ライフサイエンスコーパス: Ca2 dependent

1 findings that neurexin-neuroligin binding is Ca2+ dependent.

2 KCC stimulation was also Ca2+ dependent.

3 of uniquantal versus multiquantal events is Ca2+ dependent.

4 and DN CaM was robust, and not significantly Ca2+ dependent.

5 ase in IRS-2 expression, indicating this was Ca2+-dependent.

6 in Escherichia coli K-12, for expression of Ca2+-dependent 3'-O-deacylase activity in membranes.

7 gly, although BMP1 has long been known to be Ca2+-dependent, a property previously assumed to apply t

8 mpal neurons can preempt a large, prolonged, Ca2+ -dependent acidosis.

9 ing depolarizing potentials that can produce Ca2+-dependent action potentials at the bipolar cell ter

10 ephosphorylation of ADF/cofilin required the Ca2+-dependent activation of calcineurin (PP2B).

11 Responses to swelling involve the Ca2+-dependent activation of K+ channels, which promote

12 Ectopic expression of IRBIT resulted in Ca2+-dependent activation of NHE3 activity, whereas sile

13 Ca2+]i removal at steady-state, secondary to Ca2+-dependent activation of SR Ca2+ uptake.

14 ugh either an unknown pathway after NgR- and Ca2+-dependent activation of the epidermal growth factor

15 ty of the postsynaptic neurons involving the Ca2+-dependent activation of TRP channels.

16 neous release at a synapse as a simultaneous Ca2+-dependent activator and clamp of exocytosis.

17 Ca2+-dependent activator protein for secretion (CAPS) is

18 the calmodulin (CaM) superfamily, modulates Ca2+-dependent activity of inositol 1,4,5-trisphosphate

19 We propose that CaBP1 may regulate Ca2+-dependent activity of InsP3Rs by promoting structur

20 fast vesicle exocytosis is driven by a dual Ca2+-dependent activity of synaptotagmin-1, namely Ca2+-

21 n maintaining epithelial polarity by forming Ca2+-dependent adherens junctions between epithelial cel

22 previous studies showed the amplitude of the Ca2+ -dependent afterhyperpolarization (AHP) following s

23 ing to one of these sites, the IQ domain, is Ca2+ dependent and competitive with CaM binding.

24 constants in the rat, like the turtle, were Ca2+ dependent and faster in hair cells tuned to higher

25 hanism for Alternaria-induced ATP release is Ca2+ dependent and involves exocytosis of ATP.

26 Both the Ca2+-dependent and -independent pathways are corequired

27 sphatidylinositol polyphosphates co-activate Ca2+-dependent and -independent phospholipid binding to

28 KCNQ2-4 channels and CaM are likely to have Ca2+-dependent and Ca2+-independent components.

29 bunit C-tail in the plasma membrane inhibits Ca2+-dependent and slow voltage-dependent inactivation.

30 le to voltage-dependent K+ channels, whereas Ca2+-dependent and voltage-independent K+channels contri

31 ect of Abeta on PtdIns(4,5)P2 metabolism was Ca2+-dependent and was not observed in neurons that were

32 vation of endogenous G-proteins reduced both Ca2+-dependent, and voltage-dependent inactivation of re

33 is involved in short-term facilitation, and Ca2+-dependent Apl I contributes to intermediate-term fa

34 A hallmark of apoptotic cells is the Ca2+-dependent appearance of phosphatidylserine (PS) at

35 Fluorescence spectroscopy reveals Ca2+-dependent association of CaM with a polypeptide cor

36 Both the Mg2+-dependent and Ca2+-dependent ATP hydrolysis activities increased by mo

37 The presence of the f peptide led to reduced Ca2+-dependent ATPase activity in a reconstituted thin f

38 The Mg2+-dependent, but not the Ca2+-dependent, ATPase activity of the double mutant was

39 activity of PDP1 is greatly enhanced through Ca2+ -dependent binding of the catalytic subunit (PDP1c)

40 ependent activity of synaptotagmin-1, namely Ca2+-dependent binding both to SNARE complexes and to ph

41 synaptotagmin 1-ECFP to SNARE complexes, and Ca2+-dependent binding of synaptotagmin 1-ECFP to phosph

42 s compete with the neuronal core complex for Ca2+-dependent binding to the presynaptic Ca2+-sensor sy

43 h increases myofilament Ca2+ sensitivity via Ca2+-dependent binding to troponin C, exerts positive in

44 e O-antigen polysaccharide of V. cholerae in Ca2+-dependent biofilm development in model and true sea

45 an exopolysaccharide-dependent biofilm and a Ca2+-dependent biofilm.

