ライフサイエンスコーパス: CaMKII

1 CaMKII activity in hippocampal protein lysates exhibited

2 CaMKII activity was judged by analysis of CaMKII express

3 CaMKII inhibition had no effect if the memory was neithe

4 CaMKII inhibition prevented hyperglycaemia-induced alter

5 CaMKII is an ideal candidate for mediating activity-depe

6 CaMKII phosphorylation of RyR2, SR Ca(2+) leak and mitoc

7 CaMKII plays a critical role in decoding calcium (Ca(2+)

8 CaMKII protein abundance was increased only in sarcomere

9 CaMKII shows high conservation between Drosophila and hu

10 CaMKII, a key kinase involved in LTP, is both necessary

11 CaMKII-Cre(+):Girk2(flox/flox) mice also displayed a sel

12 CaMKII-driven inhibitory Gi-coupled designer receptors e

13 CaMKII-mediated phosphorylation level of GluN2B serine 1

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

15 nzyme Ca(2+) /calmodulin-dependent kinase 2 (CaMKII) is a crucial and well-established signalling mol

16 epidermal marker K18, suggesting that Ca(2+)/CaMKII signaling promotes neural induction by preventing

17 an essential role for the hippocampal Cav1.2/CaMKII/S831 GluA1 pathway in cocaine CPP extinction, wit

18 temporally restricted inactivation of UNC-43/CaMKII, revealed its essential roles in the transport of

19 turation, such as SAX-1/NDR kinase or UNC-43/CaMKII.

20 phosphorylation of AMPAR GluA1 subunit at a CaMKII locus (GluA1-Ser831) in CeA and lateral amygdala.

21 ired to prevent the arrhythmias induced by a CaMKII-dependent leaky RyR2.

22 tive block of CaV1 channels by isradipine, a CaMKII blocker, and siRNA knockdown of densin, and spike

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

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

25 Activation of PFC pyramidal neurons with a CaMKII-driven Gq-coupled designer receptor exclusively a

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

27 osphorylation on the serine residue within a CaMKII target motif.

28 Other rats received CaMKII-ArchT3.0 AAV2 (CaMKII-ArchT), which transduced C1 neurons and larger nu

29 gen peroxide (H2O2) affects Ca(2+)-activated CaMKII in vitro, Angiotensin II (Ang II)-induced CaMKIId

30 test, we found that expression of activated CaMKII (T286D/T305A/T306A) impaired place avoidance, a r

31 st that the CaM-binding element of activated CaMKII acts as a wedge by docking at intersubunit interf

32 lin, thus unlocking the ability of activated CaMKII holoenzymes to exchange dimers with unactivated o

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

34 tive regulator of this circuit by activating CaMKII-TAK1-NLK signalling, which, in turn, attenuates W

35 reasing the GluN2A/GluN2B ratio in BLA alpha-CaMKII-positive neurons after a weak fear memory has con

36 305/6VA and T305D) mice, we identified alpha-CaMKII inhibition upon autophosphorylation at Thr305/306

37 t GFP-GluN2A transgene specifically in alpha-CaMKII-positive neurons.

38 argeted pharmacologic inhibition of amygdala CaMKII or AMPAR activity specifically inhibited the posi

39 in secretion is also regulated by Ca(2+) and CaMKII.

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

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

42 n therapy with flecainide, beta-blockade and CaMKII inhibition, our model predicted superior therapeu

43 e UTR antagonist, TRPC4 channel blocker, and CaMKII and CREB-binding protein/p300 inhibitors.

44 duced oxidative stress, restored calcium and CaMKII homeostasis, and improved cardiac function and po

45 icate D1-dopamine receptor, NMDAR, Cdk5, and CaMKII in cortico-striatal plasticity.

46 epends on the scaffolding protein densin and CaMKII and that outlasts a depolarizing stimulus by seco

47 n, but only when coexpressed with densin and CaMKII.

48 activity that was accentuated by densin and CaMKII.

