ライフサイエンスコーパス: CaMK

1 CaMK and Pyk2 relayed signals from integrins and the ITA

2 CaMK induced expression of peroxisome proliferator-activ

3 CaMK inhibition suppressed STAT1-mediated interferon-alp

4 CaMK phosphorylates serines -259 and -498 in HDAC5, whic

5 CaMK reciprocally enhanced L-type Ca(2+) current and red

6 CaMK regulation of CP-AMPARs was also confirmed in hippo

7 CaMK stimulates MEF2 activity by dissociating class II h

8 CaMK was contained only in pyramidal neurons; GABA was c

9 CaMK-II is transiently activated in approximately four i

10 Ca2+/calmodulin-dependent protein kinase-2 [CaMK-2] [Kd = 300-400 nmol/l at 10(-5) mol/l [Ca2+]]).

11 cholangiocytes by the activation of Ca(2+) /CaMK I-dependent AC8.

12 inction recruited calcium/calmodulin (Ca(2+)/CaMK)-dependent protein kinase II (CaMKII) to the hippoc

13 lar concentration of factors such as 14-3-3, CaMK I, and other yet unknown molecules may determine th

14 ine pathway, a cAMP-dependent pathway, and a CaMK-dependent pathway.

15 expression in CA1 pyramidal neurons causes a CaMK- and PKC-dependent potentiation of AMPAR-mediated t

16 These experiments define a CaMK IV-responsive RNA element (CaRRE), which mediates t

17 um) and tobacco (Nicotiana tabacum) or for a CaMK similar to those in animals or yeast.

18 inase family as it controls the actions of a CaMK cascade involving CaMKI, CaMKIV or AMPK.

19 Local administration of a CaMK II inhibitor in the spinal cord significantly inhib

20 emonstrate that intra-amygdala infusion of a CaMK inhibitor, 1-[NO-bis-1,5-isoquinolinesulfonyl]-N-me

21 Activated CaMK-II was found enriched along the axon and in the gro

22 Within these cells, activated CaMK-II is observed at the surface and in clusters, whic

23 lized to the cell nucleus, and the activated CaMK-IV disrupted HDAC4/SRF association, leading to expo

24 ough seven genes encode catalytically active CaMK-II in early zebrafish embryos, one of these genes a

25 of LTCCs to exogenous, constitutively active CaMK and to an IQ-mimetic peptide (IQmp).

26 Overexpressing constitutively active CaMK IV, but not CaMK I or II, specifically decreases ST

27 lls and cilia, whereas constitutively active CaMK-II restores pronephric duct formation in pkd2 morph

28 In addition, CaMK inhibition substantially decreased liver damage aft

29 al polyps, but these reagents did not affect CaMK II-activated Cl(-) currents in these cells.

30 +) axon terminals were seen to innervate all CaMK(+) postsynaptic domains, including cell bodies (22%

31 alpha CaMK-II is absent from amphibians (Xenopus laevis) and h

32 ral level of glutamate receptor activity and CaMK-dependent signaling are critical for development of

33 + release was required for both Ca2+-CaM and CaMK ICa-L responses after strongly positive conditionin

34 nges control ICa-L responses to Ca2+-CaM and CaMK signalling.

35 rately test the relationship of Ca2+-CaM and CaMK to ICa-L and SR Ca2+i release during voltage clamp

36 element for ICa-L responses to Ca2+-CaM and CaMK, and the C terminus undergoes voltage-dependent ste

37 Combined inhibition of Trk, cAMP, and CaMK signaling prevents depolarization-dependent surviva

38 indicating that SKF83959 stimulates cdk5 and CaMK II activities via a PI-linked D1-like dopamine rece

39 Although cdk5 and CaMK II are physically associated in native brain tissue

40 educed labeling by about 30%, while CDK5 and CaMK II inhibitors had no effect.

41 Both PKD2-deficient and CaMK-II-deficient zebrafish embryos fail to form proneph

42 ifferentially impact DRD-2, DAT, CaMK II and CaMK IV mRNA, protein and intracellular expression compa

43 Inhibition of PKC and CaMK attenuated phosphorylation of Galpha q/11 proteins

44 osphorylation of Galpha11 protein by PKC and CaMK contributes to agonist-induced homologous desensiti

45 ctivated by NGF involves PI3K, while PKC and CaMK II are also involved, probably at subsequent stages

46 zopyran-4-one (PD98059) and by PKA, PKC, and CaMK inhibitors.

