ライフサイエンスコーパス: CaMKII

1 CaMKII (Ca(2+)-Calmodulin dependent protein kinase) delt

2 CaMKII (Ca(2+)/calmodulin-dependent kinase II) enhances

3 CaMKII (Ca(2+)/calmodulin-dependent protein kinase-II) p

4 CaMKII activity depends on the balance between activatin

5 CaMKII activity is known to regulate dynamic shifts in t

6 CaMKII inhibition also reversed the arrhythmia phenotype

7 CaMKII is activated by calcium-bound calmodulin (Ca(2+)/

8 CaMKII phosphorylates the N-lobe of the Arc GAG domain a

9 CaMKII-dependent phosphorylation may lead to longer-last

10 CaMKII-driven inhibitory Gi-coupled designer receptors e

11 CaMKII-mediated phosphorylation level of GluN2B serine 1

12 n) of calcium/calmodulin-dependent kinase 2 (CaMKII) and also that inhibition of CaMKII abolishes 8-p

13 ells contain a diverse collection of over 70 CaMKII transcripts from all four CaMKII-encoding genes.

14 II-dependent arrhythmic SR Ca(2+) leak and a CaMKII-independent uptake exacerbates atrial arrhythmoge

15 SAP97 polymorphism increases the I(to,f), a CaMKII-dependent effect that may increase the risk of ar

16 study showed that AAV-mediated delivery of a CaMKII peptide inhibitor to the heart was effective in s

17 uA1 receptor subunit at serine 831 (S831), a CaMKII site, along with an increase in total PSD GluA1.

18 not apoptosis in FRD-SR-AIP mice, in which a CaMKII inhibitor is targeted to the SR.

19 mouse) and at a later age by breeding with a CaMKII-ERT2-Cre (FIGSKO mouse).

20 signals cause calcium-calmodulin to activate CaMKII, which leads to remodeling of the actin filament

21 ecific, mutation-dependent role of activated CaMKII in HCM progression and a precise therapeutic targ

22 a significantly increased level of activated CaMKII.

23 pressed NaV1.2 channels exposed to activated CaMKII had enhanced persistent current and depolarized c

24 ntracellular Ca(2+), which in turn activates CaMKII and, further downstream, the transcription factor

25 almodulin (CaM), the protein which activates CaMKII in the presence of calcium.

26 ing changes could be fully reversed by acute CaMKII inhibition (AIP [autocamtide-2 related inhibitory

27 Although CaMKII may have taken the spotlight, it is a member of a

28 pendent protein kinase II (CaMKII), although CaMKII phosphorylated four other Myo1c sites.

29 es in nuclear and time-averaged [Ca(2+)] and CaMKII activation occurred.

30 -1beta caused NLRP3-signaling activation and CaMKII-dependent RyR2/phospholamban hyperphosphorylation

31 n of ROS-dependent activation of the ATM and CaMKII proapoptotic signaling cascades.

32 cantly enhanced [(3) H]ryanodine binding and CaMKII phosphorylation of RyR2-S2814 residue vs. normogl

33 elta) is implicated in myocardial death, and CaMKII can be activated by ROS (ox-CaMKII) through oxida

34 activity that was accentuated by densin and CaMKII.

35 ut early spatio-temporal Ca(2+) handling and CaMKII activation in hypertrophy and HF.

36 KATP) current contributes to I/R injury, and CaMKII promotes sequestration of KATP from myocardial ce

37 n kinase II (CaMKII)-mediated mechanism, and CaMKII inhibition prevents both increased intracellular

38 Shank3 and CaMKII were previously shown to bind L-type calcium chan

39 ant cross talk between beta-AR signaling and CaMKII activation presenting CaMKII as a possible downst

40 of the worm homologs of a NMDAR subunit and CaMKII.

41 ld-type CaMKII locus, but only viability and CaMKII localization are rescued by genomic fosmids lacki

42 lanines disrupts CaMKII binding in vitro and CaMKII association with Shank3 in heterologous cells.