46 ggers the fusion of docked vesicles by local Ca2+-dependent buckling of the plasma membrane together

47 response to perforation, host cells undergo Ca2+ -dependent but K+ -independent resealing of their p

48 This increased spontaneous release remained Ca2+ dependent but was activated at lower Ca2+ concentra

49 e of Arabidopsis thaliana encodes a class of Ca2+-dependent Ca2+-release channel that is known from n

50 dicate that in smooth muscle, stimulation of Ca2+-dependent, calcineurin-mediated nuclear import and

51 aining period with Ca2+-independent, but not Ca2+-dependent, CaMKII.

52 y excitable endocrine cells and suggest that Ca2+-dependent cAMP oscillations are derived from an inc

53 To determine the function of the Ca2+-dependent cell adhesion molecule, N-cadherin, in mu

54 inding, the mechanism of Ca2+ signaling, and Ca2+-dependent cell adhesion, while avoiding the complex

55 ntaining stimulus fidelity in the control of Ca2+-dependent cell function.

56 moke, modulates neuronal activity to produce Ca2+-dependent changes in gene transcription.

57 es 4114-4142 is involved in the mechanism of Ca2+-dependent channel regulation.

58 Recently a novel cGMP-activated Ca2+-dependent Cl- channel has been described in rat mes

59 dulin (CaM) on single channel cGMP-activated Ca2+-dependent Cl- current (ICl(cGMP,Ca) in inside-out p

60 We suggest that this effect may be due to Ca2+-dependent competition between Gbetagamma and synapt

61 ase only correlate with their effects on the Ca2+-dependent component.

62 The Ca2+-dependent components of the AHP have been attribute

63 f known crystal structures, indicates that a Ca2+-dependent conformation of the ATPase headpiece is r

64 The Ca2+-dependent conformational change is required for S10

65 antibodies of our patient mainly recognized Ca2+-dependent conformational epitopes and targeted matu

66 In liposomes, the purified VDAC displays Ca2+-dependent control of the molecular cut-off size and

67 h-clamp recording and Ca2+ uncaging revealed Ca2+-dependent corelease of ACh and GABA from, and the p

68 An inhibitor of calpain, a Ca2+-dependent cysteine protease, partially suppressed m

69 3 protects pancreas and salivary glands from Ca2+-dependent damage.

70 We conclude that ARF6 plays a role in Ca2+-dependent DCV exocytosis by regulating the activity

71 priming as a PIP2 binding protein to enhance Ca2+-dependent DCV exocytosis.

72 timately leading to excessive stimulation of Ca2+-dependent degradative pathways.

73 Similarly, Ca2+ -dependent degranulation, integrin alpha(IIb)beta3

74 regulates sporulation perhaps by controlling Ca2+-dependent desensitization of Git3p.

75 , NMDA receptor activation resulted in rapid Ca2+-dependent detachment and disintegration of oligoden

76 ne (C6PS) to bovine factor Xa (FXa) leads to Ca2+-dependent dimerization in solution.

77 uces the inhibitory action of GABA through a Ca2+-dependent downregulation of KCC2 function.

78 f NMDAR-mediated currents is not a result of Ca2+-dependent effects on the NMDAR.

79 e local SR Ca2+ release required to activate Ca2+-dependent eNOS/NOi production from subsarcolemmal c

80 Tissue transglutaminase (TGase) is a Ca2+-dependent enzyme that catalyzes cross-linking of in

81 Cytosolic phospholipase A2 (cPLA2) is a Ca2+-dependent enzyme that mediates agonist-dependent ar

82 ry phospholipases comprise a large family of Ca2+-dependent enzymes that liberate arachidonic acid (A

83 These results suggest HvCDPK1 may mediate Ca2+-dependent events of the GA response, such as contro

84 ein-coupled receptors control Ca2+ entry and Ca2+-dependent events such as neurotransmitter and hormo

85 DR7, is involved in vesicle mobilization and Ca2+-dependent exocytosis at synapses.

86 functions as an essential component for the Ca2+-dependent exocytosis of dense-core vesicles in neur

87 particles activates a phosphoinositide- and Ca2+-dependent exocytosis pathway to provide membranes n

88 pores, we treat cells with ATP to stimulate Ca2+-dependent exocytosis, increase intracellular alkali

89 es in several cell types, where it regulates Ca2+-dependent exocytosis.

