ライフサイエンスコーパス: CaM

1 CaM adopts a highly compact conformation in which its op

2 CaM also modulates NaV1.5 and the ryanodine receptor, Ry

3 CaM and CML regulate a wide range of target proteins and

4 CaM binds to and stimulates PI3Kalpha/Akt signaling, pro

5 CaM can thereby replace a missing receptor-tyrosine kina

6 CaM contacts the KCNQ1 voltage sensor through a specific

7 CaM is shown to be absolutely necessary for efficient ac

8 CaM specifically targeted the highly polybasic anchor re

9 CaM triggered an increase in hydrodynamic volume in both

10 CaM/CMLs decode and relay information encrypted by the s

11 M368 on KCa3.1 and M72 on CaM at the KCa3.1-CaM-BD/CaM interface.

12 s transfected with pcDNA3.1-myc-His-Phe(138)-CaM, the lysoPC-induced TRPC6-CaM dissociation and TRPC6

13 Here we present the NMR structure of Ca(2+)-CaM bound to two molecules of ER-alpha (residues 287-305

14 Data indicate that both PIP2 and Ca(2+)-CaM perform the same function on IKS channel gating by p

15 hat the diverse IQD members sequester Ca(2+)-CaM signaling modules to specific subcellular sites for

16 ts displayed increased autonomous and Ca(2+)-CaM stimulated activities.

17 dered CaMKK2 virtually insensitive to Ca(2+)-CaM stimulation.

18 insensitivity to gating modulation by Ca(2+)-CaM.

19 It was shown experimentally that Ca(2+)/CaM (holoCaM) binds to the CaMKII peptide with overwhelm

20 data demonstrate that the complex of Ca(2+)/CaM and K-Ras4B is stable in the presence of anionic mem

21 on) by 6-fold and lowers the EC50 for Ca(2+)/CaM binding to activated eEF-2K (Thr-348 phosphorylated)

22 is unusual regulation was mediated by Ca(2+)/CaM binding to the substrate sites resulting in protecti

23 -terminus as important for binding to Ca(2+)/CaM by interacting with R126 on CaM.

24 Thus, Ca(2+)/CaM control of actin dynamics seems to be a much more br

25 reduced sensitivity of the kinase to Ca(2+)/CaM inhibition.

26 study, we investigated the effect of Ca(2+)/CaM on the interaction of GDP- and GTP-loaded K-Ras4B wi

27 her examine the inhibitory effects of Ca(2+)/CaM on the Kv7.4 channel.

28 c insights into the critical roles of Ca(2+)/CaM regulation of the Kv7.4 channel under physiological

29 of LAVP-mediated autoinhibiton during Ca(2+)/CaM stimulation.

30 Accordingly, increased binding of Ca(2+)/CaM to PSD-95 induced by a chronic increase in Ca(2+) in

31 pon Ca(2+) influx, Ca(2+)/calmodulin (Ca(2+)/CaM) binding to the N-terminus of PSD-95 mediates postsy

32 tional change upon Ca(2+)/calmodulin (Ca(2+)/CaM) binding.

33 n Ca(2+) and Ca(2+)-bound calmodulin (Ca(2+)/CaM) to relieve autoinhibition of the catalytic subunit

34 om phosphorylation in the presence of Ca(2+)/CaM, a mechanism that favors phosphorylation by prolonge

35 which lack activity in the absence of Ca(2+)/CaM, cMLCK has constitutive activity that is stimulated

36 desensitization of the CNG channel by Ca(2+)/CaM, interact to regulate the olfactory response.

37 s progressively removed by Ca(2+) and Ca(2+)/CaM, whereas LAVP remains engaged.

38 d found that CPK28 is a high affinity Ca(2+)/CaM-binding protein.

39 tion of action potential duration and Ca(2+)/CaM-dependent inactivation after treatment.

40 ycling properties, and (3) diminished Ca(2+)/CaM-dependent inactivation of L-type Ca(2+) channels.

41 kt by phosphorylation at Thr-308 in a Ca(2+)/CaM-dependent manner.

