ライフサイエンスコーパス: CaM kinase

1 (2+)/calmodulin-dependent protein kinase II (CaM kinase).

2 for signaling pathways controlled by IGF and CaM kinase.

3 er-82) following induction of the endogenous CaM kinase.

4 vity via a novel signaling pathway involving CaM kinase.

5 s additional predictions for the dynamics of CaM kinases.

6 not cause a calcium flux, also activated the CaM kinases.

7 ition of Ca(2+) influx or Ca(2+)/calmodulin (CaM) kinases.

8 of a pathway involving CaM kinase kinase and CaM kinase 4 that induces synaptic depression of AMPAR a

9 AMPAR subunit, indicating that downstream of CaM kinase activation divergent pathways regulate homeos

10 te a novel mechanism by which ROI can induce CaM kinase activation in T lymphocytes.

11 Inhibition of either phase of CaM kinase activity blocks adipogenesis and expression o

12 strated the presence of calmodulin-dependent CaM kinase activity in the parasite.

13 CaM kinase activity is increased in active muscle and in

14 CaM kinase activity was increased 5-fold in cells subjec

15 To determine whether CaM-kinase activity regulates CPEB-dependent mRNA transl

16 ession of myogenesis also can be overcome by CaM kinase and insulin-like growth factor (IGF) signalin

17 binds to Mint 1, and the region between the CaM kinase and PDZ domains interacts with Velis, resulti

18 Functional interactions between CaM kinases and mitogen-activated protein (MAP) kinases

19 oth the calcium-calmodulin-dependent kinase (CaM kinase) and the mitogen-activated protein (MAP) kina

20 Although the CaM kinases appear to be required for this response, inc

21 alcium/calmodulin-dependent protein kinases (CaM kinases) are a family of related kinases that are ac

22 These results identify the CaM kinases as potential targets that can be used to min

23 CaM kinase blockade with the calmodulin antagonist W-7 r

24 ion of calcium/calmodulin-dependent protein (CaM)kinases blocked activity-induced MeCP2 serine 421 ph

25 Ca(2+)/calmodulin-dependent protein kinase (CaM kinase) blocked increases in P-CREB and c-fos levels

26 CCaMK differs from the animal CaM kinases by its dual ability to bind free calcium, vi

27 Inhibition of Ca(2+)/CaM kinase (CaM-K) slowed the current decay, the rate of

28 A putative CaM kinase (CaMK) cDNA of C. gloeosporioides was cloned

29 tivates the phosphatase calcineurin (Cn) and CaM kinase (CaMK)II.

30 uence significantly similar to those of both CaM kinases (CaMKs) and doublecortin, the product of the

31 ossess high sequence identity with mammalian CaM kinases (CaMKs) I/IV and CaMKKalpha/beta, respective

32 esponses to elevated calcium are mediated by CaM kinases (CaMKs), a family of protein kinases whose a

33 d activates a plethora of enzymes, including CaM kinases (CaMKs).

34 These results demonstrate that the CaM kinase cascade is negatively regulated in cells by t

35 roximately 1 pM, compared with 30 nM for the CaM-kinase complex, indicating that activation of autoin

36 ical for vertebrates) is phosphorylated by a CaM kinase-dependent mechanism.

37 nt 1 bind to the same site on the N-terminal CaM kinase domain of CASK and compete with each other fo

38 We now demonstrate that the N-terminal CaM kinase domain of CASK binds to a novel brain-specifi

39 The CaM kinase domain of CASK binds to Mint 1, and the regio

40 rminal calcium/calmodulin-dependent protein (CaM) kinase domain, central PSD-95, Dlg, and ZO-1/2 doma

41 tion crystal structures reveal that the CASK CaM-kinase domain adopts a constitutively active conform

42 ue MAGUK protein that contains an N-terminal CaM-kinase domain besides the typical MAGUK domains.