47 PKD2 and CaMK-II deficiencies are synergistic, supporting their e

48 pendent on upstream activation of ERK1/2 and CaMKs.

49 e of PKC translocation was apparent, PKC and CaMKs were required for activation and nuclear transloca

50 transduction network through which Rem2 and CaMKs function to restrict dendritic complexity.

51 Jun NH(2)-terminal kinase, protein kinase B, CaMK II, protein kinase Calpha, and protein kinase Cdelt

52 irtually every pyramidal cell appeared to be CaMK(+), the cell bodies of small nonpyramidal neurons w

53 We conclude that beta CaMK-II expression and activity are necessary for proper

54 f beta2 CaMK-II (camk2b2), but not the beta1 CaMK-II (camk2b1) paralog, exhibit bradycardia, elongate

55 alphaKAP, beta2 CaMK-II and gamma1 CaMK-II antisense morpholino oligonuc

56 and gamma1 CaMK-II; however, alphaKAP, beta2 CaMK-II and the RyR3 ryanodine receptor were also necess

57 Morphants of beta2 CaMK-II (camk2b2), but not the beta1 CaMK-II (camk2b1) p

58 oneal M that was attenuated with biochemical CaMK inhibition or CaMKIalpha small interfering RNA (siR

59 Both CaMK and IQmp induced a modal gating shift in LTCCs that

60 Both CaMK and IQmp were able to induce a modal gating shift i

61 ction of DNA synthesis in mesangial cells by CaMK II 290.

62 ylation of the APC/C inhibitor XErp1/Emi2 by CaMK II renders it a good substrate for Plx1, and phosph

63 Phosphorylation of class II HDACs by CaMK results in CRM1-dependent nuclear export of HDAC/RF

64 Neuronal behavior is influenced by CaMK-II, the type II Ca2+/calmodulin-dependent protein k

65 Activation of the c-fos promoter by CaMK II 290 was also blocked by COOH-terminal Src kinase

66 ked activation of the c-fos gene promoter by CaMK II 290, a constitutively active form of CaMK IIalph

67 gets at sites similar to those recognized by CaMK pathways.

68 In contrast, gamma(C) CaMK-II is uniformly cytosolic.

69 of a structurally similar isozyme, gamma(C) CaMK-II, which does not induce neurite outgrowth.

70 alize like full-length delta(E) and gamma(C) CaMK-II.

71 pendent mechanism for SRF activation by Ca2+/CaMK-mediated signaling.

72 targets of SOM+ terminals were small-caliber CaMK+ dendrites and dendritic spines, some of which were

73 y lower compared with that of the calmodulin-CaMK-2 association (K0.5 = 40 micromol/l [Ca2+], maximal

74 ism resolves long-standing puzzles about CaM/CaMK-dependent signaling to the nucleus.

75 To further define the mechanisms that confer CaMK responsiveness to HDAC4 and -5, we performed yeast

76 a heterologous gene is sufficient to confer CaMK IV repression on an otherwise constitutive exon.

77 Prolonged Ca(2)(+) stimulation converts CaMK-II into an activated state that, in the zebrafish,

78 notypes can be restored by ectopic cytosolic CaMK-II expression in tbx5 morphants.

79 de B gp120 differentially impact DRD-2, DAT, CaMK II and CaMK IV mRNA, protein and intracellular expr

80 B and C gp120 and/or METH on the DRD-2, DAT, CaMKs and CREBP transcription.

81 vels and, like CaMK-II inhibitors, decreased CaMK-II activation.

82 delta CaMK-II is the only gene with both central and C-termina

83 y in mammals, whereas beta, gamma, and delta CaMK-IIs are expressed in most tissues.

84 efine a targeting domain for gamma and delta CaMK-IIs that is in between the central variable and ass

85 argeting differences between gamma and delta CaMK-IIs.