90 pses in the central nervous system (CNS) for Ca2+-dependent exocytosis.

91 l stability and, surprisingly, is capable of Ca2+-dependent F-actin bundling, suggesting that D6 cont

92 that the Ca2+ sensor calmodulin can trigger Ca2+-dependent facilitation (CDF) of channel opening.

93 Ca2+-dependent facilitation (CDF) of voltage-gated calci

94 the channel C terminus, controls the form of Ca2+-dependent facilitation (CDF), an activity-dependent

95 CaV2.1 channels with beta2a subunits undergo Ca2+-dependent facilitation and inactivation attributabl

96 nted Ca2+-dependent inactivation, and caused Ca2+-dependent facilitation of currents evoked by step d

97 f injury and toward the plasma membrane in a Ca2+-dependent fashion in response to a newly designed i

98 mmalian cell surfaces in a concentration and Ca2+-dependent fashion.

99 mammalian nerve terminals, show two types of Ca2+-dependent feedback regulation-inactivation (CDI) an

100 factor-like repeat dramatically altered the Ca2+-dependent fluorescence transition for the Asn-700 c

101 for NAADP in differentiation, and (iii) that Ca2+-dependent function can be messenger-specific.

102 of Ca2+ signals and influences a variety of Ca2+-dependent functions.

103 rs, suggesting that the parasite expresses a Ca2+ dependent, furin-like protease activity.

104 To further define elements of the Ca2+-dependent GA response machinery, we have cloned a C

105 g, mitochondrial and nuclear signalling, and Ca2+-dependent gene regulation, but their existence rais

106 RabA4b recruitment of PI-4Kbeta1 results in Ca2+-dependent generation of PI-4P on this compartment,

107 The mechanism underlying Ca2+-dependent glutamate release from astrocytes is most

108 Although these proteins mediate Ca2+-dependent glutamate release from astrocytes, it is

109 Ts abolished mechanically and agonist-evoked Ca2+-dependent glutamate release from astrocytes.

110 tion of migration by M3 was mediated through Ca2+-dependent guanylyl cyclase-cyclic GMP-protein kinas

111 oscopy reveals this peptide binds within the Ca2+-dependent hydrophobic pocket of S100A1.

112 n, shows rapid, self-incompatibility-induced Ca2+-dependent hyperphosphorylation in vivo.

113 Extensive functional data suggests that this Ca2+-dependent inactivation (CDI) requires both calmodul

114 IHCs show generally weak-to-absent Ca2+-dependent inactivation (CDI), potentially permittin

115 c BAPTA, which promotes release by hampering Ca2+-dependent inactivation (CDI).

116 Although the molecular details underlying Ca2+-dependent inactivation have been characterized, lit

117 ast with those of CaM, which promoted strong Ca2+-dependent inactivation of Ca(v)1.2 with these same

118 Based on previous findings that Ca2+-dependent inactivation of Ca(v)2.1 (P/Q-type) Ca2+

119 We conclude that Ca2+-dependent inactivation of Ca(v)2.1 depends on a sub

120 importance of buffer kinetics in modulating Ca2+-dependent inactivation of Ca(v)2.1.

121 ldendrin causes a more modest suppression of Ca2+-dependent inactivation of Cav1.2 through a differen

122 We conclude that, in NCX KO myocytes, Ca2+-dependent inactivation of I(Ca) reduces I(Ca) ampli

123 Ca2+ extrusion is, in part, attributable to Ca2+-dependent inactivation of PMCAs.

124 terminal alpha(1C)-LA/IQ region and mediates Ca2+-dependent inactivation of the channel.

125 us or its deletion inhibit both voltage- and Ca2+-dependent inactivation of the current.