42 between CaM and two specific targets, Ca(2+)/CaM-dependent protein kinase II (CaMKII) and neurogranin

43 CaMKK2 (Ca(2+)/CaM-dependent protein kinase kinase 2) is a central memb

44 to CPK regulation, as is the case for Ca(2+)/CaM-dependent protein kinases outside the plant lineage,

45 almodulin (CaM) activates a family of Ca(2+)/CaM-dependent protein kinases.

46 MLCK4 has only Ca(2+)/CaM-independent activity with comparable Vmax and Km val

47 eously lacking NCKX4 (NCKX4(-/-)) and Ca(2+)/CaM-mediated CNG channel desensitization (CNGB1(DeltaCaM

48 ficiently by autonomous compared with Ca(2+)/CaM-stimulated CaMKII activity.

49 a(2+)-responsive and was inhibited by Ca(2+)/CaM.

50 tutive activity that is stimulated by Ca(2+)/CaM.

51 tivates pure CaMKII in the absence of Ca(2+)/CaM.

52 (Ca)-binding affinity, ryanodine receptor 2-CaM binding, Ca handling, L-type Ca current, and action

53 to generate models of the KCa3.1 and KCa2.3 CaM-BD/CaM complexes with SKA-121.

54 CaM-positive cases were compared with the 33 CaM-negative cases, CaM-positive cases had a more severe

55 When the clinical sequelae of these 5 CaM-positive cases were compared with the 33 CaM-negativ

56 ly transfected with pcDNA3.1-myc-His-Phe(99)-CaM, but not in ECs transfected with pcDNA3.1-myc-His-Ph

57 aining detailed structural information for a CaM-K-Ras complex is still challenging.

58 In this study, a CaM-independent activation mechanism for smMLCK by mecha

59 mpared with long QT syndrome D96V-CaM, A103V-CaM had significantly less effects on L-type Ca current

60 Even a 1:3 mixture of A103V-CaM:WT-CaM activated Ca waves, demonstrating functional

61 1 may promote lysosome fission by activating CaM.

62 cells, we demonstrate that inhibition of Akt-CaM binding attenuated Akt activation.

63 reduction versus WT-CaM), but did not alter CaM binding to ryanodine receptor 2.

64 ntervention capable of specifically altering CaM expression and potentially attenuating LQTS-triggere

65 Although CaM binds over 100 proteins, practical limitations cause

66 on of Ser-500 is found to require Ca(2+) and CaM and is inhibited by mutations that compromise bindin

67 ry site (Ser-500) integrates with Ca(2+) and CaM to influence eEF-2K activity.

68 lation of Ser-500 integrates with Ca(2+) and CaM to regulate eEF-2K.

69 y results revealed that the gating brake and CaM bind each other with high-nanomolar affinity.

70 nt kinase, and TRPML1, lysosomal calcium and CaM play essential regulatory roles in the mTORC1 signal

71 etails of the interplay between membrane and CaM binding to Akt may help in the development of potent

72 as on Ca(2+)/calmodulin (CaM) signaling and CaM association.

73 ect that is influenced by both [Ca(2+)] and [CaM].

74 ain melting transitions of Ca(2+)-free (apo) CaM (reduction in alpha-helix structure by 13% (CD) and

75 ular Dynamics (MD) simulations show that apo-CaM exists in dynamic equilibrium with holo-like conform

76 cent structural characterization of the AQP0-CaM complex, the mechanism by which CaM modulates AQP0 r

77 rs calcium sensitivity by modifying the AQP0-CaM interaction interface, particularly at an arginine-r

78 of the K-Ras4B HVR that stably wraps around CaM's acidic linker.

79 rk contrast to the actions of arrhythmogenic CaM mutations N54I, D96V, N98S, and D130G, which all dim

80 as the mechanistic effects of arrhythmogenic CaM mutations.

81 eptor, RyR2), and it appears that attenuated CaM Ca(2+) binding correlates with impaired CaM-dependen

82 erate models of the KCa3.1 and KCa2.3 CaM-BD/CaM complexes with SKA-121.

83 ivators bind relatively "deep" in the CaM-BD/CaM interface and hydrogen bond with E54 on CaM.

84 of the benzothiazoles/oxazoles to the CaM-BD/CaM interface and then used computational modeling softw

85 n KCa3.1 and M72 on CaM at the KCa3.1-CaM-BD/CaM interface.