86 The C-terminal 95 residues of delta CaMK-II also has no targeting capability but can efficie

87 indicate that persistent activation of delta CaMK-II by laminin stabilizes nascent embryonic axons th

88 rt for the placement of the vertebrate delta CaMK-II as the earliest diverging vertebrate gene.

89 ight microscopic observations revealed dense CaMK staining in the ABL.

90 rafish embryos and mouse fibroblasts doubles CaMK-II expression.

91 TLR4-dependent ROS production and downstream CaMK-mediated signaling.

92 delta(E) CaMK-II co-localizes with filamentous actin in the perin

93 Constitutively active delta(E) CaMK-II induces F-actin-rich extensions, thereby support

94 the subcellular targeting domain of delta(E) CaMK-II, an isozyme that induces neurite outgrowth, and

95 Endogenous CaMK is targeted to LTCCs in excised cell membrane patch

96 eption of some dendritic spines, can exhibit CaMK immunoreactivity.

97 oplasmic localization of HDAC7 by expressing CaMK I.

98 In fact, CaMK-II suppression results in additional ciliated hair

99 e show in hippocampal neurons that the fast, CaMK-dependent pathway can be followed by a slower pathw

100 forebrain-restricted SPL deletion (SPL(fl/fl/CaMK)) caused marked accumulation of S1P.

101 that 14-3-3 binding to HDAC5 is required for CaMK-dependent disruption of MEF2-HDAC complexes and nuc

102 hes, the present findings support a role for CaMK kinase in mediating mGluR5-dependent cyclic adenosi

103 t development, but support implied roles for CaMK-II in adult heart remodeling.

104 idea that S18 could be a novel substrate for CaMK II, thus providing a potential link between Ca(2+)-

105 ngs identify MEF2 as a downstream target for CaMK signaling in the hypertrophic heart and suggest tha

106 Roles for CaMKs in modulating gene transcription are well establis

107 an antagonist for Ca(2+)/CaM rather than for CaMKs.

108 nodine receptor were also necessary for full CaMK-II activation.

109 beta and gamma CaMK-II genes show strong sequence similarity and have c

110 alphaKAP, beta2 CaMK-II and gamma1 CaMK-II antisense morpholino oligonucleotides, as well a

111 ntact KV, the PKD2 Ca(2+) channel and gamma1 CaMK-II; however, alphaKAP, beta2 CaMK-II and the RyR3 r

112 K-II is activated by laminin, and if so, how CaMK-II influences axonal growth and stability.

113 cium-calmodulin-dependent protein kinase II (CaMK II) activation also prevented NGF-induced sensitisa

114 cium/calmodulin-dependent protein kinase II (CaMK II) activities.

115 (2+)/calmodulin-activated protein kinase II (CaMK II) is abundantly expressed in vascular smooth musc

116 cium/calmodulin-dependent protein kinase II (CaMK II) is found throughout the CNS.

117 Ca2+/calmodulin-dependent protein kinase II (CaMK II), which is activated by elevated [Ca2+]i, increa

118 Ca2+-calmodulin-dependent protein kinase II (CaMK) and a calmodulin (CaM)-binding 'IQ' domain (IQ) ar

119 (LTCC) C terminus and calmodulin kinase II (CaMK) both signal increases in LTCC opening probability

120 cium/calmodulin-dependent protein kinase II (CaMK) has been shown to play a critical role in long-ter

121 cium/calmodulin-dependent protein kinase II (CaMK) immunoreactivity as a marker.

122 tivate Ca2+-CaM-dependent protein kinase II (CaMK) to increase ICa.

123 cium/calmodulin-dependent protein kinase II (CaMK) was used as a marker for pyramidal cells, the prin

124 cium/calmodulin-dependent protein kinase II (CaMK).

125 cium/calmodulin-dependent protein kinase II (CaMK); previous studies have shown that the vast majorit

126 (2+)/calmodulin-dependent protein kinase II (CaMK-II) isozyme variability is the result of alternativ

127 almodulin-dependent protein kinase, type II (CaMK-II) is an evolutionarily conserved protein.

128 PKD2 suppression inactivates CaMK-II in pronephric cells and cilia, whereas constitut

129 molecules and signaling pathways, including CaMK, PKA, Casein kinase-II, and the Raf-MEK-ERK and PI-

130 Engineered Ca2+-independent CaMK and IQmp each markedly increased LTCC open probabil

131 c1 in vivo and that this activation involves CaMK II and PKC, but not 3-phosphoinositides.

