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1 orphogenic processes is CaMK-II, a conserved calmodulin-dependent protein kinase.
2 uptake; one of them encoded CaMK4, a calcium/calmodulin-dependent protein kinase.
3 crease its activity in BTICs, whereas Ca(2+)-calmodulin-dependent protein kinase 2 (CAMK2) inhibited
4 (Ede1) that can function upstream of Ca(2+)/calmodulin-dependent protein kinase 2 (Cmk2) to suppress
5 hanistically, CaMKK2 signals through Ca(2+) /calmodulin-dependent protein kinase 4 (CaMKIV) to contro
7 d dysregulation of Na and Ca handling and Ca/calmodulin-dependent protein kinase and are especially p
8 ined increase in cytosolic Ca(2+), activated calmodulin-dependent protein kinase and the calpain-casp
9 r new protein synthesis and required calcium/calmodulin-dependent protein kinases and the nuclear cal
10 resulting in c-Jun N-terminal kinase, Ca(2+)/calmodulin-dependent protein kinase, and cyclic adenosin
11 by NMDA receptor activation, requires Ca2+ /calmodulin-dependent protein kinase, and is mediated by
12 cannabinoid type 1 (CB1) receptor and Ca(2+)/calmodulin-dependent protein kinase beta, activates AMP-
13 olerance, as did mutants in the gene calcium/calmodulin-dependent protein kinase (caki), encoding the
15 Psi Here, we characterize a role for calcium/calmodulin-dependent protein kinase (CaMK) I in the regu
16 f D-myo-inositol 1,4,5-trisphosphate/Ca(2+) /calmodulin-dependent protein kinase (CaMK) I. gamma-Amin
17 II could also induce the phosphorylation of calmodulin-dependent protein kinase (CaMK) II and cAMP r
18 ostretrieval bilateral inhibition of calcium/calmodulin-dependent protein kinase (CaMK) II in dorsal
19 +)-dependent binding of S100B to the calcium/calmodulin-dependent protein kinase (CaMK)-type domain o
20 2 model of Huntington disease and the Ca(2+)/calmodulin-dependent protein kinase (CaMK)/p25 double-tr
21 wn that the cytoplasmically oriented calcium/calmodulin-dependent protein kinase (CaMK)Ialpha regulat
22 gnaling in the inner ear is the type II Ca2+/calmodulin-dependent protein kinase (CaMK-II), which is
23 ore than 20 years, we have known that Ca(2+)/calmodulin-dependent protein kinase (CaMKII) activation
24 and the ensuing activation of the Ca(2+) and calmodulin-dependent protein kinase (CaMKII) are require
27 lation of RyR2 phosphorylation at the Ca(2+)/calmodulin-dependent protein kinase (CaMKII) site (S2814
29 prevent the arrhythmias induced by a Ca(2+) -calmodulin-dependent protein kinase (CaMKII)-dependent l
34 plex dephosphorylates and inactivates Ca2(+)/calmodulin-dependent protein kinase I (CaMKI), an upstre
39 sphorylation sites in Cx36 and evidence that calmodulin dependent protein kinase II (CaMKII) may pote
41 er brain regions, using Thy1-Cre and calcium/calmodulin dependent protein kinase II alpha-Cre for abl
42 is critically regulated by the alpha-calcium/calmodulin-dependent protein kinase II (alpha-CaMKII), a
43 , a model of memory formation, requires Ca2+.calmodulin-dependent protein kinase II (alphaCaMKII) act
47 sion of glutamate receptor 2 and beta Ca(2+)/calmodulin-dependent protein kinase II (betaCaMKII).