49 hannels, the scaffolding protein densin, and CaMKII could generate a facilitation of channel activity

50 llular mechanisms whereby calcium influx and CaMKII control Ras activity remain elusive.

51 hippocampal long-term potentiation (LTP) and CaMKII activity was totally abolished by treatment with

52 PKA and CaMKII do not affect HR by a unique target site governin

53 However, the impact of specific PKA and CaMKII phosphorylation sites on HR is unknown.

54 e systematically evaluated validated PKA and CaMKII target sites on phospholamban and the ryanodine r

55 on NMDAR (N-methyl-d-aspartate receptor) and CaMKII signalling and on postsynaptically synthesized BD

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

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

58 ins postnatally, and its deletion attenuated CaMKII and Rac1 activity, reduced GluN1 glutamate recept

59 Autophosphorylation triggers autonomous CaMKII activity, but does not impair GluN2B binding, ano

60 tion HCM (P=0.01), as was autophosphorylated CaMKII (P<0.01), suggestive of constitutive activation.

61 ysis to identify balanced regulation between CaMKII (activator) and PP1 (inhibitor) and then the mode

62 tion site or inhibiting Drp1 activity blocks CaMKII- or ISO-induced mPTP opening and myocyte death in

63 Both CaMKII and PKA phosphorylate a number of protein targets

64 induced depalmitoylation was also blocked by CaMKII inhibition.

65 Phosphorylation by CaMKII inhibited AKAP79/150 association with F-actin; it

66 These increases were prevented by CaMKII inhibition.

67 minishes ventricular arrhythmias promoted by CaMKII phosphorylation of S2814 on RyR2.

68 acellular Na and Ca overload with consequent CaMKII activation enhancing late INa and the L-type Ca c

69 In contrast, CaMKII inhibition by expression of AC3-I has been shown

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

71 he synapse is normal, maternally contributed CaMKII does not localize to synapses.

72 ma-8, but not TARPgamma-2/3/4, as a critical CaMKII substrate for LTP.

73 Moreover, the CaV1.3-densin-CaMKII interaction gave rise to an outward tail current

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

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

76 s physiological SANC rate responses, despite CaMKII inhibition.

77 nus-tagged CaMKIIalpha to identify a dimeric CaMKII.

78 o genetically engineer monomeric and dimeric CaMKII and evaluate how their activity compares to the w

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

80 decreased p38 MAPK activation via diminished CaMKII signaling.

81 revent the in vitro interaction also disrupt CaMKII association with intact LTCC complexes isolated b

82 Drosophila CaMKII-null mutants remain viable throughout development

83 tration of distinct functions for Drosophila CaMKII mRNA variants.

84 h pulse during repetitive Ca(2+) elevations, CaMKII activity increased in a stepwise manner.

85 Inhibitors of PKC, p38, ERK, CaMKII, STAT3, and CREB partially blocked the activation

86 ed the hyperactive phenotypes of Plcg1(f/f); CaMKII mice.

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

88 To account for CaMKII activation dynamics during spine depolarization w

89 th only at high concentrations necessary for CaMKII/NMDAR disruption (20 mum) but not at lower concen

90 into a spiral form that can release or gain CaMKII dimers.

91 calmodulin-dependent protein kinase II gene (CaMKII) was generated using homologous recombination.

92 gic (GAD67+) interneurons and glutamatergic (CaMKII+) interneurons in the mPFC expressed M1-AChR.

93 xide and nitric oxide, as a mediator of GPCR-CaMKII signaling.

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

95 Unlike the holoCaM-CaMKII peptide, whose structure can be determined by cry

96 However, how CaMKII gives rise to LTP is currently unknown.

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

98 s been spent in attempting to understand how CaMKII activation gives rise to this phenomenon.

99 We show that the human CaMKII holoenzyme exists in dodecameric and tetradecamer

100 cium/calmodulin-dependent protein kinase II (CaMKII) activation.