86 This is possible, in part, because CaM binding proteins are "tuned" to different Ca2+ flux

87 We focused on binding between CaM and two specific targets, Ca(2+)/CaM-dependent prote

88 and reveals a regulatory interaction between CaM and KCNQ1 that may explain CaM-mediated LQTS.

89 converts an endothermal interaction between CaM and the CaM-binding domain (CaMBD) of RyR2 into an e

90 data indicate a distinct interaction between CaM-F142L and the RyR2 CaMBD, which may explain the stro

91 molecular mechanism of the interplay between CaM and membrane binding is not established.

92 assumes a helical conformation upon binding CaM, with associated conformational changes to both CaM

93 I(3,4,5)P3 is required for membrane binding, CaM displacement, and Akt activation.

94 Both CaM and K-Ras4B HVR are highly flexible molecules, sugge

95 p to the hydrophobic pockets located at both CaM lobes further enhanced CaM-HVR complex stability.

96 th associated conformational changes to both CaM lobes as indicated by amide chemical shifts of the a

97 gating, and that (2) TRPV1 and Ca(2+)-bound CaM but not Ca(2+)-free CaM were preassociated in restin

98 a(2+)-free CaM and inhibited by Ca(2+)-bound CaM.

99 ar [S100A1], which promoted a shift of bound CaM to a lower FRET orientation (without altering the am

100 T detects two structural states of RyR-bound CaM, which respond to [Ca(2+)] and are isoform-specific.

101 he stronger CaM-dependent RyR2 inhibition by CaM-F142L, despite its reduced Ca(2+) binding.

102 ta evidence of allosteric CNGC regulation by CaM.

103 Using an explicit model of Ca2+, CaM, and seven highly-expressed hippocampal CaM binding

104 the binding and activation dynamics of Ca2+/CaM signal transduction and can be used to guide focused

105 observations of decreased activation of Ca2+/CaM-dependent protein kinase II in knockout models of ne

106 In this work, we view Ca2+/CaM as a limiting resource in the signal transduction pa

107 on and increased cytosolic Ca(2+), calcified CaM N lobe interacts with helix B in place of PIP2 to li

108 al the competition of PIP2 and the calcified CaM N lobe to a previously unidentified site in Kv7.1 he

109 Calmodulin (CaM) and closely related calmodulin-like (CML) polypepti

110 Calmodulin (CaM) has been shown to regulate DR5-mediated apoptotic s

111 Calmodulin (CaM) is a Ca(2+)-sensing protein that is highly conserve

112 Calmodulin (CaM) mutations are associated with severe forms of long

113 Calmodulin (CaM), a Ca(2+)-sensing protein, is constitutively bound

114 ent on Abp1 as well as on Ca(2+)/calmodulin (CaM) signaling and CaM association.

115 izing the CNG channel via Ca(2+)/calmodulin (CaM), to reduce the response.

116 f LQTS is a disruption of Ca(2+)/calmodulin (CaM)-dependent inactivation of L-type Ca(2+) channels.

117 apse strength require the Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) and its autono

118 We observed that Ca(2+)/calmodulin (CaM)-dependent protein kinase kinase 2 (beta) (CaMKK2) i

119 ylation in the absence of Ca(2+)/calmodulin (CaM).

120 ulates lysosome fusion through a calmodulin (CaM)-dependent mechanism.

121 ents of the beta-tubulin (BenA), calmodulin (CaM), and RNA polymerase II second largest subunit (RPB2

122 imal Kv7.1 C terminus (CT) binds calmodulin (CaM) and phosphatidylinositol-4,5-bisphosphate (PIP2), b

123 investigated the impact of bound calmodulin (CaM)-target compound structure on the affinity of calciu

124 TRPC6 channels is not known, but calmodulin (CaM) contributes to the regulation of TRPC channels.

125 Calcium signalling mediated by Calmodulin (CaM) and calmodulin-like (CML) proteins is critical to p

126 synthase (eNOS) is triggered by calmodulin (CaM) binding and is often further regulated by phosphory

127 ast cancer cells is modulated by calmodulin (CaM).

