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1 in MC pretreated with inhibitors of calcium calmodulin kinase.
2 d in part by increases in cell [Ca2+] and Ca-calmodulin kinase.
3 tivation of protein kinase C but not calcium calmodulin kinase.
5 tinocyte cultures with KN93, an inhibitor of calmodulin kinase 2, known to phosphorylate Ser-325 in C
6 bited more than 100-fold selectivity against calmodulin kinase 2; casein kinase-1 and -2; CDK1 and -4
9 tained reduction of intracellular Ca(2+) and calmodulin kinase activity, ranolazine prevented the dev
10 nstrate an important role for the calmodulin/calmodulin kinase and cAMP/protein kinase A pathways in
12 avium, activate Ca(2+)-dependent calmodulin/calmodulin kinase and MAPK pathways in murine macrophage
13 anner that is dependent on Ca(2+) and Ca(2+)/calmodulin kinases and independent of ERKs, p38 MAPK, an
15 38 and p42/44 MAP kinases, protein kinase C, calmodulin kinase, and tyrosine kinase, showing that HGF
16 evation of [Ca2+]i and activation of calcium calmodulin kinases are upstream mediators of ET-1-induce
20 MKIV) is the nuclear effector of the Ca(2+) /calmodulin kinase (CaMK) pathway where it coordinates tr
21 2c receptor on VMH neurons, serotonin uses a calmodulin kinase (CaMK)-dependent signaling cascade inv
25 ermine the role of PPT intracellular calcium/calmodulin kinase (CaMKII) signaling in the regulation o
26 exhibit attenuated calcium release, reduced calmodulin kinase (CaMKII) signaling, and impaired muscl
28 t, trifluoperazine, an antagonist of calcium/calmodulin kinases, completely blocked H(2)O(2)-induced
29 ependence, and is clearly different from the calmodulin kinase-dependent mechanism by which AngII mod
30 omologous to a CNS protein containing a Ca2+/calmodulin kinase domain, suggesting that the DCX protei
32 omain protein composed of an N-terminal Ca2+/calmodulin-kinase domain, central PDZ and SH3 domains, a
34 contrast, inhibitors of protein kinase A and calmodulin kinases had no effect on CREB phosphorylation
35 pendent protein kinase, protein kinase C and calmodulin kinases have been implicated in calcium-signa
36 C (PKC) activity and not protein kinase A or calmodulin kinase; however, the identity and role of the
39 binding of the calmodulin-binding domain of calmodulin kinase I on the fast internal dynamics of cal
40 ion (Ca(2+))-dependent activation of Ca(2+)/calmodulin kinase-I (CaMKI), which triggers cAMP respons
41 ozygous for a null mutation of alpha-calcium-calmodulin kinase II (alpha-CaMKII+/-) show normal learn
44 ion 286 mutated to alanine (A)] in the alpha calmodulin kinase II (alphaCaMKIIT286A) than in mice def
45 ctivation of the calmodulin-dependent enzyme calmodulin kinase II (CaM kinase II) was studied in PC12
46 ylated by protein kinase C (PKC) and calcium/calmodulin kinase II (CaMK II) after stimulation with ag
47 L-type Ca(2+) channel (LTCC) C terminus and calmodulin kinase II (CaMK) both signal increases in LTC
48 diator of cAMP-protein kinase (PKA) and Ca2+-calmodulin kinase II (CAMK-II) activation, we tested whe
49 otein (alphakap), encoded within the calcium/calmodulin kinase II (camk2) alpha gene, was recently fo
50 -C and TnI phosphorylation using the calcium/calmodulin kinase II (CaMK2) inhibitor autocamtide-2 rel
51 ompanied by changes in protein expression of calmodulin kinase II (CaMKII) (P<0.05) and calmodulin ki
53 Such changes were related to enhanced Ca(2+)/calmodulin kinase II (CaMKII) activity and increased pho
57 GT-1 DNA binding, phosphorylation by calcium/calmodulin kinase II (CaMKII) increased the binding acti
64 ctivation and inhibited by Ca2+ through Ca2+/calmodulin kinase II (CaMKII) phosphorylation at Ser-107
65 51-300) of mouse Emi2 that also contained a calmodulin kinase II (CaMKII) phosphorylation motif and
66 ted increase in calcium (Ca(2+)) levels, via calmodulin kinase II (CaMKII) phosphorylation, inhibits
68 everses LTS, and specific inhibitors of Ca2+/calmodulin kinase II (CaMKII) prevent induction and inhi
69 k-out mice (C3KO), Ca(2+) release and Ca(2+)/calmodulin kinase II (CaMKII) signaling are attenuated.
