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1 CaMKIV activates PGC-1alpha largely through the binding
2 CaMKIV and calspermin expression in the testis are stage
3 CaMKIV and CaMKIIalpha respond differently to substituti
4 CaMKIV does not phosphorylate RORalpha or its ligand-bin
5 CaMKIV inhibition in MRL/lpr mice resulted in significan
6 CaMKIV is found in multiple tissues, including brain, th
7 CaMKIV is highly enriched in the nucleus and thought to
8 CaMKIV phosphorylates HDAC4 in vitro and promotes its nu
9 CaMKIV protein levels were also increased in the nucleus
10 CaMKIV-mediated nuclear export of Cabin1 is likely to ac
11 CaMKIV-mTOR-dependent autophagy was fundamentally import
12 CaMKIV/Gr-deficient mice exhibited impaired neuronal cAM
13 CaMKIV/Gr-deficient thymocytes exhibited impaired positi
14 onse to an increase in intracellular Ca(2+), CaMKIV binds Ca(2+)/CaM and becomes phosphorylated on T2
15 lterations in other components of the Ca(2+)-CaMKIV signaling cascade: the ratio of phosphorylated to
16 response to sustained activation of a Ca(2+)-CaMKIV signaling pathway, resulting from growth of cultu
19 STO609 (a CaMKIV kinase inhibitor), KN93 (a CaMKIV inhibitor), or we utilized cells from which CaMKI
20 al Mphi were incubated with either STO609 (a CaMKIV kinase inhibitor), KN93 (a CaMKIV inhibitor), or
22 In this study, we demonstrate that activated CaMKIV/Gr induces transcription from the BZLF1 promoter
24 r, despite impaired LTP and CREB activation, CaMKIV/Gr-deficient mice exhibited no obvious deficits i
25 ith vectors expressing constitutively active CaMKIV and calcineurin, we have demonstrated that each p
26 signalling pathway via constitutively active CaMKIV prevents nuclear entry of HDAC4 and HDAC4-mediate
31 vation of gene expression by calcineurin and CaMKIV is common to members of the TNF cytokine family.
37 pendent protein kinases-I and -IV (CaMKI and CaMKIV) also induce hypertrophic responses in cardiomyoc
38 ependent protein kinases I and IV (CaMKI and CaMKIV) are closely related by primary sequence and pred
39 ependent protein kinases I and IV (CaMKI and CaMKIV, respectively) require phosphorylation on an equi
44 (2+)/calmodulin-activated kinases CaMKK2 and CaMKIV are highly expressed in the brain where they play
45 vely, these findings suggest that CaMKK2 and CaMKIV may represent potential targets for hepatic cance
46 d PFC CaMKII but increased PFC CaMKKbeta and CaMKIV levels, suggesting the involvement of PFC CaMK pa
47 nt signaling cascade involving CaMKKbeta and CaMKIV to decrease the sympathetic tone and increase bon
51 CaMKIV in the cerebellum, Wild-type (WT) and CaMKIV KO mice were tested with delay eyeblink condition
52 dent protein kinase IV (Camk4; also known as CaMKIV), a multifunctional serine/threonine protein kina
53 ond event, involving protein kinases such as CaMKIV, leads to efficient nuclear export of the HDAC4.1
54 that CaMKK2 serves as a scaffold to assemble CaMKIV with key components of the mammalian target of ra
55 consider the possible implications of axonal CaMKIV in the context of the unique properties of IB4-bi
56 which correlated with an interaction between CaMKIV and HMGB1 and with CaMKIV phosphorylation of HMGB
58 ave examined the expression patterns of both CaMKIV and calspermin in mouse testis and unexpectedly f
63 phosphorylated with similar efficiencies by CaMKIV, whereas the Leu-substituted peptide is preferred
64 e phosphorylation on Ser 133 is increased by CaMKIV following serotonin treatment of hypothalamic exp
66 iptional activation of the BZLF1 promoter by CaMKIV/Gr is dependent on the CREB/AP1 binding element Z
69 in addition to the classical nuclear calcium-CaMKIV-CREB/CBP (cAMP-response element-binding protein/C
72 ant consequences in the regulation of CaMKI, CaMKIV, protein kinase B, and ERK signaling pathways.