128 of one or two subunits, calcium-calmodulin (CaM)-dependent protein kinase II (CaMKII) is composed of

129 ates AKAP79 through its effector calmodulin (CaM), but the molecular basis of this regulation was pre

130 It also engages calmodulin (CaM) to reduce subsequent NMDA receptor activity in a pr

131 How calmodulin (CaM) acts in KRAS-driven cancers is a vastly important q

132 study, where we synthesize human calmodulin (CaM) by using a CFPS kit and prove the structural integr

133 In calmodulin (CaM)-rich environments, oncogenic KRAS plays a critical

134 llular Ca(2+) sensors, including calmodulin (CaM) 3, CaM7 and several CaM-like proteins, pointing to

135 -7 on SG recruitment may involve calmodulin (CaM), pretreatment of islets with CaM blocker calmidazol

136 y (cryo-EM) structure of a KCNQ1/calmodulin (CaM) complex.

137 a(2+) binding to the C-domain of calmodulin (CaM) by an unknown mechanism.

138 TORC1 by inducing association of calmodulin (CaM) with mTOR.

139 ctor 2 kinase (eEF-2K), the only calmodulin (CaM)-dependent member of the unique alpha-kinase family,

140 acellular Ca(2+)-sensing protein calmodulin (CaM) are arrhythmogenic, yet their underlying mechanisms

141 alcium-binding messenger protein Calmodulin (CaM) as a function of temperature and Ca(2+) concentrati

142 lcium-binding messenger protein, calmodulin (CaM), and phosphorylation of the CaM-binding site abolis

143 um to its intracellular receptor calmodulin (CaM) activates a family of Ca(2+)/CaM-dependent protein

144 The calcium-sensor calmodulin (CaM) acts as a common activator of the networks responsi

145 are gated by calcium binding to calmodulin (CaM) molecules associated with the calmodulin-binding do

146 alpha is modulated by Ca(2+) via calmodulin (CaM).

147 Furthermore, whether calmodulin (CaM) contributes to CPK regulation, as is the case for C

148 gements and its interaction with Calmodulin (CaM) under activation by chemical agonists and temperatu

149 C termini, which associate with calmodulin (CaM), a universal calcium sensor.

150 d that at elevated calcium levels in cancer, CaM recruits PI3Kalpha to the membrane and extracts K-Ra

151 ed loop, which sits outside of the canonical CaM-binding site on the AQP0 cytosolic face, mechanicall

152 ere compared with the 33 CaM-negative cases, CaM-positive cases had a more severe phenotype with an a

153 Notably, collapsed CaM is observed after binding of an extended CaM to K-Ra

154 he AQP0 cytosolic face, mechanically couples CaM to the pore-gating residues of the second constricti

155 Compared with long QT syndrome D96V-CaM, A103V-CaM had significantly less effects on L-type

156 I, D96V, N98S, and D130G, which all diminish CaM-dependent RyR2 inhibition.

157 n PI(3,4,5)P3 is able to completely displace CaM.

158 sociated with the calmodulin-binding domain (CaM-BD) of these channels.

159 Consequently, E2 doubles CaM-eNOS interaction and also promotes dual phosphorylat

160 l characterization of 1 novel variant, E141G-CaM, revealed an 11-fold reduction in Ca(2+)-binding aff

161 mbrane, as conformational plasticity enables CaM to orient efficiently to the polybasic HVR anchor, w

162 Furthermore, CaM-F142L enhanced CaM-dependent RyR2 inhibition at the single channel leve

163 s located at both CaM lobes further enhanced CaM-HVR complex stability.

164 ction between CaM and KCNQ1 that may explain CaM-mediated LQTS.

165 ns, we observe that nSH2 prefers an extended CaM conformation, whereas cSH2 prefers a collapsed confo

166 CaM is observed after binding of an extended CaM to K-Ras4B.

167 erpinnings of lowered affinity of Ca(2+) for CaM in the presence of Ng13-49 by showing that the N-ter

168 computed the changes in Ca(2+) affinity for CaM with and without binding targets in atomistic models

169 in return increases the Ca(2+) affinity for CaM.