101 (2+)/calmodulin-dependent protein kinase II (CaMKII) and Ca(2+)/cAMP response element-binding protein

102 almodulin (CaM)-dependent protein kinase II (CaMKII) and its autonomous activity generated by Thr-286

103 ets, Ca(2+)/CaM-dependent protein kinase II (CaMKII) and neurogranin (Ng), as they both regulate CaM-

104 (2+)/calmodulin-dependent protein kinase II (CaMKII) and Polo-like kinase-2 (PLK2) decreases its affi

105 (2+)/calmodulin-dependent protein kinase II (CaMKII) and protein kinase A (PKA) both in vitro and in

106 (2+)/calmodulin-dependent protein kinase II (CaMKII) assembles into large 12-meric holoenzymes, which

107 ), by Ca(2+)/calmodulin-dependent kinase II (CaMKII) at a serine 616 (S616) site.

108 cium/calmodulin-dependent protein kinase II (CaMKII) binds to and modulates NMDAR activity.

109 (2+)/calmodulin-dependent protein kinase II (CaMKII) is also activated in response to betaAR stimulat

110 almodulin (CaM)-dependent protein kinase II (CaMKII) is composed of 8-14 subunits arranged as pairs a

111 cium/calmodulin-dependent protein kinase II (CaMKII) is increased and plays a key role in the potenti

112 ecause calcium/calmodulin protein kinase II (CaMKII) is known to modify persistent current and channe

113 cium/calmodulin-dependent protein kinase II (CaMKII) overactivity plays a crucial role in the pathoph

114 (2+)/calmodulin-dependent protein kinase II (CaMKII) oxidation controls excitability and viability.

115 ing, calcium/calmodulin-dependent kinase II (CaMKII) phosphorylates OGT, which in turn promotes O-Glc

116 2+) /calmodulin-dependent protein kinase II (CaMKII) phosphorylation of RyR2-S2814 residue vs. normog

117 m (Ca(2+)) levels, via calmodulin kinase II (CaMKII) phosphorylation, inhibits proximal GRASP localiz

118 2+) release and Ca(2+)/calmodulin kinase II (CaMKII) signaling are attenuated.

119 cium/calmodulin-dependent protein kinase II (CaMKII) specific inhibitor tatCN21 peptide.

120 (2+)/calmodulin-dependent protein kinase II (CaMKII) strongly interacts with a novel binding motif in

121 (2+)/calmodulin-dependent protein kinase II (CaMKII) to dendritic spine synapses is determined in par

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

123 (2+)/calmodulin-dependent protein kinase II (CaMKII) to the NMDA-type glutamate receptor (NMDAR) subu

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

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

126 cium/calmodulin-dependent protein kinase II (CaMKII), a key synaptic signaling molecule for learning

127 (2+)/calmodulin-dependent protein kinase II (CaMKII), an oligomeric enzyme that is critical for learn

128 (2+)/calmodulin-dependent protein kinase II (CaMKII), led to an inhibition of the neural marker PAX6

129 ding calmodulin-dependent protein kinase II (CaMKII), RhoA, and Cdc42, and the spine volume can be de

130 cium/calmodulin-dependent protein kinase II (CaMKII)-delta and -gamma isoforms.

131 (2+)/calmodulin-dependent protein kinase II (CaMKII)-dependent alterations in NaV1.5 channel inactiva

132 in kinase A (PKA)- and calmodulin kinase II (CaMKII)-mediated enhancement of Ca(2+) uptake and releas

133 n of calcium/calmodulin-dependent kinase II (CaMKII).

134 (2+)/calmodulin-dependent protein kinase II (CaMKII).

135 (2+)/calmodulin-dependent protein kinase II (CaMKII).

136 in (Ca(2+)/CaM) dependent protein kinase-II (CaMKII) subunits form a complex that modulates synaptic

137 calmodulin-dependent protein kinase type II (CaMKII) were similar in HCM samples compared with contro

138 ata show that ONOO(-) participates in Ang II-CaMKII signaling.

139 nduced HF is not associated with a change in CaMKII activity.

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

141 h beta-AR blockers revealed no difference in CaMKII activity when compared with non-beta-AR blocker-t

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

143 potentials (mEJPs) is significantly lower in CaMKII mutants.

