ライフサイエンスコーパス: CaM kinase II

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

2 CaM kinase II appears localized on midzone microtubules

3 CaM kinase II assembled with alphaKAP retains normal enz

4 CaM kinase II displays a biphasic increase in autonomous

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

6 CaM kinase II subunits containing the 38-amino acid inse

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

8 CaM kinase II-dependent substrate phosphorylation and au

9 of myosin light chain kinase (RS-20, M-13), CaM kinase II, and the myristoylated alanine-rich protei

10 Transient expression of wild-type delta 2 CaM kinase II in COS-7 cells resulted in increased ERK2

11 y pretreating cells with 30 mumol/L KN-93, a CaM kinase II inhibitor.

12 Site-directed mutagenesis of a CaM kinase II consensus site (Ser-1076 to Ala-1076) in I

13 n was also inhibited in cells treated with a CaM kinase II inhibitor, KN-93, or with CaM kinase II an

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

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

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

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

18 In addition, constitutively activated CaM kinase II inhibits the enzyme.

19 [Ca2+]i over a physiological range activates CaM kinase II in VSM and that this process is facilitate

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

21 ition, no change in the mRNA levels of alpha CaM kinase II was seen.

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

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

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

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

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

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

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

29 RS-20 produced a 9-fold and CaM kinase II a 6.3-fold increase in C-terminal Ca2+ aff

30 Phosphorylation of MAP kinase and CaM kinase II by NE, studied by 32P incorporation and im

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

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

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

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

35 tu Ca2+ dependence for generating autonomous CaM kinase II was determined in cells selectively permea

36 tion and consequent generation of autonomous CaM kinase II activity.

37 fter tetanic stimulation, autophosphorylated CaM kinase II (P-CaMKII) is significantly increased in a

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

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

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

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

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

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

44 Boiled CaM kinase II had no effect.

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

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

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

48 e to direct phosphorylation of the enzyme by CaM kinase II in vivo.

49 zyme stimulated by CaM, was not inhibited by CaM kinase II or IV.

50 ovel pathway for activation of MAP kinase by CaM kinase II appears to be mediated through stimulation

51 mponent of ERK1/2 activation was mediated by CaM kinase II.

52 ways in VSM cells may be mediated in part by CaM kinase II-dependent activation of ERK1/2.

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

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

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

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

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

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

59 95-Ala437 except Ser416 is phosphorylated by CaM kinase II, (4) a number of amino acids in the tau mo

60 calmodulin are also mildly phosphorylated by CaM kinase II.

61 kingly similar to that generated in vitro by CaM kinase II, most notably with regard to the increased

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

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

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

65 hich are primarily glutamatergic and contain CaM kinase II.

66 In contrast, CaM kinase II was unable to activate either ATF1 or CREB

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

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

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

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

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

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

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

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

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

76 NE (10 microM) enhanced CaM kinase II and MAP kinase activity.

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

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

79 the first demonstrated anchoring protein for CaM kinase II.

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

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

82 ower than that of other known substrates for CaM kinase II, suggesting that the receptor is a high af

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

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

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

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

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

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

89 almodulin (CaM)-dependent protein kinase II (CaM kinase II) and development of the Ca2+/CaM-independe

90 Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) and mitogen-activated protein kinase (MAP

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

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

93 (2+)/calmodulin-dependent protein kinase II (CaM kinase II) at Thr(286) results in calmodulin (CaM) t

94 (2+)/calmodulin-dependent protein kinase II (CaM kinase II) at Thr-286 generates Ca(2+)-independent a

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

96 Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) gamma-subunits were cloned from a porcine

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

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

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

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

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

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

103 Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) sites without affecting synapsin I levels

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

105 (2+)/calmodulin dependent protein kinase II (CaM kinase II) which is abundantly expressed in VSMC.

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

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

108 Ca2+/calmodulin-dependent protein kinase II (CaM kinase II), an abundant protein kinase located at po

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

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

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

112 Ca2+/calmodulin-dependent protein kinase II (CaM kinase II); thus, it was postulated that the Ca(2+)-

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

114 (2+)-calmodulin-dependent protein kinase II (CaM-kinase II) is a ubiquitous Ser/Thr-directed protein

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

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

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

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

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

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

121 des did not alter the NE-induced increase in CaM kinase II activity.

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

123 omoting extracellular Ca2+ influx, increases CaM kinase II activity, leading to activation of MAP kin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 xpressed in COS cells resulted in multimeric CaM kinase II holoenzymes (470 kDa) with activation and

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

142 t increase in staining for nonphosphorylated CaM kinase II.

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

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

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

146 ous reflecting nearly complete activation of CaM kinase II and a Hill slope of 3, indicating a highly

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

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

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

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

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

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

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

154 also inhibit the CaM-mediated activation of CaM kinase II.

155 OH-terminal variable region in activation of CaM kinase II.

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

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

158 mate state of phosphorylation of an array of CaM kinase II molecules could be sensitive to the tempor

159 te that such a mechanism may allow arrays of CaM kinase II molecules in postsynaptic densities to act

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

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

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

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

164 ion in the conserved "association" domain of CaM kinase II subunits.

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

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

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

168 Equally effective, however, is inhibition of CaM kinase II activity at 24-48 h after induction, durin

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

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

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

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

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

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

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

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

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

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

179 Two temporally-distinct phases of CaM kinase II activation, either 6 to 12 h or 24 to 48 h

180 This correlated with 32P phosphorylation of CaM kinase II delta-subunits in situ and was abolished b

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

182 A model for the regulation of CaM kinase II is presented based on the following report

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

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

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

186 ntary to the translation initiation sites of CaM kinase II and MAP kinase, NE-induced AA release was

187 One of the best substrates of CaM kinase II in vitro that could function in secretory

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

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

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

191 tors with NE in VSMC caused translocation of CaM kinase II, MAP kinase, and cPLA2 to the nuclear enve

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

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

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

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

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

197 )1.2(I1624E) hearts, the activity of phospho-CaM kinase II and phospho-MAPK was increased.

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

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

200 orylation, and specifically that presynaptic CaM kinase II activity and synapsin I phosphorylation ma

201 to mobilize intracellular Ca2+ but prevented CaM kinase II and ERK1/2 activation with almost identica

202 crude parietal cell homogenate and purified CaM kinase II in a calcium/calmodulin-dependent manner.

203 ed by Western analysis of partially purified CaM kinase II from carotid arterial smooth muscle and br

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

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

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

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

208 g in identification of alternatively spliced CaM kinase II gammaB- and gammaC-subunits and a novel ga

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

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

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

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

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

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

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

216 Collectively, these data suggest that CaM kinase II can activate MAP kinase, which in turn act

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

218 These data suggest that CaM kinase II regulates the activity of III-AC by direct

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

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

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

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

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

224 amino-5-phosphonopentanoic acid (APV) or the CaM kinase II inhibitor KN-62.

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

226 u and was abolished by pretreatment with the CaM kinase II inhibitor KN-93.

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

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

229 9,000 (LIN-2A) with regions of similarity to CaM kinase II and membrane-associated guanylate kinases.

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

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

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

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

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

235 the NR2B subunit and phosphorylated it with CaM kinase II in vitro.

236 th a CaM kinase II inhibitor, KN-93, or with CaM kinase II antisense oligonucleotide.