43 will be important for optimizing artificial CaMKII activation for clinical use to manage infertility

44 activity-dependent gene expression, such as CaMKII, Shank3, and L-type calcium channels, are often m

45 structural protection of autophosphorylated CaMKII by Ca2+/CaM may be an important mechanism for reg

46 computational model to investigate how beta CaMKII regulates the direction of plasticity in cerebell

47 imental observations that indicate that beta CaMKII controls the direction of plasticity at PF-PC syn

48 ce of autophosphorylation is flipped between CaMKII variants with longer and shorter linkers.

49 that Ca2+/CaM and protein phosphatases bind CaMKII at nearby or overlapping sites, we compare model

50 studies revealed that Shank3 binding to both CaMKII and LTCCs is important for increased phosphorylat

51 For the principal isoforms in the brain, CaMKII-alpha, with a ~30 residue linker, readily acquire

52 ecreased in HF when Ca(2+) was buffered, but CaMKII-mediated Ca(2+)-dependent facilitation upregulate

53 implying that phosphorylation of Thr(17) by CaMKII may become crucial for 14-3-3 recruitment to Delt

54 investigate modulation of Nav1.6 function by CaMKII signaling.

55 ous actin (F-actin) networks cross-linked by CaMKII.

56 Mutant Arc that cannot be phosphorylated by CaMKII enhances metabotropic receptor-dependent depressi

57 ion was CaMKII independent (not prevented by CaMKII inhibition).

58 first direct evidence for memory storage by CaMKII.

59 Ps/min, p = 0.004); these were suppressed by CaMKII inhibition.

60 y tuned through the interactions of Ng, CaM, CaMKII, and PP1, providing a mechanism to precisely cont

61 How Na(V) -CaM, CaMKII and FGF/fibroblast growth factor homologous facto

62 efore, Tiam1 binding results in constitutive CaMKII activation, which in turn persistently phosphoryl

63 Here, we show that complexes containing CaMKII and Shank3, a postsynaptic scaffolding protein kn

64 In contrast, CaMKII peptide increases Ca(2+) affinity for the C-domai

65 Cytosolic CaMKII and the MCU participate in a regulatory circuit,

66 s are important in revealing a CaV1.3-densin-CaMKII interaction that extends the contribution of CaV1

67 ng different components of the CaV1.3-densin-CaMKII interaction, identifying an important role for Ca

68 model of post-synaptic plasticity describing CaMKII, PKA, and PKC pathways and their contribution to

69 ilar networks were formed by three different CaMKII species with a 10-fold length difference in the l

70 nus-tagged CaMKIIalpha to identify a dimeric CaMKII.

71 n hydrodynamic volume in both WT and dimeric CaMKII without altering subunit stoichiometry or the net

72 )Arg-Arg-Lys(951) to three alanines disrupts CaMKII binding in vitro and CaMKII association with Shan

73 Drosophila CaMKII-null mutants remain viable throughout development

74 Either CaMKII-inhibition (by autocamtide-2-related peptide) or

75 in pathophysiological processes has elevated CaMKII to a key target in the management of numerous dis

76 ly, to detect the activity of all endogenous CaMKII variants simultaneously, we constructed a substra

77 FRESCA enables assessment of endogenous CaMKII activity in real-time by both fertilization and a

78 understanding the complex pool of endogenous CaMKII splice variants.

79 ncies, neurogranin promotes LTP by enhancing CaMKII autophosphorylation.

80 ndent protein kinase-II) protein-expression, CaMKII-dependent phosphorylation of the cardiac RyR2 (ry

81 a1 (PLCgamma1) in the forebrain (Plcg1(f/f); CaMKII) exhibit hyperactivity, decreased anxiety-like be

82 irst employed the one existing biosensor for CaMKII activation.

83 lts from the different affinities of CaM for CaMKII depending on the number of calcium ions bound to

84 Our data highlight an integral role for CaMKII in neuronal TRPV4-associated Ca(2+) responses, th

85 MKII activity, FRESCA (FRET-based sensor for CaMKII activity).

86 we constructed a substrate-based sensor for CaMKII activity, FRESCA (FRET-based sensor for CaMKII ac

87 of over 70 CaMKII transcripts from all four CaMKII-encoding genes.

88 Vertebrate genomes encode four CaMKII homologs: CaMKIIalpha, CaMKIIbeta, CaMKIIgamma, a

89 actin filaments at random, whereas at higher CaMKII/F-actin ratios, filaments bundled.