126 negative feedback loop, calmodulin mediates Ca2+-dependent inactivation of the NMDA receptor by disp

127 1 greatly prolonged Ca2+ currents, prevented Ca2+-dependent inactivation, and caused Ca2+-dependent f

128 itions when the channel gating, voltage- and Ca2+-dependent inactivation, and plasma-membrane targeti

129 tant but different roles in the voltage- and Ca2+-dependent inactivation, as well as beta subunit mod

130 As the Ca2+-sensor for Ca2+-dependent inactivation, calmodulin (CaM) has been p

131 a negative feedback regulation by Ca2+ ions, Ca2+-dependent inactivation, which is important for rest

132 er than the one tethered to LA/IQ to support Ca2+-dependent inactivation.

133 litates calcium channel gating, and supports Ca2+-dependent inactivation.

134 a-free Ca(v)1.2 channels but did not support Ca2+-dependent inactivation.

135 d astrocyte neuroprotection is mediated by a Ca2+-dependent increase in mitochondrial metabolism.

136 These phenotypes are caused by a Ca2+-dependent increase in neurotransmitter release effi

137 vascular endothelium to sTNF-alpha induced a Ca2+-dependent increase of mitochondrial H2O2 that cause

138 The Ca2+-dependent inhibition of bTREK-1 by AngII was blunte

139 However, PLB did not affect the Ca2+-dependent inhibition of Ca-ATPase phosphorylation b

140 We have shown previously that the Ca2+-dependent inhibition of lens epithelial cell-to-cel

141 Previously Ca2+-dependent inhibition of NHE3 was demonstrated in th

142 data suggest a common mechanism by which the Ca2+-dependent inhibition of the alpha-class of gap junc

143 gh these two pathways, but ACTH displayed no Ca2+-dependent inhibition.

144 use S100A1 has recently been identified as a Ca2+-dependent inotropic factor in the heart, this study

145 For alpha1B receptors the Ca2+-dependent Ins(1,4,5)P3 production may serve to augm

146 A Ca2+ -dependent interaction occurs between calmodulin-li

147 k from several laboratories has documented a Ca2+-dependent interaction between ERalpha and calmoduli

148 Here we show that Ca2+-dependent interaction of the synaptotagmin VII C(2)

149 s provide trans-synaptic connectivity by the Ca2+-dependent interaction of their alternatively splice

150 y charged residue (R233Q in rat) showed that Ca2+-dependent interactions between the C2A domain and m

151 can regulate Ca2+ sensing and the subsequent Ca2+-dependent interactions mediated by Syt C2 domains.

152 ta-catenin was not affected by disruption of Ca2+-dependent intercellular cadherin interactions.

153 r our understanding of contraction and other Ca2+-dependent intracellular processes.

154 Anti-M3R-positive serum had no effect on Ca2+-dependent ion channel activation evoked by the dire

155 ular Ca2+ waves and their role in activating Ca2+-dependent ion channels in CA1 pyramidal neurons.

156 ease in [Ca2+]i and consequent activation of Ca2+-dependent ion channels in individual mouse and huma

157 . increased number) of the small-conductance Ca2+ -dependent K+ (SK) channels, or their interaction w

158 erpolarization mediated by small-conductance Ca2+-dependent K+ (SK) channels was critical for the pre

159 minent CA2+ transients to various stimuli, a CA2+-dependent K+ channel may help SON astrocytes with K

160 iving force through CFTR after activation of Ca2+-dependent K+ channels.

161 L-type Ca2+ channels, and large-conductance Ca2+-dependent K+ current (I(BK)).

162 s probably underlain by a small-conductance, CA2+-dependent, K+ type 3 (SK3) channel.

163 age-related increase in the amplitude of the Ca2+-dependent, K+-mediated afterhyperpolarization (AHP)

164 ific enzyme inhibitors showed that up-stream Ca2+-dependent kinase(s) is required for the inducing ef

165 This pathway is believed to use Ca2+-dependent local interactions among IP3 receptors (I

166 ons responded to depolarizing current with a Ca2+-dependent low-threshold potential.