43 The CASK CaM-kinase domain is presumed to be a catalytically inac

44 The CASK CaM-kinase domain phosphorylates itself and at least one

45 y activated by KCl requires Ca2+/calmodulin (CaM) kinase for CREB phosphorylation in both neuronal ty

46 Mutants defective in the unc-43/CaM kinase gene showed a defect in SDQR and AVM position

47 ith membrane depolarization, suggesting that CaM kinase has an important role in the pathway leading

48 Both CaM kinase I and CaM kinase IV are able to phosphorylate

49 ection with constitutively active mutants of CaM kinase I or CaM kinase IV specifically blocks nuclea

50 for cAMP-dependent protein kinase (PKA) and CaM Kinase I, and a large central C domain that binds AT

51 report that intracellular infusion of active CaM-kinase I (CaMKI) into cultured hippocampal neurons e

52 kinase (STO-609), the upstream activator of CaM-kinase I (CaMKI), as well as by transfection with do

53 nsiently expressed each of three isoforms of CaM kinase II (alpha, deltaB, and deltaC) along with an

54 Ca(2+)-dependent signaling through CaM Kinase II (CaMKII) and calcineurin was suggested to

55 CaM kinase II (CaMKII) but not CaMKIV, the major nuclear

56 otein kinase A (PKA), MAP kinase (MAPK), and CaM kinase II (CAMKII) in the vicinity of the synapse, a

57 lations indicate that the Ca(v)1.2-activated CaM kinase II (CaMKII) mediates cocaine-induced increase

58 roteins activated by the increase in Ca2+ is CaM kinase II (CaMKII).

59 The effect of PEP-19 on CaM kinase II activation was not attributable to changes

60 The inhibition in CaM kinase II activity and the development of epilepsy w

61 The decrement in CaM kinase II activity associated with low Mg2+ treatmen

62 persistent, post-translational alteration of CaM kinase II activity in a model of epilepsy characteri

63 ncubating cells with only PDGF-AB stimulated CaM kinase II activity in an insulin- and 8-Br-cGMP-inhi

64 The findings of this study demonstrate that CaM kinase II activity is decreased in association with

65 aptosomal membrane fractions were tested for CaM kinase II activity towards endogenous substrates.

66 In addition, the inhibition of CaM kinase II activity was associated in time and region

67 indicating that the long-lasting decrease in CaM kinase II activity was dependent on N-methyl-D-aspar

68 High intracellular Ca2+ ([Ca]i)-stimulated CaM kinase II activity was inhibited by 8-Br-cGMP by an

69 T-3 release depends on extracellular sodium, CaM kinase II activity, and requires intact microtubules

70 ed component of VSMC migration by inhibiting CaM kinase II activity.

71 ion-dependent, Ca(2+)/calmodulin-independent CaM kinase II activity.

72 rylated by brain supernatant and recombinant CaM kinase II alpha-subunit showed that (1) brain supern

73 Expression of deltaB-CaM kinase II also potentiated phenylephrine-mediated AN

74 These results suggest that both CaM kinase II and 3 phosphoinositides mediate betaAR-ind

75 prevented the nuclear localization of deltaB-CaM kinase II and also blocked its effects on ANF report

76 rs of protein phosphatase 2A (PP2A), induced CaM kinase II and IV activity in these cells.

77 treatment results in the activation of both CaM kinase II and IV in Jurkat T lymphocytes.

78 )1.2(I1624E) hearts, the activity of phospho-CaM kinase II and phospho-MAPK was increased.

79 rectly or indirectly involves calmodulin and CaM kinase II and represents a possible mechanism used b

80 o assign a function to the deltaB isoform of CaM kinase II and to link its nuclear localization to su

81 CaM kinase II appears localized on midzone microtubules

82 Mechanistically, CaM kinase II appears to be involved in secretory steps

83 IV specifically blocks nuclear targeting of CaM kinase II as a result of phosphorylation of a Ser im

84 CaM kinase II assembled with alphaKAP retains normal enz

85 cGMP inhibits CaM kinase II at a post-[Ca]i step by a protein phosphat

86 bes of calmodulin and autophosphorylation of CaM kinase II at Thr(286) induces a further decrease in

87 The net decrease in CaM kinase II autophosphorylation and substrate phosphor

88 this work, we characterize the mechanism of CaM kinase II autophosphorylation.