48 a marker for cholinergic terminals; calcium/calmodulin-dependent protein kinase II (CaMK) was used a
50 e Cl(-) currents can be attributed to Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activati
51 stically, this effect was mediated by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activati
52 calmodulin, but was not dependent on calcium/calmodulin-dependent protein kinase II (CaMKII) activati
53 tate (NMDA) receptor activation, and Calcium/calmodulin-dependent protein kinase II (CaMKII) activati
55 ctivity in mutant cultures was lower, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activity
56 tamine exposure transiently increases Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) alpha ex
57 y (SOCE) and sequential activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and Ca(2
59 reduced activation of PLCgamma-alpha-calcium/calmodulin-dependent protein kinase II (CaMKII) and PI3K
62 kinase signaling pathways, including Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and prot
63 phorylated at serine 409 (Ser-409) by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and prot
64 hibitory peptide (mAIP) selective for Ca2+ / calmodulin-dependent protein kinase II (CaMKII) and U012
65 cription factor DeltaFosB and protein kinase calmodulin-dependent protein kinase II (CaMKII) are co-r
67 d the contribution of multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) as a med
72 e classic regulators of this current, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) but not
73 ulation; (5) inhibiting either PKA or Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) during b
74 imulation; (5) inhibiting either PKA or Ca2+/calmodulin-dependent protein kinase II (CaMKII) during b
75 lum (SR) Ca(2+) release that involves Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) effects
76 activation of the multifunctional Ca(2+) and calmodulin-dependent protein kinase II (CaMKII) favors m
82 o signal neuronal cells and activate calcium calmodulin-dependent protein kinase II (CaMKII) in neuro
83 ctly associates with and targets the calcium/calmodulin-dependent protein kinase II (CaMKII) in pancr
84 iew, the functions of multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in VSM p
92 e heart; however, the multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is also
96 Here we show that the activity of calcium/calmodulin-dependent protein kinase II (CaMKII) is incre
97 w that Ca(2+)-dependent activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is requi
99 Considerable evidence suggests that calcium/calmodulin-dependent protein kinase II (CaMKII) overacti
101 nhanced [(3) H]ryanodine binding and Ca(2+) /calmodulin-dependent protein kinase II (CaMKII) phosphor
102 ated Ca(2+) channels (VGCCs) leads to Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) phosphor
106 nel activity reduced EGF receptor (EGFR) and calmodulin-dependent protein kinase II (CAMKII) signalin
107 is downstream of Dalpha7 nAChRs and Calcium/calmodulin-dependent protein kinase II (CaMKII) signalin
109 treated wild-type C57BL/6 mice with calcium/calmodulin-dependent protein kinase II (CaMKII) specific
112 esulted in compromised signaling from Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) to myosi
113 which in turn requires binding of the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) to the N
114 protein GW182 increases expression of a Ca2+/calmodulin-dependent protein kinase II (CaMKII) translat
117 nificantly increased the activity of calcium/calmodulin-dependent protein kinase II (CaMKII) while re
118 ought to determine how activation of calcium/calmodulin-dependent protein kinase II (CaMKII), a centr
119 CaMK2N2 are endogenous inhibitors of calcium/calmodulin-dependent protein kinase II (CaMKII), a key s
120 reduces FRET between the NMDARcd and calcium/calmodulin-dependent protein kinase II (CaMKII), a proce
121 following: 1) that autophosphorylated Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), an impo
122 triggers the exchange of subunits in Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), an olig
123 embranes, synGAP is phosphorylated by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), another
124 ono pentanoic acid; the inhibitor of calcium/calmodulin-dependent protein kinase II (CaMKII), autocam
125 ed its effects on phosphorylation of calcium/calmodulin-dependent protein kinase II (CaMKII), extrace
126 vented by pharmacological blockade of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), it was
127 tream effector of WNT/Ca(2+) pathway, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), led to