167 ng the RGR sequence binds to calmodulin in a Ca2+ -dependent manner with a Kd < or =1.5 microm; conce

168 2F domain bound syntaxin 1A and SNAP-25 in a Ca2+-dependent manner (with optimal 61 microm free Ca2+

169 rburst cells release GABA in a prolonged and Ca2+-dependent manner and inhibit each other laterally v

170 that a single CaM binds to two NR1 CTs in a Ca2+-dependent manner and promotes their reversible "dim

171 CaM bound directly to TRE17 in a Ca2+-dependent manner both in vitro and in vivo.

172 function of its binding target proteins in a Ca2+-dependent manner in the process of restoration of e

173 hat astrocytes release gliotransmitters in a Ca2+-dependent manner to affect synaptic transmission.

174 nd p38 mitogen-activated protein kinase in a Ca2+-dependent manner, but influx by extra-cellular Ca2+

175 effectively compete with Par-4 binding in a Ca2+-dependent manner, providing a route for Ca2+-mediat

176 I and II and also interact dynamically, in a Ca2+-dependent manner, with the alpha(1C)-IQ region.

177 phosphorylated by soybean cell extract in a Ca2+-dependent manner.

178 retinal guanylate cyclase (GC) activity in a Ca2+-dependent manner.

179 oteins that can interact with membranes in a Ca2+-dependent manner.

180 P) secretion in a thromboxane A2 (TxA2)- and Ca2+-dependent manner.

181 inal (ct) CaM binding regions bound CaM in a Ca2+-dependent manner.

182 main that bound the Cav1.3 II-III loop, in a Ca2+-dependent manner.

183 e found that agrin-G3 binds sialic acid in a Ca2+-dependent manner.

184 otif binds the Ca2+ sensor, calmodulin, in a Ca2+-dependent manner; and a proline-rich N-terminal reg

185 We show that activation of ERK1, a Ca2+-dependent MAP kinase response, is required for both

186 ] modulates adipocyte lipid metabolism via a Ca2+-dependent mechanism and inhibits adipocyte UCP2 exp

187 f Epac modulates KATP channel activity via a Ca2+-dependent mechanism involving the activation of Ca2

188 n of axonal action potentials and, through a Ca2+-dependent mechanism, the average amplitude of the p

189 nd the C2 domain that is responsible for the Ca2+-dependent membrane binding.

190 5 and synaptotagmin 1, two proteins from the Ca2+-dependent membrane fusion machinery.

191 Ca2+-dependent membrane interaction has long been recogn

192 mV by concerted increases in ATP demand and Ca2+-dependent metabolic activation.

193 Therefore, t-FcepsilonRIbeta mediates Ca2+ -dependent microtubule formation, which promotes de

194 ls IP3Rs and CACNA1A were downregulated, and Ca2+-dependent mitochondrial transport proteins MIRO1 an

195 Thus, Syt VII regulates the Ca2+-dependent mobilization of lysosomes as a supplement

196 We developed a Ca2+-dependent model of cell damage for salivary gland a

197 ght-scattering experiments indicate that the Ca2+-dependent monomer-polymer transitions of the mutant

198 traction in striated muscles is regulated by Ca2+-dependent movement of tropomyosin-troponin on thin

199 ated at the metaphase-anaphase transition by Ca2+-dependent myosin light chain kinase (MLCK) activity

200 s), inducing glutamate receptor-independent, Ca2+ -dependent, neuronal injury inhibited by ASIC block

201 ce generation and exercise capacity, reduced Ca2+-dependent neutral protease calpain activity and pla

202 ptotagmin 1, we observed no major changes in Ca2+-dependent or -independent activities, indicating th

203 ons (NMJs) and synapses of the CNS through a Ca2+ -dependent pathway.

204 lation is dependent upon the activation of a Ca2+-dependent pathway as shown by anti-CD80 mAb-induced

205 Remarkably, this Ca2+-dependent pathway cannot be activated by the global

206 The novel Ca2+-dependent pathway is distinctive in its lack of ATP

207 These results identify a novel Ca2+-dependent pathway that signals from fibrocystin loc

208 ated inhibition of bTREK-1 through the novel Ca2+-dependent pathway was blocked by the AT1 receptor a

209 1 agonist) agonists via Ca2+-independent and Ca2+-dependent pathways, respectively, in sensory neuron

210 Reinforcing a role for Syt VII in Ca2+-dependent phagocytosis, particle uptake in Syt VII-

211 Syt VII was required for a form of Ca2+-dependent phagolysosome fusion that is analogous to

212 overexpression of the constitutively active Ca2+-dependent phosphatase calcineurin (CAN) causes seve