90 ed the Ca(2+)/CaM sensitivity of hippocampal CaMKII variants spanning a broad range of linker lengths

91 In the hippocampus, CaMKII is required for learning and memory.

92 ound complexes of apoCaM-Ng13-49 and holoCaM-CaMKII delineates the importance of CaM's progressive me

93 These results provide a mechanism how CaMKII can indeed mediate not only LTP but also LTD thro

94 ncing or inhibiting Ca/calmodulin kinase II (CaMKII) abolished the p.P888L-induced Kv4.3 charge incre

95 Ca2+/calmodulin-dependent protein kinase II (CaMKII) accounts for up to 2 percent of all brain protei

96 ncreased mitochondrial calmodulin kinase II (CaMKII) activation and left ventricular dilation in mice

97 (2+)/calmodulin-dependent protein kinase II (CaMKII) activation are required for embryogenesis, as we

98 cium/calmodulin-dependent protein kinase II (CaMKII) and calcineurin (CaN) both bind open calmodulin,

99 KC) betaII, or calcium-calmodulin kinase II (CaMKII) and inhibition by Galphai/o, novel PKC isoforms,

100 (2+)/calmodulin-dependent protein kinase II (CaMKII) and protein kinase A (PKA) both in vitro and in

101 f the Ca(2+)/calmodulin-dependent kinase II (CaMKII) and the phosphorylation of the mitochondrial fis

102 onal Ca(2+)/CaM-dependent protein kinase II (CaMKII) are independently linked to excitability disorde

103 (2+)/calmodulin-dependent protein kinase II (CaMKII) at Thr(17) beta-Adrenergic stimulation and PKA-d

104 (2+)/calmodulin-dependent protein kinase II (CaMKII) differ in the lengths and sequences of disordere

105 -AR downstream protein kinase CaM kinase II (CaMKII) directly binds and phosphorylates H3S28.

106 host calcium/calmodulin-dependent kinase II (CaMKII) for inhibition.

107 Calcium-calmodulin-dependent kinase II (CaMKII) has an important role in dendritic spine remodel

108 Calmodulin-dependent kinase II (CaMKII) has long been known to play an important role in

109 cium calmodulin-dependent protein kinase II (CaMKII) is a dodecameric holoenzyme important for encodi

110 cium/calmodulin-dependent protein kinase II (CaMKII) is a multifunctional serine/threonine protein ki

111 (2+)/calmodulin-dependent protein kinase II (CaMKII) is an oligomeric enzyme with crucial roles in ne

112 2+) /calmodulin-dependent protein kinase II (CaMKII) phosphorylation of RyR2-S2814 residue vs. normog

113 cium/calmodulin-dependent protein kinase II (CaMKII) plays a central role in Ca(2+) signaling through

114 Calcium/calmodulin-dependent kinase II (CaMKII) plays a key role in the plasticity of dendritic

115 cium-calmodulin dependent protein kinase II (CaMKII) regulates many forms of synaptic plasticity, but

116 (2+)/calmodulin-dependent protein kinase II (CaMKII) strongly interacts with a novel binding motif in

117 n (Ca(2+)/CaMK)-dependent protein kinase II (CaMKII) to the hippocampal PSD.

118 cium/calmodulin-dependent protein kinase II (CaMKII) was blocked with KN-93, the inhibitory effect of

119 almodulin (CaM)-dependent protein kinase II (CaMKII) was touted as a memory molecule, even before its

120 th factors (FGF) or CaM-dependent kinase II (CaMKII)) that can also modify channel function or exert

121 n by Ca(2+)/CaM-dependent protein kinase II (CaMKII), although CaMKII phosphorylated four other Myo1c

122 (2+)/calmodulin-dependent protein kinase II (CaMKII), an adrenergically activated kinase that contrib

123 cium/calmodulin-dependent protein kinase II (CaMKII), protein kinase A (PKA), protein kinase C (PKC),

124 zing calmodulin-dependent protein kinase II (CaMKII), Raf, and MAPK/ERK kinase 1/2 (MEK1/2).