71 ac myocyte apoptosis by activation of Ca(2+)/calmodulin kinase II (CaMKII), independently of PKA sign
72 a second Ca2+-activated signaling molecule, calmodulin kinase II (CaMKII), were increased in hearts
74 reases depend on protein kinase A (PKA)- and calmodulin kinase II (CaMKII)-mediated enhancement of Ca
77 s mediated by direct interaction between the Calmodulin Kinase II (CKII)-like domain of mLin-2 and th
80 ontrast, currents were not attenuated by the calmodulin kinase II 281-309 peptide (10 micrometer), an
81 out inhibition of calcium elevation, calcium-calmodulin kinase II activation, or cystic fibrosis tran
82 l relationship between a decrease in calcium/calmodulin kinase II activity and the development of sei
87 a(2+) disturbances, this results from Ca(2+)-calmodulin kinase II and reactive oxygen species-mediate
88 dependent Ca(2+) entry, activation of Ca(2+)/calmodulin kinase II and subsequent gating of CLC-3 link
89 tion with the protein effector alpha calcium-calmodulin kinase II and the regulation of the mTOR path
90 mice were bred with mice expressing an alpha-calmodulin kinase II Cre to selectively inactivate Dicer
91 tion of protein kinase C isoforms or calcium calmodulin kinase II did not alter the BzATP-induced inc
93 fluorescent images of COS1 cells expressing calmodulin kinase II fused with enhanced yellow fluoresc
95 n), completely inhibited by KN-62, a calcium-calmodulin kinase II inhibitor, and only partially repre
96 e I, calphostin C, and Ro31-8220 but not the calmodulin kinase II inhibitor, Kn-93, suggesting a role
97 to play a role in targeting multiple calcium/calmodulin kinase II isoforms to specific subcellular lo
99 al LTP-mice heterozygous for a alpha-calcium calmodulin kinase II mutation (alpha CaMKII +/-) have lo
100 casein kinase (CK) I or II, but not calcium-calmodulin kinase II or protein kinase A, inhibited DNA
101 tion was dependent on the calcium/calmodulin/calmodulin kinase II pathway in both M. smegmatis- and M
102 sing a decoy peptide representing the Ca(2+)/calmodulin kinase II phosphorylation site on CLC-3, we s
103 on was driven by a forebrain-specific Ca(2+) calmodulin kinase II promoter system resulting in high l
105 eta(IV)-spectrin, to bind and recruit Ca(2+)/calmodulin kinase II to the channel at a cellular locati
106 s inhibited by intracellular calcium through calmodulin kinase II, AC3 may serve as an important inte
107 te, or the calcium-responsive kinase calcium calmodulin kinase II, CpG-induced TNFalpha secretion was
108 ecific phosphorylation events on Erk 1/2 and calmodulin kinase II, two proteins required for CA1 hipp
109 chanistically, this regulation appears to be calmodulin kinase II-dependent and mediated through the
110 ivated by PGE(2) in human arterial SMCs is a calmodulin kinase II-inhibited AC with characteristics s
111 en probability was linked to enhance calcium-calmodulin kinase II-mediated phosphorylation in non-nat
112 Esophageal acid exposure induced calcium calmodulin kinase II-mediated phosphorylation of the sub
118 l inhibitors of calmodulin kinase kinase and calmodulin kinases II and III do not inhibit EGF-induced
119 the hippocampus requires activation of Ca2+/calmodulin-kinase II (CaM-KII), which phosphorylates Ser
121 tracellular calcium, elevated calmodulin and calmodulin-kinase II expression, whereas calcium chelati
124 lar signaling molecules calcineurin, calcium calmodulin kinase IIalpha (CAMKIIalpha) and the receptor
125 signaling molecules calcineurin and calcium calmodulin kinase IIalpha (CAMKIIalpha); and the recepto
128 tested this hypothesis in mice with calcium calmodulin kinase IIalpha-Cre-mediated forebrain GR dele
131 tein expression of Orai1, STIM1, and calcium-calmodulin kinase IIdelta2 (CamKIIdelta2); increased pro
132 cells, but neither protein phosphatase-1 nor calmodulin kinase III (EF-2 kinase) activity was affecte
134 itor of protein kinase Cdelta (PKCdelta) and calmodulin kinase III, abrogated the up-regulation at bo
135 rt that both calmodulin inhibitor (CaMI) and calmodulin kinase inhibitor could also enhance cleavage
138 )-dependent CREB/c-fos activation via Ca(2+)-calmodulin kinase IV (CaMKIV) induces transcriptional re
139 can bind to T cells and activate the Ca(2+)-calmodulin kinase IV (CaMKIV) signaling cascade, resulti
140 iologic synaptic stimulation recruits a fast calmodulin kinase IV (CaMKIV)-dependent pathway that dom
141 y co-transfection with constitutively active calmodulin kinase IV and protein kinase A, and binding o
143 ampal neurons demonstrates a role for Ca(2+)/calmodulin kinase kinase (CaMKK) and its downstream targ
145 LKB1, upstream kinases for AMPK; STO-609, a calmodulin kinase kinase beta inhibitor, had the same ef
146 K phosphorylation was inhibited by siRNA for calmodulin kinase kinase beta, but not LKB1, upstream ki
148 e corresponding to the CaM-binding domain of calmodulin kinase kinase, along with the thermodynamic u
150 ular signaling pathways involving Ca2+, Ca2+/calmodulin kinase, mitogen-activated protein kinase, cyc
151 t activation is mediated directly by neither calmodulin kinases nor phosphatidylinositol 3-kinase (PI
153 We also report that signaling via the Ca(2+)/calmodulin kinase pathway functions upstream of the MAPK
157 as used to identify a broad range of calcium calmodulin kinase superfamily members, including CHK2, C
158 f kinases that are components of the calcium calmodulin kinase superfamily, including CHK2, AMP kinas
160 el (CaV1.1) facilitates activation of Ca(2+)/calmodulin kinase type II (CaMKII) and Ca(2+) store refi
162 e of Ca2+ and the absence of endogenous Ca2+/calmodulin kinase type II or protein kinase C activity,
163 pecific for the alpha subunit of the calcium/calmodulin kinase were used to decrease the expression o
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