128 athway is a kinase cascade involving calcium/calmodulin-dependent protein kinase II (CaMKII), p38alph
129 tors of transient spine expansion, including calmodulin-dependent protein kinase II (CaMKII), RhoA, a
130 d Ang II activate the multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), the inh
131 scular smooth muscle (VSM) expresses calcium/calmodulin-dependent protein kinase II (CaMKII)-delta an
132 ators of myocardial excitability, and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)-dependen
133 lism regulates oocyte cell death via calcium/calmodulin-dependent protein kinase II (CaMKII)-mediated
134 Although many studies have focused on Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)-mediated
135 he hypotheses that (1) inhibition of Ca(2+) /calmodulin-dependent protein kinase II (CAMKII)-mediated
136 o the model reveal that inclusion of Ca(2+) /calmodulin-dependent protein kinase II (CAMKII)-mediated
149 tor DeltaFosB and the brain-enriched calcium/calmodulin-dependent protein kinase II (CaMKIIalpha) are
151 ites by protein kinase A (Ser-7) and calcium-calmodulin-dependent protein kinase II (Ser-13) and at m
153 id) receptor activation, calcium and calcium/calmodulin-dependent protein kinase II activity, but not
154 increase in oxidation-dependent calcium and calmodulin-dependent protein kinase II activity, which c
156 bunit, Rpt6, by the plasticity kinase Ca(2+)/calmodulin-dependent protein kinase II alpha (CaMKIIalph
157 entanyl decreased the activity of the Ca(2+)/calmodulin-dependent protein kinase II alpha (CaMKIIalph
158 Alcohol-sensitive proteins included calcium/calmodulin-dependent protein kinase II alpha (CaMKIIalph
160 ling molecules, calcineurin, Ras, and Ca(2+)/calmodulin-dependent protein kinase II and implicates Ca
161 itive deficits via altered levels of calcium/calmodulin-dependent protein kinase II and N-methyl-D-as
162 ociated with reduced levels of total calcium/calmodulin-dependent protein kinase II and N-methyl-D-as
163 lated to higher activation of nuclear Ca(2+)/calmodulin-dependent protein kinase II and nuclear expor
164 o be independent of their effects on calcium/calmodulin-dependent protein kinase II and PKA, respecti
165 rrhythmic manifestations, related to Ca(2+) /calmodulin-dependent protein kinase II and ryanodine rec
166 it that mediates dephosphorylation of Ca(2+)/calmodulin-dependent protein kinase II and tyrosine hydr
167 es and Thr-287 autophosphorylation of Ca(2+)/calmodulin-dependent protein kinase II beta (CaMKIIbeta)
168 However, double knockdown of pygo and Ca2+/calmodulin-dependent protein kinase II caused additional
169 , inhibitors, and a dominant negative Ca(2+)/calmodulin-dependent protein kinase II construct block A
171 nt and function, including Titin and calcium/calmodulin-dependent protein kinase II delta (Camk2d).
173 he mechanical effects of the kinases calcium/calmodulin-dependent protein kinase II delta (CaMKIIdelt
174 myocytes from arrhythmia-susceptible calcium calmodulin-dependent protein kinase II delta C (CaMKIIde
176 the LTP kinase dependency from PKA to Ca2(+)/calmodulin-dependent protein kinase II during synapse ma
180 A null mutation of the Drosophila calcium/calmodulin-dependent protein kinase II gene (CaMKII) was
181 hereas inhibiting protein kinase A or Ca(2+)/calmodulin-dependent protein kinase II had no effect.
182 ion and subsequent activation of calcium and calmodulin-dependent protein kinase II has a causal role
183 eam signaling protein, PKC-alpha, and Ca(2+)/calmodulin-dependent protein kinase II in endothelial ce
184 2B, also referred to as Pyk2) and of calcium/calmodulin-dependent protein kinase II in wild-type brai
185 rolled firing rate adaptation whereas Ca(2+)/Calmodulin-dependent protein kinase II induced a delayed
186 ia inhibition of ryanodine receptors, Ca(2+)/calmodulin-dependent protein kinase II inhibition, or by
188 Development of organ-specific calcium and calmodulin-dependent protein kinase II inhibitors may re
189 ignal-regulated kinase activators and Ca(2+)/calmodulin-dependent protein kinase II inhibitors showed
191 rom transgenic mice expressing a calcium and calmodulin-dependent protein kinase II inhibitory peptid
194 es including JNK, GSK3alpha/beta, and Ca(2+)/calmodulin-dependent protein kinase II is increased sign
197 on synapsin I, two of which are known Ca(2+)/calmodulin-dependent protein kinase II phosphorylation s
199 ignaling kinases protein kinase C and Ca(2+)/Calmodulin-dependent protein kinase II to AngII-mediated
201 as phosphorylation of substrates for calcium/calmodulin-dependent protein kinase II was unchanged.