125 cium/calmodulin-dependent protein kinase II (CaMKII), which is not the case at distal segments.

126 (2+)/calmodulin-dependent protein kinase II (CaMKII)-dependent alterations in NaV1.5 channel inactiva

127 (2+)/calmodulin-dependent protein kinase II (CaMKII)-mediated mechanism, and CaMKII inhibition preven

128 cium-dependent kinase (calmodulin kinase II [CaMKII]) via the AC3I peptide and diltiazem, an L-type c

129 otoactivation produced similar BP changes in CaMKII-ArchT-treated rats.

130 y to report the conclusion of the decline in CaMKII's activity, not for the measurement of the interv

131 lving a regulatory C-terminal alpha-helix in CaMKII.

132 hing frequency (FR), whereas FR increased in CaMKII-ArchT rats.

133 The dual action of JNK2 in CaMKII-dependent arrhythmic SR Ca(2+) leak and a CaMKII-

134 The selective loss of the long 3'UTR mRNA in CaMKII-null larvae allows us to test its role in plastic

135 These alterations of pERK occurred in CaMKII-expressing neurons, suggesting changes in efferen

136 hat Ng plays an important modulatory role in CaMKII phosphorylation following a surge of high calcium

137 data suggest that Ca(2+)/CaM sensitivity in CaMKII is homolog dependent and includes substantial con

138 Whereas, in CaMKII-deficient myocytes, acute catecholaminergic stimu

139 Increased CaMKII (Ca/calmodulin-dependent protein kinase II) activ

140 2-phosphorylation by inhibition of increased CaMKII activity.

141 l myocardium of patients with SDB, increased CaMKII-dependent phosphorylation of Na(V)1.5 results in

142 SDB consistent with significantly increased CaMKII-dependent cardiac Na channel phosphorylation (Na(

143 was independently associated with increased CaMKII activity, enhanced late I(Na) and correlated with

144 nd gradual relaxation of calcium-independent CaMKII measure a 6-min time window to coordinate two mal

145 however, in the case of AKAP79/150, indirect CaMKII effects on palmitoylation are more important than

146 alities and activation of NLRP3-inflammasome/CaMKII signaling are evident in atrial cardiomyocytes fr

147 BSA 9 inhibited CaMKII activity with an IC(50) value of 0.79 muM and dis

148 interact with CaMKII, effectively inhibiting CaMKII activation.

149 However, with JNK2-CaMKII-driven SR Ca(2+) leak present, the JNK2-enhanced

150 acerbated Ca(2+) /calmodulin-protein kinase (CaMKII) activity, ryanodine receptor 2 (RyR2) phosphoryl

151 ide (9) showed superior properties as a lead CaMKII inhibitor and antiviral agent.

152 Mice with myocardial and mitochondrial CaMKII overexpression (mtCaMKII) have severe dilated car

153 By contrast, mice with genetic mitochondrial CaMKII inhibition are protected from left ventricular di

154 vide a pharmacological target for modulating CaMKII activity.

155 meric mutant, WT-holoenzyme, and a monomeric CaMKII oligomerization-domain deletion mutant control.

156 lation frequency results in high peak mutant CaMKII(T286A) activity that is sufficient for inducing p

157 viral (HSV) expression of dominant-negative CaMKII-alpha (K42M) in the hippocampus.

158 In Purkinje neurons, CaMKII phosphorylation acutely reverses Arc's synaptic a

159 suggest that other Ca(2+)/CaM-dependent, non-CaMKII activities should be considered in KN-93-based me

160 Thus, this novel CaMKII-Shank3 interaction is essential for the initiatio

161 The (peri)nuclear CaMKII accumulation also correlated with enhanced HDAC4

162 was decreased by 3-Hz pacing, while nuclear CaMKII phosphorylation was increased.

163 d STOC activity (i) occurs via activation of CaMKII and (ii) is driven by changes in the underlying b

164 We have previously reported an activation of CaMKII during transition to HF in long-term VO.

165 Previously, we showed that activation of CaMKII triggers the exchange of subunits between holoenz

166 U was associated with baseline activation of CaMKII, mitochondrial fragmentation due to increased Drp

167 in mammalian cells shows that activation of CaMKII-alpha results in the destabilization of the holoe

168 ctivity and increased relative activation of CaMKII-expressing projection neurons.