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

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

146 this was paralled neither by a reduction in CaMKII autophosphorylation, oxidation, and substrate bin

147 um-dependent downstream effectors, including CaMKII.

148 Memantine increased CaMKII activity in the APP23 mouse hippocampus, and mema

149 m for increasing baseline Ca(2+)-independent CaMKII activity.

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

151 mobilized Ca(2+) : 8-pCPT-AM fails to induce CaMKII activation following intracellular Ca(2+) store d

152 Epac-induced CaMKII activation is probably initiated by inositol 1,4,

153 l inactivation in the heart, we investigated CaMKII as a plausible modulator of neuronal sodium chann

154 e with a mutant NMDAR GluN2B subunit that is CaMKII binding-incompetent, any tatCN21 effects that are

155 calcium release, reduced calmodulin kinase (CaMKII) signaling, and impaired muscle adaptation to exe

156 Ca(2+)/calmodulin-dependent protein kinase (CaMKII) activation is both necessary and sufficient for

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

158 Ca(2+) -calmodulin-dependent protein kinase (CaMKII) constitutive pseudo-phosphorylation of the ryano

159 Ca(2+)/calmodulin-dependent protein kinase (CaMKII), resulting in disruption of its PDZ-mediated int

160 Ca(2+) -calmodulin-dependent protein kinase (CaMKII)-dependent leaky RyR2.

161 tase-1, as well the serine/threonine kinases CaMKII and PKA.

162 , are significantly impaired in mice lacking CaMKII phosphorylation sites of TARPgamma-8.

163 potentiation but was associated with lesser CaMKII activation.

164 am of chronic beta-AR stimulation that links CaMKII, Drp1 and mPTP to bridge cytosolic stress signal

165 tress fibers and the colocalized, long-lived CaMKII tracks.

166 Meanwhile, CaMKII can also promote K63-linked ubiquitination of inh

167 Here, we measured CaMKII activity in spines using fast-framing two-photon

168 ntial for peroxynitrite (ONOO(-)) to mediate CaMKII activation and downstream Kv4.3 channel mRNA dest

169 date a pathway downstream of Ca(2+)-mediated CaMKII activation that is dysfunctional in C3KO mice, le

170 IP3 receptors blocks both 8-pCPT-AM-mediated CaMKII phosphorylation and STOC activity.

171 nd cognition, such as the MAP kinases, MKPs, CaMKII, CREB, Fyn, and Tau.

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

173 eanwhile, via regulation of the KIF17 motor, CaMKII (activated by the NMDAR pathway) may further faci

174 ed de novo CAMK2A mutation disrupts multiple CaMKII functions, induces synaptic deficits, and causes

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

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

177 acking GIRK2 in forebrain pyramidal neurons (CaMKII-Cre(+):Girk2(flox/flox) mice) exhibited diminishe

178 tocrine signalling mechanism involving NMDAR-CaMKII-dependent BDNF release from stimulated dendritic

179 In contrast to normal CaMKII substrates, the substrate sites within the AKAP79

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

181 s, but is dispensable for, the activation of CaMKII and LTP.

182 c lesions in mice demonstrated activation of CaMKII.

183 24 hours) was regulated by the activation of CaMKII.

184 ow that a critical step is the activation of CaMKII.

185 CaMKII activity was judged by analysis of CaMKII expression, autophosphorylation, and oxidation an

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

187 Blockade of CaMKII selectively in presynaptic Abeta-LTMRs removes do

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

189 Thr286 phosphorylation slows the decay of CaMKII and thus lowers the frequency required to induce

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

191 isms involved in LTP induction downstream of CaMKII activation.

192 that the calmodulin (CaM)-binding element of CaMKII can bind to the hub of the holoenzyme and destabi

193 l synthesis requiring the long 3'UTR form of CaMKII mRNA and a process that requires zygotic transcri

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

195 By contrast, inhibition of CaMKII attenuated persistent current, evoked a hyperpola

196 Also, the inhibition of CaMKII in the hypothalamus reduces elevated blood pressu

197 Intra-basolateral amygdala inhibition of CaMKII promoted memory extinction and disrupted reconsol

198 Therefore, inhibition of CaMKII represents a novel mechanism for memory-based add

199 producing turning assays with inhibitions of CaMKII and PP1.