89 spectrometry, and kinetic studies show that CaM kinase II binds to cPLA(2) resulting in cPLA(2) phos

90 Peptide and pharmacologic inhibitors of CaM kinase II blocked the transit into anaphase, both in

91 to the approximate time when calmodulin and CaM kinase II colocalize at several points in the activa

92 n CaM specifically stabilize the trapped CaM-CaM kinase II complex.

93 ophosphorylation rate was independent of the CaM kinase II concentration, results corroborating intra

94 Rat forebrain CaM kinase II consists of heteromers composed of alpha a

95 However, CaM kinase II could be fully activated when calcium infl

96 To directly determine whether CaM kinase II could regulate ANF gene expression, we tra

97 In RBL-2H3 m1 cells, inhibition of CaM kinase II decreased Thr-1940 phosphorylation, and in

98 Conversely, CaM kinase II decreases the rates of dissociation of Ca(

99 CaM kinase II displays a biphasic increase in autonomous

100 Boiled CaM kinase II had no effect.

101 The deltaB isoform of CaM kinase II has been shown to exhibit nuclear localiza

102 embly with other more abundant subunits into CaM kinase II heteromultimers.

103 gene of alpha-CaM kinase II, can target the CaM kinase II holoenzyme to the SR membrane.

104 rylation occurs between subunits within each CaM kinase II holoenzyme.

105 Moreover, the recently discovered ability of CaM kinase II holoenzymes to self-associate has raised q

106 The subunit composition of CaM kinase II holoenzymes was analyzed by immunoprecipit

107 ized into a model describing the assembly of CaM kinase II holoenzymes.

108 alpha (50 kDa) and beta (60 kDa) subunits of CaM kinase II in association with the induction of SRS a

109 man NMHC-IIA was phosphorylated by activated CaM kinase II in HeLa cells, while wild type was not.

110 -resistant cells, consistent with a role for CaM kinase II in mediating the antiproliferative effect

111 Activation of CaM kinase II in norepinephrine-stimulated vascular smoo

112 study demonstrated that PEP-19 can regulate CaM kinase II in situ in a manner that was dependent on

113 d by protein kinase A, protein kinase C, and CaM kinase II in situ.

114 ide evidence that MAP-2 is phosphorylated by CaM kinase II in the pancreatic beta-cell in situ, and t

115 An understanding of the role of CaM kinase II in the pancreatic beta-cell is dependent o

116 tablishes that synapsin I is a substrate for CaM kinase II in the pancreatic beta-cell, this event ap

117 serine 831 is specifically phosphorylated by CaM kinase II in transfected cells expressing GluR1 as w

118 -IIA carboxyl terminus was phosphorylated by CaM kinase II in vitro, while mutation of Thr-1940 to Al

119 oactivator p300, which was phosphorylated by CaM kinase II in vitro.

120 ized and associated with rat skeletal muscle CaM kinase II in vivo.

121 Using a biochemical approach we confirm that CaM kinase II increases in activity 5 min after egg acti

122 e affinity of calmodulin for Ca(2+), whereas CaM kinase II increases the calmodulin affinity for Ca(2

123 The selective CaM kinase II inhibitor KN-93 (1 microM), but not the in

124 sing cells by Ca(2+) was not affected by the CaM kinase II inhibitor KN-93 but was partially attenuat

125 ryanodine, or when calmodulin antagonists or CaM kinase II inhibitors were present.

126 Adipogenesis was blocked effectively by CaM kinase II inhibitors, either KN-62 or KN-93, if the

127 There was no effect of CaM kinase II inhibitors, KN-93 and KN-62, on M1-muscari

128 protein/DNA interaction studies suggest that CaM kinase II inhibits binding of the myogenic factor, m

129 ha-subunit showed that (1) brain supernatant CaM kinase II is mainly responsible for the phosphorylat

130 CaM kinase II is not expressed and p135 SynGAP is expres

131 Thus, a biphasic activation of CaM kinase II is obligate for the progression of the emb

132 h its unique regulatory properties, however, CaM kinase II is predicted to serve in more specialized

133 can co-assemble with catalytically competent CaM kinase II isoforms and target them to the membrane r