170 nding proteins, we find that competition for CaM binding serves as a tuning mechanism: the presence o

171 herefore screened a subset of plant CPKs for CaM binding and found that CPK28 is a high affinity Ca(2

172 our knowledge, novel functional evidence for CaM preassociation to NMDA receptors in living cells.

173 al apoptosis also play an important role for CaM-DR5 binding.

174 of high-nanomolar affinity binding sites for CaM at its universal gating brake and its unique form of

175 show that this allosteric loop is vital for CaM regulation of the channels, facilitating cooperativi

176 rwhelmingly higher affinity than Ca(2+)-free CaM (apoCaM); the binding of CaMKII peptide to CaM in re

177 ase channel RyR1 is activated by Ca(2+)-free CaM and inhibited by Ca(2+)-bound CaM.

178 PV1 and Ca(2+)-bound CaM but not Ca(2+)-free CaM were preassociated in resting live cells, while caps

179 Furthermore, CaM-F142L enhanced CaM-dependent RyR2 inhibition at the

180 CaM, and seven highly-expressed hippocampal CaM binding proteins, we find that competition for CaM b

181 he more thermally stable Ca(2+)-bound (holo) CaM.

182 Cav2) and sodium channels possess homologous CaM-binding motifs, known as IQ motifs in their C termin

183 How CaM specifically targets K-Ras and how it extracts it fr

184 CaM Ca(2+) binding correlates with impaired CaM-dependent RyR2 inhibition.

185 Exposed glutamate residues in CaM (Glu-11, Glu-14, Glu-84, and Glu-87) form salt bridg

186 E2 substantially increases CaM binding to estrogen receptor alpha and GPER/GPR30.

187 These findings suggest that lysoPC induces CaM phosphorylation at Tyr(99) by a Src family kinase an

188 ine phosphorylation of AQP0 does not inhibit CaM binding to the whole AQP0 protein.

189 ortment of platform proteins for integrating CaM-dependent Ca(2+) signaling at multiple cellular site

190 n four distinct members of the intracellular CaM target network, including GPER/GPR30 itself and estr

191 Transfection of cells with full-length CaM slightly increased the ability of estrogen to enhanc

192 A103V modestly lowered CaM Ca-binding affinity (3-fold reduction versus WT-CaM)

193 While many CaM-binding proteins have been identified, few have been

194 lar allosteric interactions may also mediate CaM modulation of the properties of other CaM-regulated

195 Moreover, CaM is capable of stimulating the kinase activity of mTO

196 We identified a novel CaM mutation-A103V-in CALM3 in 1 of 12 patients (8%), a

197 C) substrate is identified in the absence of CaM, indicating restored substrate-binding capability du

198 amide chemical shifts of the amino acids of CaM in (1)H-(15)N HSQC NMR spectra.

199 d Ca(2+) is shown to enhance the affinity of CaM toward eEF-2K.

200 orientation (without altering the amount of CaM bound to RyR).

201 ily emerged as possibly the largest class of CaM-interacting proteins with undefined molecular functi

202 We therefore looked at the conservation of CaM sequences over deep evolutionary time, focusing prim

203 nd sharpens the Ca2+ frequency-dependence of CaM binding proteins.

204 ncreases Ca(2+) affinity for the C-domain of CaM by stabilizing the two Ca(2+) binding loops.

205 +) binding loops particularly at C-domain of CaM, enabling Ca(2+) release.

206 ct of competitive binding on the dynamics of CaM binding partner activation.

207 Ca(2+), sub-states in the folded ensemble of CaM's C-terminal domain present chemically and stericall

208 ia charge inversion by ectopic expression of CaM(R)(126E), as determined by analysis of miniature exc

209 The primary function of CaM is to transduce Ca(2+) concentration into cellular s

210 Our findings support the generality of CaM shuttling to drive nuclear CaMK activity, and they a

211 holoCaM-CaMKII delineates the importance of CaM's progressive mechanism of target binding on its Ca(

212 (2+) binding to CaM and impair inhibition of CaM-regulated Ca(2+) channels like the cardiac Ca(2+) re

213 st, expression of either the N- or C-lobe of CaM abrogated estrogen-stimulated transcription of the e

214 to Akt(PHD) displaces the C-terminal lobe of CaM but not the weakly binding N-terminal lobe.