200 ically encoded, light-inducible inhibitor of CaMKII activity.

201 er important synaptic protein interaction of CaMKII.

202 The lack of CaMKII modulation by beta-AR blocker treatment was confi

203 te that TARPgamma-8 is a crucial mediator of CaMKII-dependent LTP and therefore a molecular target th

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

205 therapy in patients and in a mouse model of CaMKII-induced HF is not associated with a change in CaM

206 AR blockers are not based on a modulation of CaMKII.

207 The inhibition phase of CaMKII, which lasted 10 to 20 minutes after administrati

208 nding nor a change in the phosphorylation of CaMKII downstream target proteins (n>/=11).

209 Increased phosphorylation of CaMKII, phospholamban, and ryanodine receptor 2 was dete

210 2 Ser-409 phosphorylation in the presence of CaMKII, and this phosphorylation was reduced in the pres

211 Zygotic production of CaMKII mRNA with a long 3'-untranslated region is necess

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

213 enase 2 via the mitochondrial recruitment of CaMKII (Ca(2+)/calmodulin-dependent protein kinase II),

214 o better define the biological regulation of CaMKII activation and signaling by Ang II, we evaluated

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

216 These data argue that regulation of CaMKII localization and levels by local transcriptional

217 o our knowledge, this is the first report of CaMKII activation triggering cellular activity known to

218 o our knowledge, this is the first report of CaMKII initiating cellular activity linked to vasorelaxa

219 on LTP, strongly support a critical role of CaMKII in LTP maintenance and memory storage.

220 In this study, we determined the role of CaMKII in regulating NMDAR activity of PVN presympatheti

221 rprisingly little is known about the role of CaMKII.

222 investigating the phosphorylation status of CaMKII downstream targets.

223 The structures of CaMKII from two distantly diverged organisms suggest tha

224 This suggests that targeting of CaMKII and the regulation of autophagic degradation of I

225 y Kalirin and Trio as the elusive targets of CaMKII phosphorylation responsible for AMPA receptor up-

226 ocess that requires zygotic transcription of CaMKII mRNA.

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

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

229 NCX1 blockade impacted on CaMKII signalling to down-regulate cardiac gene expressi

230 Y1 receptor expression was localized on CaMKII-positive pyramidal projection neurons and GAD67-p

231 fect of chronic beta-AR blocker treatment on CaMKII activity in human and experimental HF.

232 nrelated to the CaMKII/GluN2B interaction or CaMKII activity.

233 lts suggest that activation of either PKA or CaMKII is sufficient to speed SR refilling, but activati

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

235 r enhancing SR Ca(2+) uptake by PKA (S16) or CaMKII (T17) to alanines did not affect HR in vivo or in

236 acement of ryanodine receptor PKA (S2808) or CaMKII (S2814) target sites failed to affect HR response

237 The CaMKII inhibitor tatCN21 or CaMKII mutations that inhibit GluN2B association by bloc

238 ator of synaptic development and plasticity, CaMKII has important roles in both normal and pathologic

239 ization and/or stabilization of postsynaptic CaMKII (Ca(2+)/calmodulin-dependent protein kinase II) a

240 ted with distinct regulation of postsynaptic CaMKII.

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

242 MPA receptor expression, and that preventing CaMKII signaling through Kalirin and Trio prevents LTP i

243 The abundant synaptic protein CaMKII is necessary for long-term potentiation (LTP) and

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

245 ONOO(-) oxidizes and modestly activates pure CaMKII in the absence of Ca(2+)/CaM.

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

247 n to the defects in regulation of mEJP rate, CaMKII protein is largely lost from synapses in the muta

248 Other rats received CaMKII-ArchT3.0 AAV2 (CaMKII-ArchT), which transduced C1

249 We conclude that regulated CaMKII isoform composition is an important determinant o

250 ment of AMPAR-mediated transmission requires CaMKII phosphorylation sites of TARPgamma-8.