213 Here, we studied the Ca2+-dependent phosphatase calcineurin, which regulates

214 smitter release, was proposed to function by Ca2+-dependent phospholipid binding and/or by Ca2+-depen

215 ese results reveal clear distinctions in the Ca2+-dependent phospholipid binding modes of the synapto

216 Ca2+-dependent phospholipid binding to the C2A and C2B d

217 Annexin XI, a member of the Ca2+-dependent, phospholipid-binding protein family, is

218 Here we report how multiple Ca2+-dependent phosphorylation sites within the transcri

219 by expressing a dominant-negative isoform of Ca2+-dependent PKC (apl-I).

220 , which are eventually turned off by a D1/D5-Ca2+-dependent PKC mechanism.

221 without affecting the expression of group IV Ca2+-dependent PLA2.

222 the susceptibility of neighboring neurons to Ca2+-dependent plasticity.

223 These data suggest that Ca2+-dependent postsynaptic fusion of glutamate-loaded v

224 cle exocytosis by acting at a rate-limiting, Ca2+-dependent prefusion step.

225 recursor to the core complex formed during a Ca2+-dependent priming step of exocytosis.

226 ough TRPV4 predisposes RGCs to activation of Ca2+ -dependent proapoptotic signaling pathways, indicat

227 TP, connexin hemichannels, and intracellular Ca2+ -dependent process.

228 ulate mitochondrial ADP-phosphorylation in a Ca2+-dependent process that fulfills the genetic criteri

229 t PMA-induced mucin secretion is, in fact, a Ca2+-dependent process under the conditions of low bulk

230 triphosphate) is generally accepted to be a Ca2+-dependent process.

231 r increasing intracellular Ca2+ and studying Ca2+ -dependent processes.

232 well as the relationships among the various Ca2+-dependent processes remain largely unknown.

233 appeared to be regulated by [Ca2+]i, and/or Ca2+-dependent processes, as it was significantly enhanc

234 Our model includes Ca2+ -dependent production of IP3 at the plasma membrane

235 nd severe NAD+ /ATP depletion that stimulate Ca2+ -dependent programmed necrosis, unique to this new

236 Here, we report that the Ca2+-dependent protein cross-linking enzyme tissue trans

237 to the multigene transglutaminase family of Ca2+-dependent protein cross-linking enzymes.

238 dent GA response machinery, we have cloned a Ca2+-dependent protein kinase (HvCDPK1) from these cells

239 activates ERK indirectly, via recruitment of Ca2+-dependent protein kinase C alpha and betaI.

240 ase1 (CDPK1), which is predicted to encode a Ca2+-dependent protein kinase, resulted in significantly

241 Silencing Ca2+-dependent protein kinase1 (CDPK1), which is predict

242 s an ideal approach to the identification of Ca2+-dependent protein-protein interactions, which are i

243 ong-term potentiation (LTP) triggered robust Ca2+-dependent Ras activation in single spines that deca

244 ng alpha2-integrin was activated due to both Ca2+-dependent recruitment of Ca2+/calmodulin-dependent

245 n's interaction with myosin and mediates the Ca2+ -dependent regulation of contraction by troponin in

246 mitochondrial oxidative phosphorylation and Ca2+ -dependent regulation of Krebs cycle dehydrogenases

247 Thus, CaM imparts Ca2+-dependent regulation not only to mature Ca(V)1.2 ch

248 lectrophoresis and by the loss and regain of Ca2+-dependent regulation of ATPase activity.

249 e rod photoresponse, indicating that dynamic Ca2+-dependent regulation of cGMP synthesis was preserve

250 surface liquid (ASL) through both cAMP- and Ca2+-dependent regulation of ion and water transport.

251 on with CaM could afford the opportunity for Ca2+-dependent regulation of membrane targeting.

252 transients in myocytes, we demonstrate that Ca2+-dependent regulation of NCX is preserved in Delta56

253 e, whereas the Slo1 cytosolic module confers Ca2+-dependent regulation on the Slo3 pore module.

254 n the force-producing state and period 5 for Ca2+-dependent regulation with troponin.

255 Many of these Ca2+-dependent regulatory processes operate in cardiomyo

256 spontaneous and evoked release used the same Ca2+-dependent release mechanism.