134 taM-CaM kinase II, is one of the predominant CaM kinase II isoforms associated with alphaKAP in skele

135 In CaM kinase II isolated from rat forebrain, however, the

136 microtubule-associated protein 2, and alpha-CaM Kinase II leader sequences enhanced translation, whe

137 Therefore, CaM kinase II may represent a previously unappreciated a

138 ions caused us to test whether activation of CaM kinase II mediated the chromosomal transit into an a

139 It is proposed that the activation of CaM kinase II mediates some of the actions of Ca2+ on th

140 chain reaction, we show that alpha- and beta-CaM kinase II mRNAs are simultaneously present in the ma

141 nsfecting VSMCs with a constitutively active CaM kinase II mutant blocked the inhibition by insulin o

142 ations E120A, M124A, and E120A/M124A and the CaM kinase II mutations F293A, F293E, N294A, N294P, and

143 RC3 dampens the effects of CaM kinase II on Ca(2+) dissociation by increasing the r

144 ered, has an IC50 = 50 nM for MLCK, inhibits CaM kinase II only at 4000-fold higher concentrations, a

145 and tautomycin suggest that heparin inhibits CaM kinase II phosphorylation by activating protein phos

146 s indicate that Ser-831 is the major site of CaM kinase II phosphorylation on GluR1.

147 ation of surface AMPA receptors on the major CaM kinase II phosphorylation site.

148 s further show that Phe(293) and Asn(294) in CaM kinase II play dual roles, because they likely desta

149 We measured dissociation kinetics of CaM and CaM kinase II proteins by using a fluorescently modified

150 We conclude that CaM kinase II regulates SK channels in murine coloni myo

151 sgenic mouse overexpressing a mutant form of CaM kinase II selectively in superficial layers of media

152 Experiments with a monomeric CaM kinase II showed that phosphorylation of this constr

153 We have also identified residues in CaM and CaM kinase II that interact in the trapped state by muta

154 The ability of CaM kinase II to autophosphorylate through an intraholoe

155 In particular, the ability of CaM kinase II to remain active after cell stimulation is

156 creased further by the addition of exogenous CaM kinase II to synaptosomal membrane fractions.

157 Application of autothiophosphorlated CaM kinase II to the cytoplasmic surface of excised patc

158 ggestion is supported by the localization of CaM kinase II to the insulin secretory granule and by th

159 The ability of deltaB-CaM kinase II to transactivate a truncated ANF promoter,

160 Once autophosphorylated, beta-CaM kinase II traps calmodulin by reducing the rate of c

161 ugh a voltage-dependent Ca2+ channel and the CaM kinase II UNC-43.

162 entration range shown to activate endogenous CaM kinase II under identical conditions.

163 nt and closely correlated with activation of CaM kinase II under similar experimental conditions.

164 IIA fusion protein was not phosphorylated by CaM kinase II unless Ala-1940 was mutated to Thr.

165 d a stable phenotype that failed to activate CaM kinase II upon depolarization in high K(+).

166 e transferred to the CaM-binding domain from CaM kinase II via a ternary complex.

167 The frequency response of CaM kinase II was modulated by several factors, includin

168 In addition, a chimeric alpha-CaM kinase II which contains the nuclear localization si

169 rall phosphorylation of the delta-subunit of CaM kinase II which is consistent with inhibition of aut

170 f calmodulin by calmidazolium or blockade of CaM kinase II with either KN93 or autocamtide-2-related

171 s in calcium/calmodulin-dependent kinase II (CaM kinase II) activity associated with epileptogenesis.