169 c lesions in mice demonstrated activation of CaMKII.

170 24 hours) was regulated by the activation of CaMKII.

171 -molecule fluorescence intensity analysis of CaMKII-alpha expressed in mammalian cells shows that act

172 Genome-wide analysis of CaMKII-mediated H3S28p in response to chronic beta-AR st

173 mulation results suggest that the balance of CaMKII-mediated phosphorylation and protein phosphatase

174 han Ca(2+)-free CaM (apoCaM); the binding of CaMKII peptide to CaM in return increases the Ca(2+) aff

175 LTD, but limits LTP by precluding binding of CaMKII with calmodulin.

176 CaN activity, thus increasing the chance of CaMKII trans-autophosphorylation at high-frequency calci

177 uctural model for the dodecameric complex of CaMKII with F-actin.

178 l and pathological metabolic consequences of CaMKII signaling in mitochondria.

179 the rapid formation of a RAKEC consisting of CaMKII and Tiam1, a Rac-GEF.

180 ages due to a large maternal contribution of CaMKII mRNA, which consists of a short 3'-untranslated r

181 r-/-) mice with myeloid-specific deletion of CaMKII had smaller necrotic cores with concomitantly thi

182 We also show that the regulatory domain of CaMKII may bind either calmodulin or F-actin, but not bo

183 nding interface involves multiple domains of CaMKII.

184 echanism by which the structural dynamics of CaMKII establishes the link between calcium signaling an

185 urogranin (Ng), in governing the dynamics of CaMKII is not yet fully understood.

186 he effect of Ca2+ signals on the dynamics of CaMKII phosphorylation in the postsynaptic density (PSD)

187 omputational simulations to model effects of CaMKII inhibition on Nav1.6 function demonstrate dramati

188 udying the cellular and in vivo functions of CaMKII.

189 Here, we report the heterogeneity of CaMKII transcripts in three complex samples of human hip

190 omic sequencing led to the identification of CaMKII-dependent H3S28p target genes.

191 inase 2 (CaMKII) and also that inhibition of CaMKII abolishes 8-pCPT-AM-induced increases in STOC act

192 In contrast, inhibition of CaMKII in R92L animals led to worsened myocellular calci

193 Inhibition of CaMKII led to recovery of diastolic function and partial

194 Inhibition of CaMKII may be useful for prevention or treatment of arrh

195 We show that inhibition of CaMKII, a Ser/Thr protein kinase associated with excitab

196 ents have indicated that the beta isoform of CaMKII controls the bidirectional inversion of plasticit

197 bunit activation and regulate maintenance of CaMKII autophosphorylation.

198 el against previous experimental measures of CaMKII activity and investigate molecular mechanisms of

199 vity and investigate molecular mechanisms of CaMKII regulation.

200 t them, suggesting that the initial 1 min of CaMKII activation is sufficient for inducing LTP and sLT

201 tin bundles arising from the multivalence of CaMKII.

202 ibition of mitochondrial fragmentation or of CaMKII in the cytosol.

203 ) oscillations, but the resultant pattern of CaMKII activity remains largely unclear.

204 e measured an increase in phosphorylation of CaMKII in R92W animals by 6 months of age, indicating in

205 vestigate the dynamics of phosphorylation of CaMKII monomers and dodecameric holoenzymes.

206 2 Ser-409 phosphorylation in the presence of CaMKII, and this phosphorylation was reduced in the pres

207 However, the properties of CaMKII that mediate Ca(2+) signals in spines remain elus

208 ity in the R92W animals despite reduction of CaMKII activation, likely indicating improvement in myoc

209 f ketamine led to differential regulation of CaMKII function, manifested as autoinhibition (pT305 pho

210 Release of CaMKII from F-actin, triggered by calcium-calmodulin, wa

211 Our results show how the responsiveness of CaMKII holoenzymes to calcium signals can be tuned by va

212 dated the model's predictions on the role of CaMKII-Gbetagamma and CaN-Gbetagamma interactions in med

213 ation/MS of Nav1.6 reveal potential sites of CaMKII phosphorylation, specifically Ser-561 and Ser-641

214 g site leading to the autoactivated state of CaMKII.