132 or of many of these morphogenic processes is CaMK-II, a conserved calmodulin-dependent protein kinase

133 CaMKII, one of the key CaMKs, plays a significant role in mediating cellular re

134 Signaling by the Ca(2+)/calmodulin kinase (CaMK) cascade has been implicated in neuronal gene trans

135 Calmodulin kinase (CaMK) has characteristics suitable for an ECC coordinati

136 Calmodulin kinase (CaMK) II is linked to arrhythmia mechanisms in cellular

137 r effector of the Ca(2+) /calmodulin kinase (CaMK) pathway where it coordinates transcriptional respo

138 neurons, serotonin uses a calmodulin kinase (CaMK)-dependent signaling cascade involving CaMKKbeta an

139 H(2)O(2) activates Ca(2+)/calmodulin kinase (CaMK)II, which also impairs I(Na) inactivation and promo

140 phosphatase calcineurin (Cn) and CaM kinase (CaMK)II.

141 KC) and calcium/calmodulin dependent kinase (CaMK) consensus site in Galpha11 significantly reduced D

142 ided by calcium/calmodulin-dependent kinase (CaMK) disrupt the interaction of MITR and HDACs with HP1

143 tion of calcium calmodulin-dependent kinase (CaMK) has no effect, but pERK is reduced by inhibition o

144 nctional Ca(2+)/calmodulin-dependent kinase (CaMK) II.

145 of the calcium/calmodulin-dependent kinase (CaMK) inhibitor KN93 to depolarizing medium.

146 through Ca(2+)/calmodulin-dependent kinase (CaMK) IV.

147 part by calcium/calmodulin-dependent kinase (CaMK)-mediated phosphorylation.

148 including Ca2+/calmodulin-dependent kinase (CaMK).

149 rin) and Ca(2+)/calmodulin-dependent kinase (CaMK).

150 Calcium/calmodulin-dependent protein kinase (CaMK) activation induces mitochondrial biogenesis in res

151 calcium/calmodulin-dependent protein kinase (CaMK) and extracellular signal-regulated kinase 1/2 (ERK

152 calcium/calmodulin-dependent protein kinase (CaMK) cascade that is comprised of CaMK kinase (CaMKK) a

153 m/calmodulin (CaM)-dependent protein kinase (CaMK) I and insulin-like growth factor (IGF) II (Igf2) i

154 calcium/calmodulin-dependent protein kinase (CaMK) I in the regulation of these mechanisms.

155 Ca(2+) /calmodulin-dependent protein kinase (CaMK) I. gamma-Aminobutyric acid (GABA) affects cell fun

156 tion of calmodulin-dependent protein kinase (CaMK) II and cAMP response element-binding protein (CREB

157 calcium/calmodulin-dependent protein kinase (CaMK) II in dorsal CA1 does not affect retention of this

158 cked by calmodulin-dependent protein kinase (CaMK) inhibitor KN-62.

159 calcium/calmodulin-dependent protein kinase (CaMK) IV serine phosphorylates and mediates the release

160 calcium calmodulin-dependent protein kinase (CaMK) pathway, a major pathway of CREB activation--fear

161 Calcium/calmodulin-dependent protein kinase (CaMK) signaling promotes myogenesis by disrupting MEF2-H

162 Ca(2+)/calmodulin-dependent protein kinase (CaMK) type IV, which was attenuated by calpain inhibitor

163 Ca(2+)/calmodulin-dependent protein kinase (CaMK), and cyclic adenosine 3',5'-monophosphate-responsi

164 calcium-calmodulin-dependent protein kinase (CaMK)-dependent binding of 14-3-3 to phosphoserines 259

165 of Ca2+/calmodulin-dependent protein kinase (CaMK)-IV prevented SRF/HDAC4 interaction and derepressed

166 calcium/calmodulin-dependent protein kinase (CaMK)-type domain of RSK1 is reminiscent of the better k

167 Ca(2+)/calmodulin-dependent protein kinase (CaMK)/p25 double-transgenic model of tauopathic degenera

168 calcium/calmodulin-dependent protein kinase (CaMK)Ialpha regulates the inflammatory phenotype of the