172 Ca2+/calmodulin-dependent protein kinase II (CaM Kinase II) activity was evaluated in a well-characte

173 t of calmodulin-dependent protein kinase II (CaM kinase II) and synaptic vesicles in the enhanced Ca2

174 Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) are concentrated postsynaptically at glut

175 (2+)/calmodulin-dependent protein kinase II (CaM kinase II) at Thr(286) results in calmodulin (CaM) t

176 (2+)/calmodulin-dependent protein kinase II (CaM kinase II) at Thr-286 generates Ca(2+)-independent a

177 cium/calmodulin-dependent protein kinase II (CaM kinase II) can specifically suppress nAChR promoter

178 Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) in the secretion of insulin from the panc

179 and calmodulin-dependent protein kinase II (CaM kinase II) in vitro showed that the enzyme can decod

180 of driving the spindle (with its associated CaM kinase II) into an anaphase configuration in a perme

181 ts of Ca(2+)/calmodulin-dependent kinase II (CaM kinase II) into holoenzymes is an important structur

182 Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) is present in a membrane-bound form that

183 cium/calmodulin-dependent protein kinase II (CaM kinase II) is tightly associated with the meiotic sp

184 the role of calmodulin-dependent kinase II (CaM kinase II) membrane phosphorylation on GABAA recepto

185 association of calmodulin (colocalized with CaM kinase II) on the meiotic spindle.

186 dulin-dependent enzyme calmodulin kinase II (CaM kinase II) was studied in PC12 cells that had been t

187 (2+)/calmodulin dependent protein kinase II (CaM kinase II) which is abundantly expressed in VSMC.

188 ium-/calmodulin-dependent protein kinase II (CaM kinase II), a decoder of Ca(2+) signals, and cytosol

189 cium/calmodulin-dependent protein kinase II (CaM kinase II), activated by increased intracellular cal

190 Ca2+/calmodulin-dependent protein kinase II (CaM kinase II), as isolated from brain, is a multimeric

191 al Ca2+/calmodulin-dependent protein kinase (CaM kinase II), blocked the induction of these responses

192 Ca2+/calmodulin-dependent protein kinase II (CaM kinase II), which are targeted to the nucleus by an

193 bitor of Ca(2+)/calmodulin-dependent kinase (CaM kinase II).

194 cium/calmodulin-dependent protein kinase II (CaM kinase II).

195 ut probably not Ser262, is phosphorylated by CaM kinase II, (3) no amino acid between Lys395-Ala437 e

196 95-Ala437 except Ser416 is phosphorylated by CaM kinase II, (4) a number of amino acids in the tau mo

197 CaM kinase II, a multifunctional Ca2+/calmodulin-depende

198 e receptor subtype, Ca2+ influx, activity of CaM kinase II, and function of the protein synthesis.

199 Recombinant homomers of alpha- or beta-CaM kinase II, as well as of alternatively spliced beta

200 ependent and can be induced by activation of CaM kinase II, CaM kinase IV, and protein kinase A, but

201 n encoded by a gene within the gene of alpha-CaM kinase II, can target the CaM kinase II holoenzyme t

202 inase A, protein kinase G, rhodopsin kinase, CaM kinase II, casein kinase II, or cyclin-dependent kin

203 variant of beta-CaM kinase II, termed betaM-CaM kinase II, is one of the predominant CaM kinase II i

204 y active mutant of CaM kinase IV, but not of CaM kinase II, leads to activation of the promoter in th

205 A new variant of beta-CaM kinase II, termed betaM-CaM kinase II, is one of the

206 tion (Ser-473) and activation of Akt through CaM kinase II- and 3 phosphoinositides-dependent mechani

207 ng the phosphorylation reactions blocked the CaM kinase II-dependent increase in muscimol binding.

208 ta support the hypothesis that activation of CaM kinase II-dependent phosphorylation caused an increa

209 Activation of endogenous CaM kinase II-dependent phosphorylation resulted in a si

210 cted to either basal (Mg2+ alone) or maximal CaM kinase II-dependent phosphorylation.

211 CaM kinase II-dependent substrate phosphorylation and au

212 eased phosphorylation of sites identified as CaM kinase II-specific and distinct from protein kinase

213 affinity complex between CaM and full-length CaM kinase II.

214 c or glutamatergic and can sometimes express CaM kinase II.

215 the first demonstrated anchoring protein for CaM kinase II.

216 hich are primarily glutamatergic and contain CaM kinase II.

217 ssion, albeit to a lesser extent than deltaB-CaM kinase II.

218 calmodulin are also mildly phosphorylated by CaM kinase II.

219 of a Ser immediately adjacent to the NLS of CaM kinase II.