215 -terminal sites, which bind to the N-lobe of CaM, are significantly less mobile in the presence of bo

216 -terminal sites, which bind to the C-lobe of CaM, do not show a significant Ca(2+)-dependence in mobi

217 n of the peptide with the N-terminal lobe of CaM.

218 The two lobes of CaM bind to the same site on two separate ER-alpha molec

219 gene-coding regions, in vitro measurement of CaM-Ca(2+) (Ca)-binding affinity, ryanodine receptor 2-C

220 Phosphorylation of CaM at Tyr(99) (pY99) enhances PI3Kalpha activation.

221 Blocking phosphorylation of CaM at Tyr(99) also reduced CaM association with the p85

222 lar patterns of IQD-dependent recruitment of CaM, suggesting that the diverse IQD members sequester C

223 tol-4,5-bisphosphate (PIP2), but the role of CaM in channel function is still unclear, and its possib

224 for the further investigation of the role of CaM-DR5 binding in DR5-mediated DISC formation for apopt

225 tching the changes in the chemical shifts of CaM upon Ng13-49 binding from nuclear magnetic resonance

226 We determined a crystal structure of CaM bound to a peptide encompassing its binding site in

227 ction is structurally different from that of CaM-WT at low Ca(2+) These data indicate a distinct inte

228 se results reveal that mTOR is a new type of CaM-dependent kinase, and TRPML1, lysosomal calcium and

229 ls to dissect the molecular underpinnings of CaM binding diversity.

230 y, these results add to our understanding of CaM-dependent regulation of RyR2 as well as the mechanis

231 ity to CNbeta1, decreasing its dependence on CaM, but also limited maximal enzyme activity through pe

232 /CaM interface and hydrogen bond with E54 on CaM.

233 ions with S372 and M368 on KCa3.1 and M72 on CaM at the KCa3.1-CaM-BD/CaM interface.

234 logical assay, we find that this mutation on CaM shifts the KCNQ1 voltage-activation curve.

235 ng to Ca(2+)/CaM by interacting with R126 on CaM.

236 a specific interface involving a residue on CaM that is mutated in a form of inherited LQTS.

237 Intact Ca(2+)-binding sites on CaM and an intact gating brake sequence (first 39 amino

238 rising from mutations in the gating brake or CaM.

239 ibited by intracellular Ca(2+)i chelation or CaM inhibition.

240 te CaM modulation of the properties of other CaM-regulated proteins.

241 techniques to characterize how PI(3,4,5)P3, CaM, and membrane mimetics (nanodisc) bind to Akt(PHD).

242 ne the spectrum and prevalence of pathogenic CaM variants in a cohort of genetically elusive LQTS, an

243 veil key interactions between phosphorylated CaM (pCaM) and the two SH2 domains in the p85 subunit, c

244 a Src family kinase and that phosphorylated CaM activates PI3K to produce PIP3, which promotes TRPC6

245 as4B from the membrane, organizing a K-Ras4B-CaM-PI3Kalpha ternary complex.

246 These LQTS-causative variants reduce CaM affinity to Ca(2+) and alter the properties of the c

247 osphorylation of CaM at Tyr(99) also reduced CaM association with the p85 subunit and subsequent acti

248 uding the start-Met), which markedly reduces CaM Ca(2+) binding.

249 s harbor a mutation in only 1 of 6 redundant CaM-encoding alleles, we devised a strategy using CRISPR

250 and neurogranin (Ng), as they both regulate CaM-dependent Ca(2+) signaling pathways in neurons.

251 onstrate that the prototypical Ca(2+) sensor CaM is required for the regulation of lysosome/vacuole s

252 cluding calmodulin (CaM) 3, CaM7 and several CaM-like proteins, pointing to the importance of Ca(2+)

253 e RyR2 CaMBD, which may explain the stronger CaM-dependent RyR2 inhibition by CaM-F142L, despite its

254 Surprisingly, CaM-F142L had little to no aberrant effect on RyR2-media

255 With these approaches, we estimate that CaM senses NMDA receptor Ca(2+) influx at approximately

256 Expanding on previous work, we found that CaM evolves slowly but that its evolutionary rate is sub

257 d fluorescence experiments, we observed that CaM preferentially binds unfolded K-Ras4B hypervariable