169 calcium/calmodulin-dependent protein kinase (CaMK)II and downstream MEK and ERK MAPKs that are import

170 study, Ca(2+)/CaM-dependent protein kinase (CaMK-II) is identified as a necessary target of this Ca(

171 II Ca2+/calmodulin-dependent protein kinase (CaMK-II), which is preferentially activated in hair cell

172 he function of the calcium-dependent kinases CaMK and Pyk2 'downstream' of ITAM-associated receptors

173 tional calcium/calmodulin-dependent kinases (CaMK), KN-93, arrests a variety of cell types in G(1).

174 cantly similar to those of both CaM kinases (CaMKs) and doublecortin, the product of the gene mutated

175 equence identity with mammalian CaM kinases (CaMKs) I/IV and CaMKKalpha/beta, respectively.

176 levated calcium are mediated by CaM kinases (CaMKs), a family of protein kinases whose activities are

177 plethora of enzymes, including CaM kinases (CaMKs).

178 including the calmodulin-dependent kinases (CaMKs) and the ERKs (extracellular signal-regulated kina

179 es such as the calmodulin-dependent kinases (CaMKs) and the extracellular signal-regulated kinases (E

180 Ca(2)(+)/calmodulin-dependent kinases (CaMKs) are essential for neuronal development and plasti

181 ibited several calmodulin-dependent kinases (CaMKs) competitively with Ca(2+)/calmodulin (Ca(2+)/CaM)

182 ns with Ca(2+)/calmodulin-dependent kinases (CaMKs) in rat hippocampal neurons.

183 ion of calcium/calmodulin-dependent kinases (CaMKs), a family of proteins involved in a wide range of

184 Ca(2+)/calmodulin-dependent protein kinases (CaMKs) and RARs that modulates the differentiation of my

185 Ca(2+)/calmodulin-dependent protein kinases (CaMKs) are major downstream mediators of neuronal calciu

186 Ca(2+)/calmodulin-dependent protein kinases (CaMKs) with KN-62 reduces SGN survival independently of

187 PRKs), calmodulin-dependent protein kinases (CaMKs), calcium and calmodulin-dependent protein kinases

188 f Ca2+/calmodulin-dependent protein kinases (CaMKs).

189 alcium-calmodulin-dependent protein kinases (CaMKs).

190 d Ca2+/calmodulin-dependent protein kinases (CaMKs)[corrected].

191 By comparing known CaMK-II protein and nucleotide sequences, we have now pr

192 length and phospho-CaMK-II levels and, like CaMK-II inhibitors, decreased CaMK-II activation.

193 All 38 known mammalian CaMK-II splice variants were compiled with their tissue

194 Voltage-gated channels mobilize CaMK to activate CREB initially, but they also enable ca

195 related behavior, cortical activity and mPFC CaMK components, implicating cellular and molecular mech

196 To determine which multifunctional CaMK acts in G(1), we expressed kinase-deficient forms o

197 es, as well as KV-targeted dominant negative CaMK-II, randomize organ laterality and southpaw (spaw)

198 ion using a combination of dominant-negative CaMKs (dnCaMKs) and other specific CaMK inhibitors.

199 ssing constitutively active CaMK IV, but not CaMK I or II, specifically decreases STREX inclusion in

200 report that PV+ interneurons employ a novel CaMK-dependent pathway to trigger CREB phosphorylation a

201 generality of CaM shuttling to drive nuclear CaMK activity, and they are relevant to disease pathophy

202 Continued expression and activation of CaMK-II in maculae and cristae in older embryos suggests

203 by approximately 10-fold, and the amount of CaMK kinase (an upstream activator of CaMKIV) protein an

204 ia HP1-MITR and HP1-HDAC interactions and of CaMK signaling to disrupt these interactions provides an

205 DeltaD protein accumulates in hair cells of CaMK-II morphants, indicative of defective recycling and

206 n kinase (CaMK) cascade that is comprised of CaMK kinase (CaMKK) and its primary downstream substrate

207 o retain HDAC5 in the nucleus in the face of CaMK signaling.