257 tivation of postsynaptic mGluRs triggers the Ca2+-dependent release of endocannabinoids that activate

258 In this study, we show that Ca2+-dependent resealing after permeabilization with the

259 a2+]i but stimulation of the ECs generates a Ca2+ dependent response in the VSMCs.

260 n that targets to mitochondria and increases Ca2+-dependent ROS production.

261 Q (containing glutamate)-SNARE essential for Ca2+-dependent secretory vesicle-plasma membrane fusion

262 nals; (2) reduced activity of calcineurin, a Ca2+-dependent serine/threonine phosphatase, increases s

263 DAC5) nuclear shuttling represent a critical Ca2+-dependent signaling circuit for controlling cardiac

264 How Ca2+-dependent signaling effectors are regulated in card

265 suggesting its potential role in controlling Ca2+-dependent signaling effectors such as calcineurin.

266 ceptors revealed the possible involvement of Ca2+-dependent signaling in PGE2-mediated activation of

267 Ca2+-dependent signaling is highly regulated in cardiomy

268 However, the effect of Ca2+-dependent signaling on NHE3 activity varies dependi

269 Here, we identify an NMDA receptor-mediated, Ca2+-dependent signaling pathway that couples neuronal a

270 plastic, growth-related pH changes through a Ca2+-dependent signaling pathway.

271 emaining questions in cardiac biology is how Ca2+-dependent signaling pathways are regulated under co

272 contraction coupling (ECC) and activation of Ca2+-dependent signaling pathways.

273 eract with incompatible pollen, triggering a Ca2+-dependent signalling network resulting in pollen tu

274 eract with incompatible pollen, triggering a Ca2+-dependent signalling network, resulting in the inhi

275 in complex, leading to pathological calcium (Ca2+)-dependent signals that damage muscle cells.

276 nd regulated the NR2B glutamate receptor and Ca2+-dependent signals through the beta-catenin pathway

277 electrical response composed of a transient Ca2+-dependent SK channel-mediated hyperpolarization and

278 ding sites of thin filament in two settings: Ca2+-dependent sliding speed of unloaded thin filaments

279 In hippocampal pyramidal neurons, the Ca2+ -dependent slow afterhyperpolarization (sAHP) exhib

280 at the D232N mutation dramatically increases Ca2+-dependent SNARE complex binding by native synaptota

281 a2+-dependent phospholipid binding and/or by Ca2+-dependent soluble N-ethylmaleimide-sensitive factor

282 The expressed complexes exhibited pH- and [Ca2+]-dependent specific activities that were similar to

283 ocytosis but suggest that it is not the sole Ca2+-dependent step.

284 f striated muscle contraction is achieved by Ca2+ -dependent steric modulation of myosin cross-bridge

285 loying recombinant proteins, immunoblotting, Ca2+-dependent stimulation of GC, fluorescence emission

286 The Ca2+-dependent stimulation of neurite elongation has gen

287 Ca2+-dependent stimulation of NHE3 activity was dependen

288 mpared GECI fluorescence saturation with CaM Ca2+-dependent structural transitions.

289 It was Ca2+ dependent, suggesting activation by increased [Ca2+

290 We have performed a kinetic analysis of Ca2+-dependent switching in the complex between calmodul

291 Thus, Ca2+-dependent synaptic signals can spread to couple mul

292 from synaptotagmin I knock-out mice rescued Ca2+-dependent synchronous transmitter release and reduc

293 propionate (AMPA) receptors (AMPARs) and is Ca2+-dependent, the molecular basis for AMPAR-mediated C

294 at 28 days and was associated with abnormal Ca2+-dependent tone and higher Ca(L) currents in the VSM

295 enhanced Ca(L) channel current, and elevated Ca2+-dependent tone.

296 Postsynaptic neuroligins engage in Ca2+-dependent transsynaptic interactions via their extr

297 each NCS protein by its myristoyl group, and Ca2+-dependent unmasking of different residues, may expl

298 These results suggest that Ca2+-dependent upregulation of mitochondrial O2- product

299 rsts of Na+ spikes, often riding on a slower Ca2+-dependent waveform.

300 ound that halothane binding to calmodulin is Ca2+ -dependent, which demonstrates anesthetic specifici