258 Here, we report that CaM recognizes a '1-4-7-8' pattern of hydrophobic amino

259 Recent experimental data show that CaM selectively promotes K-Ras signaling but not of N-Ra

260 ur recent crystallographic study showed that CaM embraces helices A and B with the apo C lobe and cal

261 These data suggest that CaM-induced dimerization of ER-alpha is required for est

262 Thus, high micromolar S100A1 does alter the CaM/RyR interaction, without involving competition.

263 endothermal interaction between CaM and the CaM-binding domain (CaMBD) of RyR2 into an exothermal on

264 Furthermore, the CaM D129G mutation led to bradycardia in zebrafish and a

265 KCa activators bind relatively "deep" in the CaM-BD/CaM interface and hydrogen bond with E54 on CaM.

266 sive RyR2 Ca(2+) release by manipulating the CaM-RyR2 interaction.

267 gel electrophoresis, we coarsely mapped the CaM-binding domain to a site within the CPK28 J domain t

268 vestigated the RyR2 inhibitory action of the CaM p.Phe142Leu mutation (F142L; numbered including the

269 Removal of the CaM-binding sequence in AKAP79 prevents formation of a C

270 calmodulin (CaM), and phosphorylation of the CaM-binding site abolishes calcium sensitivity.

271 eate the in vivo frequency dependence of the CaM-dependent phosphatase calcineurin.

272 The unique properties of the CaM-F142L mutation may provide novel clues on how to sup

273 Our structural model of the CaM-K-Ras4B HVR association provides plausible clues to

274 Moreover, NMR spectra revealed that the CaM-F142L-CaMBD interaction is structurally different fr

275 g site of the benzothiazoles/oxazoles to the CaM-BD/CaM interface and then used computational modelin

276 The interaction involved all three CaM domains including the central linker and both lobes.

277 tude in a process depending on Ca binding to CaM (calmodulin).

278 tations generally decrease Ca(2+) binding to CaM and impair inhibition of CaM-regulated Ca(2+) channe

279 Although an IQ motif promotes binding to CaM, an acidic sequence in PEP-19 is required to modulat

280 When bound to CaM, the probe nearest RyRp's N-terminus shows rapid rot

281 HVR association provides plausible clues to CaM's regulatory action in PI3Kalpha activation involvin

282 M (apoCaM); the binding of CaMKII peptide to CaM in return increases the Ca(2+) affinity for CaM.

283 c-His-Phe(138)-CaM, the lysoPC-induced TRPC6-CaM dissociation and TRPC6 externalization was disrupted

284 ion induced both the formation of more TRPV1/CaM complexes and conformational changes.

285 cause many models to include only one or two CaM-activated proteins.

286 in Kv7.1 helix B form a critical site where CaM competes with PIP2 to stabilize the channel open sta

287 Our findings support a model by which CaM binds to Akt to facilitate its translocation to the

288 the AQP0-CaM complex, the mechanism by which CaM modulates AQP0 remains poorly understood.

289 296, 299, 302, and 303), which explains why CaM binds two molecules of ER-alpha in a 1:2 complex and

290 ction changes in response to activation with CaM in the dimeric mutant, WT-holoenzyme, and a monomeri

291 ely disrupt the interaction of ER-alpha with CaM may be useful in the therapy of breast carcinoma.

292 T-type channels specifically associate with CaM at helix 2 of the gating brake in the I-II linker of

293 lustrate that T-type channels associate with CaM using co-immunoprecipitation experiments and single

294 Ca(2+) release in HEK293 cells compared with CaM-WT.

295 on at the single channel level compared with CaM-WT.

296 y employ similar motifs for interaction with CaM.

297 almodulin (CaM), pretreatment of islets with CaM blocker calmidazolium showed effects very similar to

298 a model in which the interaction of RyR with CaM is nonuniform along the peptide, and the primary eff

299 Even a 1:3 mixture of A103V-CaM:WT-CaM activated Ca waves, demonstrating functional dominan

300 binding affinity (3-fold reduction versus WT-CaM), but did not alter CaM binding to ryanodine recepto