220 t increase in staining for nonphosphorylated CaM kinase II.

221 This effect is not seen with phosphorylated CaM kinase II.

222 l lobe of calmodulin when in the presence of CaM kinase II.

223 ion of calcium/calmodulin-dependent protein (CaM) kinase II activity by monoclonal antibody 24.3.1 an

224 s studies have demonstrated that calmodulin (CaM) kinase II can phosphorylate and modulate AMPA recep

225 lts in a mobilization of calcium/calmodulin (CaM) kinase II to synapses and an increase in the phosph

226 Inhibition of calmodulin (CaM) kinase II with KN-62, or inclusion of the CaM inhib

227 has generally been assumed to be mediated by CaM-kinase II (CaMKII), although other members of the Ca

228 KN93, a CaM-kinase II inhibitor, had no effect on NaV1.4, sugges

229 usible model in which autophosphorylation of CaM-kinase II leads to a conformational change in the re

230 iation, and the overall Kd of CaM binding to CaM-kinase II was determined using an overlapping peptid

231 ides modeled after the CaM binding domain of CaM-kinase II were previously shown to kinetically resem

232 almodulin (CaM)-dependent protein kinase II (CaM-kinase II) induces a striking >1,000-fold increase i

233 (2+)-calmodulin-dependent protein kinase II (CaM-kinase II) is a ubiquitous Ser/Thr-directed protein

234 ion of Ca2+/CaM-dependent protein kinase II (CaM-kinase II) with 2 microM KN-62.

235 ted K+ channel, and in unc-43, which encodes CaM-kinase II, and a gain-of-function mutation in egl-30

236 Strikingly, chronic inhibition of NMDARs or CaM-Kinase II, which signals downstream of NMDARs, suppr

237 d by a signaling cascade composed of CaM and CaM-kinase II.

238 of the CaM mutants altered Ca/CaM binding to CaM-kinase II.

239 ctly on NaV1.4 and not through activation of CaM-kinase II.

240 phorylated and inhibited by the eEF2 kinase (CaM kinase III); the latter is inhibited by the S6K or R

241 I (CaMKII) but not CaMKIV, the major nuclear CaM kinase in hippocampal neurons, appeared to mediate t

242 st BAY K 8644 (300 nmol/kg), suggesting that CaM kinase-independent activation of L-type Ca(2+) curre

243 on after depolarization; the addition of the CaM kinase inhibitor KN-62 reduced the proportion of CGR

244 increase in GluA1, as did treatment with the CaM kinase inhibitor KN-93, but not the inactive analog

245 odulin antagonists W-7 and calmidazolium and CaM kinase inhibitor KN-93.

246 r BAPTA-AM or the Ca2+/calmodulin-dependent (CaM) kinase inhibitor KN93 blocked reporter gene activat

247 ptide inhibitor of CaMKII and by the general CaM-kinase inhibitor KN-93.

248 on in neurons; this was also attenuated by a CaM-kinase inhibitor.

249 CaM kinase inhibitors attenuated phosphorylation at Ser3

250 tor antagonist APV, intracellular BAPTA, the CaM kinase inhibitors KN-62 and autocamtide-2-related in

251 -dependent dendritic growth is suppressed by CaM kinase inhibitors, a constitutively active form of C

252 st W-7 and the calcium/calmodulin-dependent (CaM) kinase inhibitors KN-93 and K252a, can block oxidat

253 Two different CaM kinase inhibitory peptides (n=16) and a CaM inhibito

254 synapse, and activation of transcription by CaM kinase IV (CAMKIV) and MAPK.

255 ible for persistent CREB phosphorylation and CaM kinase IV (CaMKIV) responsible for phosphorylating t

256 ivation of Ca(2+)/CaM kinase kinase beta and CaM kinase IV (CaMKIV).