215 However, translation of CaMKII inhibition has been limited by the need for selec

216 ude that the fundamental functional units of CaMKII holoenzyme are paired catalytic-domains.

217 s useful to elucidate the temporal window of CaMKII activation required for synaptic plasticity and l

218 d in HF versus control (dependent largely on CaMKII [Ca(2+)/calmodulin-dependent protein kinase II] a

219 udy the effect of multiple calcium spikes on CaMKII holoenzyme autophosphorylation, and show that in

220 Moreover, FRESCA provides a new view on CaMKII activity, and its application in additional biolo

221 ponses to NPY or CRF required calcineurin or CaMKII, respectively.

222 ions with calmodulin, accessory proteins, or CaMKII that modulate channel activity.

223 ons, cardiomyocytes, immune cells, and other CaMKII-expressing cells.

224 eath, and CaMKII can be activated by ROS (ox-CaMKII) through oxidation of regulatory domain methionin

225 icular myocytes, but not in MMVV, showing ox-CaMKII decreases KATP availability.

226 ether, these findings support a view that ox-CaMKII and KATP are components of a signaling axis promo

227 olchicine reduced both NOX2/ROS and oxidized CaMKII, increased S325/S328/S330 phosphorylation, and pr

228 nd show that in the presence of phosphatase, CaMKII behaves as a leaky integrator of calcium signals,

229 eviously that in the absence of phosphatase, CaMKII monomers integrate over Ca2+ signals of certain f

230 P(3)R1 (IP(3)R-type 1) and of phosphorylated CaMKII (immunohistochemistry and immunoblot) while decre

231 ermore, we find that adenylate cyclase, PKA, CaMKII, and release of Ca(2+) from intracellular stores

232 ao, Gbetagamma), protein kinases (PKCbetaII, CaMKII), and forskolin, were systematically evaluated us

233 Our aim is to place CaMKII in context of the other CaM kinases and then revi

234 no-associated viral vector in which a potent CaMKII inhibitory peptide, autocamtide-2-related inhibit

235 type II delta (CaMKIIdelta), the predominant CaMKII isoform expressed in the heart, has been implicat

236 R signaling and CaMKII activation presenting CaMKII as a possible downstream mediator of detrimental

237 lude phosphatase binding and thereby prolong CaMKII autophosphorylation.

238 ed evoked spine calcium signals and promoted CaMKII activation.

239 inction-dependent changes in hippocampal PSD CaMKII expression and S831 GluA1 phosphorylation.

240 aling effector in the common synaptic NMDA-R-CaMKII-SynGap-Ras-BRaf-MEK-ERK transduction cascade.

241 volving miR-26a, leading to enhanced IP(3)R1-CaMKII-HDAC4 signaling and L-type calcium current downre

242 ction of arrhythmogenic I(Na,L), and reduced CaMKII-dependent phosphorylation of Na(v)1.5.

243 tic plasticity and the mechanisms regulating CaMKII activity.

244 s over sequential activation of PNs required CaMKII-dependent synaptic plasticity.

245 ins the architecture of the micrometer-scale CaMKII/F-actin bundles arising from the multivalence of

246 n has been limited by the need for selective CaMKII inhibition in cardiomyocytes.

247 al reflection fluorescence microscopy showed CaMKII dissociation from surface-immobilized globular ac

248 d that at physiological molar ratios, single CaMKII holoenzymes cross-linked multiple F-actin filamen

249 lore how Ca2+/CaM-binding may both stabilize CaMKII subunit activation and regulate maintenance of Ca

250 Upon synaptic stimulation, CaMKII is disengaged by calcium-calmodulin, triggering n

251 face, allows calmodulin transiently to strip CaMKII from actin assemblies so that they can reorganize

252 reate a rule-based model of a twelve-subunit CaMKII holoenzyme.

253 revented in AC3I mice, with cardiac-targeted CaMKII inhibition.

254 al creatine kinase or mitochondrial-targeted CaMKII inhibition.

