ライフサイエンスコーパス: CaMKII

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

2 nding interface involves multiple domains of CaMKII.

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

4 udying the cellular and in vivo functions of CaMKII.

5 g site leading to the autoactivated state of CaMKII.

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

7 structurally exclude each other's binding to CaMKII.

8 first direct evidence for memory storage by CaMKII.

9 tin bundles arising from the multivalence of CaMKII.

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

11 c lesions in mice demonstrated activation of CaMKII.

12 nus-tagged CaMKIIalpha to identify a dimeric CaMKII.

13 24 hours) was regulated by the activation of CaMKII.

14 activity that was accentuated by densin and CaMKII.

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

16 a significantly increased level of activated CaMKII.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 ed evoked spine calcium signals and promoted CaMKII activation.

35 irst employed the one existing biosensor for CaMKII activation.

36 interact with CaMKII, effectively inhibiting CaMKII activation.

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

38 (2+)/calmodulin-dependent protein kinase II (CaMKII) activation are required for embryogenesis, as we

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

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

41 CaMKII activity depends on the balance between activatin

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

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

44 CaMKII activity is known to regulate dynamic shifts in t

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

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

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

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

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

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

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

52 tic plasticity and the mechanisms regulating CaMKII activity.

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

54 vide a pharmacological target for modulating CaMKII activity.

55 2-phosphorylation by inhibition of increased CaMKII activity.

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

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

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

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

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

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

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

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

64 (2+)/calmodulin-dependent protein kinase II (CaMKII), an adrenergically activated kinase that contrib

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

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

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

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

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

70 ein response and the pro-apoptotic mediators CamkII and Stat1 was impaired in Trpc3-deficient M1 cell

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

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

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

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

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

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

77 (2+)/calmodulin-dependent protein kinase II (CaMKII) and protein kinase A (PKA) both in vitro and in

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

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

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

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

82 2 Ser-409 phosphorylation in the presence of CaMKII, and this phosphorylation was reduced in the pres

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

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

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

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

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

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

89 (2+)/calmodulin-dependent protein kinase II (CaMKII) at Thr(17) beta-Adrenergic stimulation and PKA-d

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

91 bunit activation and regulate maintenance of CaMKII autophosphorylation.

92 lude phosphatase binding and thereby prolong CaMKII autophosphorylation.

93 ncies, neurogranin promotes LTP by enhancing CaMKII autophosphorylation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 All CaMKIIs consist of a kinase domain, a regulatory segment

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

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

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

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

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

116 (2+)/calmodulin-dependent protein kinase II (CaMKII)-dependent alterations in NaV1.5 channel inactiva

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

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

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

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

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

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

123 CaMKII-dependent phosphorylation may lead to longer-last

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

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

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

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

128 -1beta caused NLRP3-signaling activation and CaMKII-dependent RyR2/phospholamban hyperphosphorylation

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

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

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

132 (2+)/calmodulin-dependent protein kinase II (CaMKII) differ in the lengths and sequences of disordere

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

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

135 CaMKII-driven inhibitory Gi-coupled designer receptors e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 he presence of barr2 is essential for proper CAMKII function in beta-cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 CaMKII inhibition also reversed the arrhythmia phenotype

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

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

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

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

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

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

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

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

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

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

192 al creatine kinase or mitochondrial-targeted CaMKII inhibition.

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

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

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

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

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

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

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

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

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

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

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

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

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

206 (2+)/calmodulin-dependent protein kinase II (CaMKII) is an oligomeric enzyme with crucial roles in ne

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

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

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

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

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

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

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

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

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

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

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

218 (2+)/calmodulin-dependent protein kinase II (CaMKII)-mediated mechanism, and CaMKII inhibition preven

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

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

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

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

223 CaMKII-mediated phosphorylation level of GluN2B serine 1

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

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

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

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

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

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

230 -/- mice that received a single dose of AAV9-CamKII-NPC1 as neonates (2.6 x 1011GC) or at weaning (1.

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

232 Drosophila CaMKII-null mutants remain viable throughout development

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

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

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

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

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

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

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

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

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

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

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

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

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

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

247 2+) /calmodulin-dependent protein kinase II (CaMKII) phosphorylation of RyR2-S2814 residue vs. normog

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

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

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

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

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

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

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

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

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

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

258 vity and investigate molecular mechanisms of CaMKII regulation.

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

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

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

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

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

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

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

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

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

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

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

270 understanding the complex pool of endogenous CaMKII splice variants.

271 (2+)/calmodulin-dependent protein kinase II (CaMKII) strongly interacts with a novel binding motif in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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