251 c AKAP79/150 removal, which in turn requires CaMKII activity.

252 tonomous compared with Ca(2+)/CaM-stimulated CaMKII activity.

253 I-induced SOCE via TRPC4 channels stimulates CaMKII/CREB-dependent GMC proliferation and ECM protein

254 lease, which cannot be fulfilled by synaptic CaMKII from the other pool.SIGNIFICANCE STATEMENT As a r

255 The origin of synaptic CaMKII also dictates its functionality.

256 This suggests that synaptic CaMKII accumulates by two distinct mechanisms: local syn

257 We determined binding of GFP-tagged CaMKII to tag-RFP-labeled actin cytoskeleton within live

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

259 ptide (AIP) mice, expressing the SR-targeted CaMKII inhibitor AIP, without any significant enhancemen

260 Directly targeting CaMKII may, therefore, further improve HF therapy in add

261 result not expected if a process other than CaMKII stores memory.

262 reases TARPgamma-8 phosphorylation, and that CaMKII-dependent enhancement of AMPAR-mediated transmiss

263 We conclude that CaMKII-mediated modulation of neuronal sodium current im

264 Here we tested the hypothesis that CaMKII/GluN2B binding also mediates the more elusive mai

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

266 Here we show that CaMKII can directly phosphorylate Beclin 1 at Ser90 to p

267 ng a rodent model of addiction, we show that CaMKII inhibition in the amygdala can reduce relapse-lik

268 Furthermore, we show that CaMKII phosphorylation of Kalirin is sufficient to enhan

269 Stepwise photobleaching showed that CaMKII formed oligomeric complexes.

270 Previous studies have shown that CaMKII and the RAS-ERK pathway are critical for several

271 Our findings suggest that CaMKII activity is increased in the PVN and contributes

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

273 mice with AC3-I expression, suggesting that CaMKII affects HR by modulation of SR Ca(2+) content.

274 This heterogeneity suggests that CaMKII adopts different F-actin binding modes, which is

275 The CaMKII inhibitor autocamtide-2-related inhibitory peptid

276 The CaMKII inhibitor tatCN21 or CaMKII mutations that inhibi

277 The CaMKII target pT17-phospholamban was 5.5-fold increased

278 zed by multiple subunit contacts between the CaMKII dodecamer and the F-actin cytoskeleton that stabi

279 However, the CaMKII substrate that increases AMPAR-mediated transmiss

280 It is not clear if the CaMKII holoenzyme functions as an assembly of independen

281 3 alpha1 subunit N-terminal domain or in the CaMKII catalytic domain that largely prevent the in vitr

282 Intriguingly, the CaMKII inhibitor tatCN21 reduces synaptic strength only

283 Importantly, systemic administration of the CaMKII inhibitor tatCN21 increased global protein synthe

284 Posttranslational activation of the CaMKII pathway is specific to sarcomere mutation-positiv

285 Importantly, they also demonstrate that the CaMKII/GluN2B interaction is required not only for norma

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

287 volley amplitude) that was unrelated to the CaMKII/GluN2B interaction or CaMKII activity.

288 any tatCN21 effects that are specific to the CaMKII/GluN2B interaction should be abolished, and any r

289 WT mice but not in S2814A mice, in which the CaMKII phosphorylation site on RyR2 was ablated.

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

291 of the better known binding of calmodulin to CaMKII.

292 ic events triggered by SR Ca(2+) leak due to CaMKII-dependent phosphorylation of the RyR2-S2814 site

293 Cardiac arrest and reperfusion lead to CaMKII activation and calcium long-term potentiation, wh

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

295 ne receptors may be preferentially linked to CaMKII activity.

296 Locally translated CaMKII has a privileged role in regulation of spontaneou

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

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

299 orcers and then stimulated this region using CaMKII-driven Gs-coupled designer receptors exclusively

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