208 ing an engineered Ca(2+)-independent form of CaMK and a highly specific CaMK inhibitory peptide.

209 CaMK II 290, a constitutively active form of CaMK IIalpha.

210 morpholino oligonucleotides or inhibition of CaMK-II activation by the pharmacological antagonist, KN

211 Direct inhibition of CaMK-II in 1-day-old neurons immediately froze growth co

212 KN-93, an inhibitor of CaMK II, markedly reduced force, MLCK FRET and [Ca(2+)].

213 Dual localization of CaMK and GABA immunoreactivity with confocal immunofluor

214 ethods to study the neuronal localization of CaMK, and its relationship to gamma-aminobutyric acid (G

215 hibition of either cdk5 by roscovitine or of CaMK by 2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfon

216 increased expression and phosphorylation of CaMK II in rat spinal dorsal horn neurons after noxious

217 evidence for the evolutionary relatedness of CaMK-IIs.

218 There are few, if any, known substrates of CaMK II that are physiologically relevant in vascular sm

219 ecovery of the current amplitude depended on CaMK activity.

220 C5 binding to 14-3-3 is largely dependent on CaMK signaling.

221 tory show an inhibitory effect of heparin on CaMK II phosphorylation and activity.

222 hat SKF83959-mediated stimulation of cdk5 or CaMK II is independent of the other kinase and that the

223 In vitro, control- or CaMK I-silenced small cholangiocytes were treated with G

224 IV levels, suggesting the involvement of PFC CaMK pathways in COMT-regulated cognitive function and a

225 A pharmacologic CaMK inhibitor, KN-93, did not block activation of the c

226 (CD29) also reduced axon length and phospho-CaMK-II levels and, like CaMK-II inhibitors, decreased C

227 axonal remnants exhibited diminished phospho-CaMK-II levels.

228 l disruption specifically prevents prepulse, CaMK and IQ-dependent LTCC facilitation.

229 uclear translocation, whereas a proapoptotic CaMK inhibitor stimulates HDAC4 nuclear accumulation.

230 rapid CaMK signaling to pCREB or both rapid CaMK and slow MAPK signaling deviated significantly for

231 The Ca(2+) signals that produced only rapid CaMK signaling to pCREB or both rapid CaMK and slow MAPK

232 timulation of c-Src by endothelin-1 required CaMK II activity, further supporting the notion that CaM

233 Among several CaMK-II variants detected in these cultures, the 52-kDa

234 Left-sided CaMK-II activation was most dependent on an intact KV, t

235 s detected using a phospho-Thr(287) specific CaMK-II antibody.

236 In addition, KN-93, a specific CaMK II inhibitor, blocks S18 phosphorylation in vascula

237 A specific CaMK inhibitory peptide nearly abolished I(Ca) facilitat

238 and this effect was prevented by a specific CaMK inhibitory peptide, but not by an inactive control

239 dependent form of CaMK and a highly specific CaMK inhibitory peptide.

240 -negative CaMKs (dnCaMKs) and other specific CaMK inhibitors.

241 In addition, spinal CaMK II activity enhances phosphorylation of AMPA recept

242 a suggest that drugs that selectively target CaMKs and regulate protein synthesis offer novel strateg

243 supports a model in which membrane targeted CaMK-II hetero-oligomers in nodal cells transduce the le

244 We conclude that CaMK-II is a crucial effector of PKD2 Ca(2)(+) that both

245 the ultrastructural level, it was found that CaMK was localized to pyramidal cell bodies, thick proxi

246 These findings support the hypothesis that CaMK is required for physiological I(Ca) facilitation in

247 These findings support the hypothesis that CaMK is required to functionally couple LTCC and RyR dur

248 These findings indicate that CaMK is a useful marker for pyramidal neurons in ultrast

249 Our findings indicate that CaMK-II plays a critical role in the developing ear, inf

250 favoured prolonged openings, indicating that CaMK and IQmp affect LTCCs through a common biophysical

251 activity, further supporting the notion that CaMK II acts upstream of Src in a signaling cassette.

