-induced conformational transition in troponin C inv

135 The Ca2+-induced cross-linking of this cytoskeletal element

136 We have investigated Ca2+ -induced cyclin destruction in MI and MII by using

137 Furthermore, CAPE directly inhibits Ca2+-induced cytochrome c release from isolated brain mi

138 ells, as its interruption severely increased Ca2+-induced cytotoxicity and cell mortality.

139 vity to Ca2+, as they were more sensitive to Ca2+-induced decreases in state 3 respiration and DeltaP

140 withdrawal of acetylcholine (ACh) can elicit Ca2+-induced delayed afterdepolarizations (DADs) in atri

141 dy level of about -100 pA from P13 while the Ca2+-induced DeltaCm remained relatively constant, indic

142 s been shown to protect mitochondria against Ca2+-induced deltaPsi(m) loss (2).

143 The Ca2+-induced dephosphorylation of BAD correlated with it

144 This Ca2+-induced dephosphorylation was calmodulin-dependent,

145 tochondria loaded with rhodamine 123 against Ca2+-induced depolarization.

146 amil blocked these K+ channels and inhibited Ca2+-induced differentiation, as assessed by cornified e

147 that K+ channel activation is necessary for Ca2+-induced differentiation.

148 We propose that Ca2+-induced dimerization of DREAM may partially block t

149 ith physiological studies, indicate that the Ca2+-induced dimerization of synaptotagmin is important

150 erminal half of calmodulin is sufficient for Ca2+-induced displacement of alpha-actinin.

151 Activity- and Ca2+-induced E(Cl) shifts were larger in mature neurons,

152 r GDP-bound state both effectively inhibited Ca2+-induced exocytosis but seemed to act by distinct me

153 hibition of the SM-syntaxin complex promotes Ca2+-induced exocytosis, suggesting that complex formati

154 Rab11 family (Rab11a, 11b, and 25) impaired Ca2+-induced exocytosis.

155 tures provides insight into the mechanism of Ca2+-induced fluorescence change.

156 power stroke heads (rigor.ADP/Ca2+ and rigor/Ca2+) induced further changes in the orientational distr

157 ave separate functions to underlie transient Ca2+-induced hyperpolarizations and to protect against d

158 3) and renders the channel less sensitive to Ca2+ -induced inactivation.

159 s at the molecular motif responsible for the Ca2+-induced inactivation of the channels.

160 Furthermore, this Ca2+ -induced increase in degradation of cyclin B1 requi

161 The Ca2+-induced increase in intrinsic tryptophan fluorescen

162 ereas the Ca2+ release phase was driven by a Ca2+-induced increase in IP3 sensitivity, Ca2+ release c

163 e basal contractility nor high extracellular Ca2+-induced increase in myocyte contraction.

164 All the mutations significantly reduced 2 mM Ca2+-induced increases in the 30 microM ACh response (P

165 Third, they reduced extracellular Ca2+-induced increases in the 30 microM ACh response.

166 Ca2+-induced inhibition of alpha1C voltage-gated Ca2+ ch

167 The Ca2+-induced inhibition of Topo II catalytic activity an

168 A qualitative model involving Ca2+-induced InsP3R sequestration and inactivation can a

169 after removal of the drug and to potentiate Ca2+-induced insulin secretion from electropermeabilized

170 study we examined the role of K+ channels in Ca2+-induced keratinocyte differentiation.

171 presence of physiological concentrations of Ca2+ induced less than a 2-fold increase in PKC-PH domai

172 in tryptophanyl fluorescence indicated that Ca2+ induced long range conformational changes throughou

173 the actin cytoskeleton acts as a barrier for Ca2+-induced lysosomal exocytosis.