203 Pharmacologic inhibition of calcium and calmodulin-dependent protein kinase II with 2.5 microM o
204 nd is accompanied by altered CaMKII (calcium/calmodulin-dependent protein kinase II) and flotillin-1
205 4) is the failure to activate CaMKII (Ca(2+)/calmodulin-dependent protein kinase II) and retinal dege
206 stabilization of postsynaptic CaMKII (Ca(2+)/calmodulin-dependent protein kinase II) at inhibitory sy
207 1 pathway, phospho-alphaCaMKII (alpha Ca2(+)/calmodulin-dependent protein kinase II) level in the hip
208 mitochondrial recruitment of CaMKII (Ca(2+)/calmodulin-dependent protein kinase II), which decreases
209 phosphorylation at Ser16 and CaMKII (Ca(2+)/calmodulin-dependent protein kinase II)-dependent phosph
211 ng protein, but not the activation of Ca(2+)/calmodulin-dependent protein kinase II, Akt or mitogen-a
212 mitogen-activated protein kinase, and Ca(2+)/calmodulin-dependent protein kinase II, and activators o
213 in cAMP, light-induced activation of Ca(2+) /calmodulin-dependent protein kinase II, and dopamine-ind
214 ellular protein mediators Homer1b/c, calcium/calmodulin-dependent protein kinase II, and the Alzheime
215 c activation of protein kinase A and calcium/calmodulin-dependent protein kinase II, as well as synap
216 a(2+) must first mobilize actin-bound Ca(2+)/calmodulin-dependent protein kinase II, freeing it for s
217 ng postsynaptic density-95 and alpha-calcium/calmodulin-dependent protein kinase II, normally elicite
218 glutamate-mediated Ca(2+) signaling (Ca(2+)/calmodulin-dependent protein kinase II, PPP3CA, and VISL
220 th cAMP-dependent protein kinase and calcium/calmodulin-dependent protein kinase II, whereas Ca(V)1.1
221 turn, led to the phosphorylation of calcium/calmodulin-dependent protein kinase II, which promoted b
222 ice using the CaMKIIalpha-Cre (alpha-calcium/calmodulin-dependent protein kinase II-Cre) system to KD
223 2 expression can be upregulated in a calcium/calmodulin-dependent protein kinase II-dependent manner
224 at have the ryanodine receptor 2 calcium and calmodulin-dependent protein kinase II-dependent phospho
226 used 1 Hz optogenetic stimulation of calcium/calmodulin-dependent protein kinase II-positive principa
233 FTO interacts with three isoforms of calcium/calmodulin-dependent protein kinase II: alpha, beta and
234 icity, but was absent in adult alpha-calcium/calmodulin-dependent protein kinase II;T286A (alphaCaMKI
236 pines, (3) required activation of the Ca(2+)/calmodulin-dependent protein-kinase II, (4) was restrict
239 A protein with similarities to the Ca(2+)/ calmodulin dependent protein kinase II_association domai
240 AT-C24 DAT) and thereby contained the Ca(2+)-calmodulin-dependent protein kinase IIalpha (CaMKIIalpha
241 a synapse-enriched protein kinase, Ca(2)(+)/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha
242 (Arch)-mediated optical silencing of calcium/calmodulin-dependent protein kinase IIalpha (CAMKIIalpha
243 is study, we investigated the role of Ca(2+)/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha
244 e densin C-terminal domain can target Ca(2+)/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha
245 lpha knock-out mice (BalphaKO) using calcium/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha
247 ceptors, p600 associates with the calmodulin.calmodulin-dependent protein kinase IIalpha complex.