252 immunofluorescence microscopy revealed that CaMK and GABA were found in different neuronal populatio

253 This study reveals that CaMK II contributes to central sensitization in a manner

254 Here we show that CaMK increases ICa-L after brief positive conditioning p

255 and IQmp were non-additive, suggesting that CaMK and IQmp are components of a shared signalling path

256 The CaMK cascade also participates in cross-talk with other

257 The CaMK pathway has been previously implicated in promoting

258 The CaMK pathway regulates synaptogenesis by driving the for

259 The CaMK-dependent MAPK pathway may inform the nucleus about

260 ormation was overwhelmingly dominated by the CaMK pathway between 0 and 10 min, and by the MAPK pathw

261 that eliminate gene products containing the CaMK-like and L27 domains (CASK-beta), but do not affect

262 Here, we describe a requirement for the CaMK-kinase (CaMKK) pathway upstream of ERK in LTP induc

263 We observe that CaMKIIgamma is the CaMK that is predominantly expressed in myeloid cells.

264 iew summarizes key neuronal functions of the CaMK cascade in signal transduction, gene transcription,

265 of upstream and downstream components of the CaMK cascade may serve distinct physiological functions.

266 pha) isoform is an upstream component of the CaMK cascade whose function in different behavioral and

267 addition be mediated by other members of the CaMK cascade, such as CaMKK, CaMKI, and CaMKIV.

268 proteins could influence the activity of the CaMK domain-containing protein kinases.

269 e II (CaMKII), although other members of the CaMK family are highly expressed in developing neurons.

270 e-associated' (CaMKv), a pseudokinase of the CaMK family with unknown function, as a synaptic protein

271 by BAPTA/AM, W7, and stable knockdown of the CaMK I gene.

272 s the expression of a specific member of the CaMK-II (the type II multifunctional Ca(2+)/calmodulin-d

273 n diminished RANKL-induced activation of the CaMK-MEK-ERK pathway and decreased expression of the mas

274 the hypertrophic heart and suggest that the CaMK and calcineurin pathways preferentially target diff

275 n together, this study demonstrates that the CaMK II/CREB/Wnt/beta-catenin signaling cascade plays an

276 CaMKK2 is one of the most versatile of the CaMKs and will phosphorylate and activate CaMKI, CaMKIV,

277 KN62, a pharmacological inhibitor of the CaMKs, enhances the terminal differentiation of myeloid

278 gulatory properties of DCK1 and those of the CaMKs.

279 This CaMK I-induced nuclear export of HDAC7 was abolished whe

280 dulin-dependent protein kinase) family; this CaMK-II is necessary for proper heart and fin developmen

281 elease from internal stores and acts through CaMK and MAPK pathways to sustain activated CREB.

282 o CaMK phosphorylation sites is resistant to CaMK-mediated nuclear export and acts as a dominant inhi

283 These findings show that ICa-L responses to CaMK are voltage dependent and suggest a new model of L-

284 An HDAC5 mutant lacking two CaMK phosphorylation sites is resistant to CaMK-mediated

285 Unlike CaMKs, DCK1 is not directly activated by Ca(2+)-bound Ca

286 ylation of the kinase on T200 by an upstream CaMK kinase (CaMKK).

287 mbiguously indicate that the four vertebrate CaMK-II genes arose via repeated duplications.

288 late c-fos gene expression independently via CaMK.

289 tes and dendritic spines, some of which were CaMK+.

290 Very similar results were found when CaMK-II activity was increased through the intracellular

291 myocytes were studied under conditions where CaMK activity could be controlled independently of intra

292 P-regulated phosphoprotein at Thr75, whereas CaMK II is responsible for the activation of cAMP respon

293 However, the mechanism whereby CaMK and the IQ domain are targeted to LTCCs is unknown.

294 n this study, we sought to determine whether CaMK-II is activated by laminin, and if so, how CaMK-II

295 ic peptide (IQmp), under conditions in which CaMK activity was controlled, to test the relationship b

296 -activated protein kinase (MAPK), along with CaMK.

297 The LTCC P(o) increases with CaMK and IQmp were non-additive, suggesting that CaMK an

298 immunoprecipitation of a 20-kDa protein with CaMK II.

299 Few SOM+ terminals formed synapses with CaMK+ pyramidal cell somata or large-caliber (proximal)

300 In zebrafish, CaMK-II is encoded by seven genes; the expression of one