174 A Ca2+-induced, membrane-bound enzyme was responsible for

175 ficits and that the increased sensitivity to Ca2+ induced mitochondrial permeabilization maybe a cont

176 ed from the mitochondrion via induction of a Ca2+-induced mitochondrial permeability transition and t

177 ilon resulted in a significant inhibition of Ca2+-induced mitochondrial swelling, an index of pore op

178 d particularly zinc, significantly prolonged Ca2+-induced mitogen-activated protein kinase phosphoryl

179 This Ca2+-induced mobilization of phosphatidylserine to the s

180 from brain mitochondria by antagonizing the Ca2+-induced mPT.

181 (g) No enzyme inactivation is observed for Ca2+-induced MPT.

182 -dependent transcription and antagonizes its Ca2+-induced nuclear accumulation.

183 Interestingly, the Ca2+-induced nuclear translocation of ERK and Rsk2 to th

184 pose of these experiments was to investigate Ca2+-induced opacification and proteolysis in the organ-

185 ed a striking visual tracking of the gradual Ca2+-induced opening of the gelsolin molecule and highli

186 These results indicate that the Ca2+-induced opening of the interfaces between helical s

187 Under these conditions, Ca2+-induced opening of the PTP was not blocked by cyclo

188 es expression of many genes, is activated by Ca2+-induced phosphorylation.

189 Munc18c-syntaxin complex potently amplified Ca2+-induced platelet granule secretion.

190 silon with the pore components and inhibited Ca2+-induced pore opening.

191 This movement, from a low Ca2+ to a Ca2+-induced position has been directly demonstrated by

192 rily through the cortex of the egg, and that Ca2+ -induced production of IP3 at the plasma membrane a

193 scence spectra of Ncs1p revealed significant Ca2+-induced protein conformational changes indicative o

194 e their Ca2+-induced conformational changes, Ca2+-induced protein/peptide and protein/protein interac

195 the presence of adenine nucleotides and Mg2+,Ca2+-induced PTP in non-synaptosomal brain mitochondria

196 Ca2+ -induced quenching of Ser-700 constructs required h

197 displacement of cell-surface toxicant by the Ca2+-induced reduction in cell-surface negativity.

198 othesis that a similar transition is the key Ca2+-induced regulatory event in calmodulin.

199 A Ca2+-induced reversible change in the intensities of the

200 s I and III to permeabilized cells increased Ca2+-induced secretion up to 15% and 90%, respectively,

201 ggesting a separate secretory mechanism from Ca2+-induced secretion.

202 Using Ca2+-induced SNARE complex disruption, we have analyzed

203 omol/L) and nifedipine (50 nmol/L) abolished Ca2+-induced spontaneous tone in aorta from DOCA-salt ra

204 reases in SR Ca2+ capacity, but decreases in Ca2+-induced SR Ca2+ release, leading to depressed contr

205 to the flow of information originating from Ca2+-induced stress, or to the coordinated expression of

206 ells for 5 min with 6 mum free intracellular Ca2+ induced strong secretion and a large reduction of t

207 Maximal activation with 10 microM free Ca2+ induced sustained increases in isometric force, sti

208 atnDap4]DALDA protected mitochondria against Ca2+-induced swelling.

209 ons with target molecules are triggered by a Ca2+-induced switch in electrostatic potential.

210 After Ca2+-induced targeting to alpha1C, CaMKII becomes tightl

211 of single-channel kinetics demonstrated that Ca2+ induced the appearance of long-lived closed interva

212 Addition of external Ca2+ induced the same Ca2+ release observed in maximally

213 inds to specific DNA sequences and regulates Ca2+-induced transcription of prodynorphin and c-fos gen

214 calcineurin-mediated response in yeast, the Ca2+-induced transcriptional activation of FKS2, which e

215 tein (CREB) have been implicated in cAMP and Ca2+-induced transcriptional activation.

216 n of the protein, thus blocking the putative Ca2+-induced transition.

217 h multiphoton microscopy to examine the fast Ca2+-induced transitions of acrylodan-labeled calmodulin

218 We now report that Ca2+-induced uncoupling of the bovine brain V-ATPase can