248 eract with iPLA(2)beta, including the Ca(2+)/calmodulin-dependent protein kinase IIbeta, and we have
249 d cardiomyocyte apoptosis, fibrosis, calcium/calmodulin-dependent protein kinase IIdelta phosphorylat
250 as a direct inhibitor of CaMKIIdelta (Ca(2+)/calmodulin-dependent protein kinase IIdelta) activity, a
251 se II inhibitor KN93, suggesting that Ca(2+)/calmodulin-dependent protein kinase IIdelta, a target of
252 n vascular smooth muscle (VSM) cells, Ca(2+)/calmodulin-dependent protein kinase IIdelta2 (CaMKIIdelt
253 by inflammatory signals that induce calcium/calmodulin-dependent protein kinase IIgamma (CaMKIIgamma
254 he mechanistic role of the family of calcium/calmodulin-dependent protein kinases in mediating these
256 Here, we present evidence that the calcium/calmodulin-dependent protein kinase IV (CaMK4) is increa
258 sponse to membrane depolarization and Ca(2+)/calmodulin-dependent protein kinase IV (CaMKIV) activati
259 ive oxygen species (ROS) production, calcium/calmodulin-dependent protein kinase IV (CaMKIV) activati
262 describe a novel mechanism in which calcium/calmodulin-dependent protein kinase IV (CaMKIV), through
264 almodulin-dependent protein kinase I, Ca(2+)/calmodulin-dependent protein kinase IV, and the AMP-depe
265 KN93, a small-molecule inhibitor of calcium/calmodulin-dependent protein kinase IV, targeted to CD4(
266 is regulated by the classical nuclear Ca(2+)/calmodulin-dependent protein kinase IV-CREB/CREB-binding
268 he mitotic spindle is dependent upon calcium/calmodulin-dependent protein kinase kinase (CamKK) activ
269 ersely, the DOR effect was reduced by Ca(2+)/calmodulin-dependent protein kinase kinase (CaMKK) inhib
270 alian target of rapamycin (mTOR) via calcium calmodulin-dependent protein kinase kinase (CaMKK).
271 re, we report that the expression of Ca(2+) /calmodulin-dependent protein kinase kinase 2 (CaMKK2) is
272 ally reduced by the application of a calcium/calmodulin-dependent protein kinase kinase 2 inhibitor (
273 istic target of rapamycin complex 1, calcium/calmodulin-dependent protein kinase kinase 2, and protei
276 e expression of constitutively active Ca(2+)/calmodulin-dependent protein kinase kinase alpha (caCaMK
278 PK kinases liver kinase B1 (LKB1) and Ca(2+)/calmodulin-dependent protein kinase kinase beta (CaMKKbe
279 AMPK activation by aa is mediated by Ca(2+)/calmodulin-dependent protein kinase kinase beta (CaMKKbe
282 events were blocked by inhibition of Ca(2+)/calmodulin-dependent protein kinase kinase beta, an upst
284 altered calcium signaling, transduced by the calmodulin-dependent protein kinase kinase cascade, medi
287 y AMPA-type glutamate receptors and required calmodulin-dependent protein kinase-mediated phosphoryla
288 ngation factor 2 kinase (eEF2K), an atypical calmodulin-dependent protein kinase, phosphorylates and
289 or somatostatin-positive interneurons and of calmodulin-dependent, protein kinase-positive, principal
291 alcineurin, Akt/protein kinase B, and Ca(2+)/calmodulin-dependent protein kinase signaling pathways i
292 O)-1, glutathione reductase (GSR)-1, calcium/calmodulin-dependent protein kinase type (CAMK)-IV, cAMP
294 ger, phospholamban, calcineurin, and calcium/calmodulin-dependent protein kinase type II (CaMKII) wer
295 -bisphosphate binding, protein kinase C- and calmodulin-dependent protein kinase type II phosphorylat
296 to remodeling pathways (e.g., Akt and Ca(2+)/calmodulin-dependent protein kinase type II) and develop
298 SLE T cells express high levels of calcium/calmodulin-dependent protein kinase type IV (CaMKIV), wh
300 ion approaches, we demonstrated that calcium/calmodulin-dependent protein kinase type IV, which contr
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