257 CaM kinase IV activates the transcription factor CREB, a

258 These mechanisms, which implicate CaM kinase IV and CREB in the control of BDNF expression

259 We report that CaM kinase IV and CREB play a critical role in mediating

260 n of a transcriptional program that involves CaM kinase IV and CREB-mediated signaling to the nucleus

261 Both CaM kinase I and CaM kinase IV are able to phosphorylate this Ser residue

262 inhibitors, a constitutively active form of CaM kinase IV induces dendritic growth in the absence of

263 The effects of CaM kinase IV on the promoter require an intact CRE.

264 Neuronal depolarization and CaM kinase IV signaling alter the splicing of multiple e

265 titutively active mutants of CaM kinase I or CaM kinase IV specifically blocks nuclear targeting of C

266 lular stimulation, and a kinase-dead form of CaM kinase IV suppresses dendritic growth induced by cal

267 n be induced by activation of CaM kinase II, CaM kinase IV, and protein kinase A, but not by activati

268 A constitutively active mutant of CaM kinase IV, but not of CaM kinase II, leads to activa

269 esults in the calcium-mediated activation of CaM kinase IV, phosphorylation of CREB, increased expres

270 nt negative form of CREB blocks calcium- and CaM kinase IV-induced dendritic growth.

271 ng via calcium/calmodulin-dependent protein (CaM) kinase IV and microtubule-associated protein (MAP)

272 tion and activation of CaM-KI and CaM-KIV by CaM kinase kinase (CaM-KK), regulates transcription thro

273 The CaM kinase kinase alpha (CaMKKalpha) isoform is an upstr

274 s leads to activation of a pathway involving CaM kinase kinase and CaM kinase 4 that induces synaptic

275 on, inhibition of the SOCE downstream target CaM kinase kinase beta (CaMKKbeta) or knockdown of AMPKa

276 pendent on constitutive activation of Ca(2+)/CaM kinase kinase beta and CaM kinase IV (CaMKIV).

277 s signaling through L-type calcium channels, CaM kinase kinase, and the GluA2 AMPA receptor subunit,

278 d by pharmacological inhibition (STO-609) of CaM kinase kinase, the upstream activator of CaMKI.

279 , the activation loop site for regulation by CaM kinase kinase.

280 nent of TBS LTP was blocked by inhibition of CaM-kinase kinase (CaMKK), the upstream activator of CaM

281 nhibitors of NMDA receptors (NMDARs; APV) or CaM-kinase kinase (STO-609), the upstream activator of C

282 c marker Rab7 in axons that highly expressed CAM-kinase-kinase (CAMKK), an upstream activator of CaMK

283 looxygenase (COX)-2, CyclinD1, double cortin CAM kinase-like 1 (DCAMKL+1), and CD44, compared with HE

284 lude enhanced expression of doublecortin and CaM kinase-like-1 (DCAMKL-1), Lgr5, CD133, alpha-fetopro

285 s in progenitors expressing doublecortin and CaM kinase-like-1 (DCAMKL1), stem cells expressing leuci

286 ized in the isthmus adjacent to doublecortin CaM kinase-like-1(+) putative progenitor cells.

287 that resembled that of unc-2 mutants; thus, CaM kinase may function as an effector of the UNC-2-medi

288 a mechanism involving the nuclear Ca(2+) and CaM kinase-mediated induction of Npas4, resulting in the

289 These results identify PPM1F as a CaM kinase phosphatase within fibroblasts, although it m

290 However, the sites of CaM kinase phosphorylation have not been unequivocally i

291 These results identify the site of CaM kinase phosphorylation of the GluR1 subunit and demo

292 ults are consistent with the hypothesis that CaM kinase plays a role in arrhythmias related to increa

293 nase IV (CaMKIV) activation, through special CaM kinase responsive RNA elements.

294 cing changes are mediated in part by special CaM kinase-responsive RNA elements, within or adjacent t

295 Our results show that CaM kinase sites control vesicle mobilization at low sti

296 These data indicate a role for CaM kinase stimulation and resultant threonine phosphory

297 ntly phosphorylated autocamtide-2, a classic CaM kinase substrate, which could be blocked by calmodul

298 ures inhibited PMA-induced activation of the CaM kinases, suggesting that similar to hydrogen peroxid

299 to hydrogen peroxide, PMA also activates the CaM kinases via the production of ROI.

300 he hypothesis that inhibition of calmodulin (CaM) kinase would prevent Iti.