255 Our findings argue that CaMKII-actin networks in dendritic spines maintain spine

256 Here, we tested the hypothesis that CaMKII inhibition with a cardiomyocyte-targeted gene the

257 We hypothesized that CaMKII-dependent dysregulation of Na current (I(Na)) may

258 These data also imply that CaMKII may be a yet unrecognized stress-responsive regul

259 g an inhibitory avoidance task revealed that CaMKII activity during, but not after, training is requi

260 e-cell voltage clamp of Nav1.6, we show that CaMKII inhibition in ND7/23 and HEK293 cells significant

261 nd tunable duration of activity suggest that CaMKII may time a wide variety of behavioral and cogniti

262 Our results suggest that CaMKII-dependent upregulation of I(NaL) in HF significan

263 on, but not LTM maintenance, suggesting that CaMKII activity is not required for LTM storage.

264 ls in a Purkinje cell model, suggesting that CaMKII modulation of Nav1.6 may be a powerful mechanism

265 and phosphorylated peptides derived from the CaMKII-alpha regulatory segment bind to the CaMKII-alpha

266 phorylation events that occur on each of the CaMKII holoenzyme's subunits.

267 d peptide) or IP(3)R-knockdown prevented the CaMKII-hyperphosphorylation and nuclear-to-cytosolic HDA

268 r, the pathways that negatively regulate the CaMKII/Na(v)1.5 axis are unknown and essential for the d

269 domain on Tiam1, which is homologous to the CaMKII autoinhibitory domain itself.

270 tally that Ca(2+)/CaM (holoCaM) binds to the CaMKII peptide with overwhelmingly higher affinity than

271 CaMKII-alpha regulatory segment bind to the CaMKII-alpha hub and break it into smaller oligomers.

272 Unlike the CaMKII (Ca(2+)/calmodulin-dependent kinase II)-dependent

273 ice but not in FRD-S2814A mice, in which the CaMKII site on ryanodine receptor 2 was ablated.

274 ded in channels (p.S550A Kv4.3) in which the CaMKII-phosphorylation is prevented.

275 ticity, and excitability disorders, with the CaMKII-specific peptide inhibitor CN21 reduces transient

276 ore solely reports on the activation of this CaMKII variant.

277 kinase 2) and cofilin, and signaling through CaMKII.

278 tes that the binding of filamentous actin to CaMKII can enable the beta isoform of the kinase to regu

279 structurally exclude each other's binding to CaMKII.

280 , and we show here that Shank3 also binds to CaMKII.

281 xpression signature that might contribute to CaMKII-dependent retinal diabetic complications.

282 widely believed that KN-93 binds directly to CaMKII, thus preventing kinase activation by competing w

283 hese results provide mechanistic insights to CaMKII-actin interactions at the collective network and

284 eagents, such as Sr(2+), which also leads to CaMKII activation.

285 ate that chronic beta-AR activation leads to CaMKII-mediated H3S28p in cardiomyocytes.

286 s in DRG neurons is preferentially linked to CaMKII activity.

287 N-93 binds directly to Ca(2+)/CaM and not to CaMKII.

288 expression of the nearest genes, pointing to CaMKII-dependent H3S28p as an activating histone mark.

289 by a fosmid containing the entire wild-type CaMKII locus, but only viability and CaMKII localization

290 By using CaMKII structure-guided inhibitor design, we generated f

291 onal progranulin-deficient mouse lines using CaMKII-Cre and Nestin-Cre.

292 Ca(2+) leak, JNK2-driven SERCA2 function was CaMKII independent (not prevented by CaMKII inhibition).

293 exponential dwell-time distribution, whereas CaMKII bound to F-actin networks had a long-lived fracti

294 However, whether CaMKII is required only during initial processes or whet

295 quires activating autophosphorylation, while CaMKII-beta, with a ~200 residue linker, is biased towar

296 With CaMKII blocked, the JNK2-driven SR Ca(2+) loading alone

297 ling with systems like those associated with CaMKII (Ca(2+)/calmodulin-dependent protein kinase-II),

298 SAP97 is more likely to form a complex with CaMKII than WT.

299 t the ability of Ca(2+)/CaM to interact with CaMKII, effectively inhibiting CaMKII activation.

300 c manner and is shaped by the interplay with CaMKII at proximal dendritic segments, shedding light on