73 eal a previously undefined role for a CaMKK2/CaMKIV cascade involved in cerebellar granule cell devel
76 , pathway, and the importance of this CaMKK2/CaMKIV axis in HCC growth is confirmed by the potent gro
78 fail to drive transcription, whereas certain CaMKIV mutants that possess constitutive autonomous acti
80 e depolarization requires a highly conserved CaMKIV target serine (Ser-513) of the heterogeneous ribo
82 dulin-dependent protein kinase IV-deficient (CaMKIV(-/-)) mice have been used to investigate the role
83 ults indicate that neural activity-dependent CaMKIV signaling in the neuronal nucleus plays an import
84 as identified in which PP2A dephosphorylates CaMKIV and functions as a negative regulator of CaMKIV s
85 CaMKIV-associated PP2A then dephosphorylates CaMKIV T200, thereby terminating autonomous activity and
86 sponse element-binding protein (a downstream CaMKIV substrate) was reduced by approximately 10-fold,
88 P2A association in cells results in enhanced CaMKIV-mediated gene transcription that is independent o
91 uclear translocation, it is not required for CaMKIV to interact with the nuclear adaptor protein, imp
93 to defining an important signaling role for CaMKIV in a subpopulation of T cells, we identify differ
95 r, our results support an important role for CaMKIV in nicotine reward, and suggest that CaMKIV has o
98 These studies demonstrate a pivotal role for CaMKIV in the regulation of orphan receptor-mediated tra
99 These results support an important role for CaMKIV/Gr in Ca(2+)-regulated neuronal gene transcriptio
100 se results demonstrate an important role for CaMKIV/Gr in sensitizing thymocytes to selection by low-
102 ntrast, stimulated naive CD4(+) T cells from CaMKIV(-/-) mice show normal CREB phosphorylation, induc
105 modulin-dependent protein kinase type IV/Gr (CaMKIV/Gr) is a key effector of neuronal Ca(2+) signalin
106 Ca2+/calmodulin-dependent kinase type IV/Gr (CaMKIV/Gr) is normally absent in primary human B cells,
108 tase calcineurin, and the kinase type IV/Gr (CaMKIV/Gr), which promote transcription by the MEF2 fami
111 on loop threonine (residue Thr(200) in human CaMKIV) by Ca(2+)/calmodulin-dependent kinase kinase lea
115 found that nicotine reward is attenuated in CaMKIV knockout (-/-) mice, but cocaine reward is enhanc
118 Correspondingly, there is an increase in CaMKIV interaction with O-GlcNAcase during CaMKIV activa
119 ted among rat tissues with highest levels in CaMKIV-expressing tissues such as brain, thymus, spleen,
121 n phosphatase 2A, the catalytically inactive CaMKIV proteins interact more avidly with CaM-dependent
122 ependent calcium influx results in increased CaMKIV activity, which acts to decrease nuclear C/EBPbet
124 e findings demonstrate that activity-induced CaMKIV signaling contributes to CREB/CBP-dependent trans
125 utline a virus-regulated mechanism involving CaMKIV/Gr which promotes transition from latency to prod
127 cium/calmodulin-dependent protein kinase IV (CaMKIV) activation, and interactions between nuclear fac
128 (2+)/calmodulin-dependent protein kinase IV (CaMKIV) activation, through special CaM kinase responsiv
129 )(+)/calmodulin-dependent protein kinase IV (CaMKIV) and cAMP response element binding protein mediat
130 o on calcium/calmodulin-dependent kinase IV (CaMKIV) and its pseudophosphorylated form can account fo
131 (2+)-calmodulin-dependent protein kinase IV (CaMKIV) are two proteins encoded by the Camk4 gene.
132 cium/calmodulin-dependent protein kinase IV (CaMKIV) has been implicated in the regulation of CRE-dep
133 the role of calmodulin-dependent kinase IV (CaMKIV) in mouse naive CD4+ T-cell activation remains en
134 d by calcium/calmodulin-dependent kinase IV (CaMKIV) in transcriptional activation of TNF family gene
135 activation via Ca(2+)-calmodulin kinase IV (CaMKIV) induces transcriptional regulation of osteoclast
136 cium/calmodulin-dependent protein kinase IV (CaMKIV) is a member of the broad substrate specificity c
137 Calcium/calmodulin-dependent kinase IV (CaMKIV) is a multifunctional serine/threonine kinase tha
138 cium/calmodulin-dependent protein kinase IV (CaMKIV) is a nuclear protein kinase that responds to acu
140 that calmodulin-dependent protein kinase IV (CaMKIV) is present in c-Kit+ ScaI+ Lin(-/low) hematopoie
141 Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) or CaMKIIdeltaB, both of which localize to the n
142 rough Ca(2+)/calmodulin-dependent kinase IV (CaMKIV) pathway, rather than the mitogen-activated prote
143 cium/calmodulin-dependent protein kinase IV (CaMKIV) phosphorylates the downstream transcription fact
144 (2+)/calmodulin-dependent protein kinase IV (CaMKIV) potentiates RORalpha-dependent transcription 20-
145 tent CREB phosphorylation and CaM kinase IV (CaMKIV) responsible for phosphorylating the CREB coactiv
146 nd activate the Ca(2+)-calmodulin kinase IV (CaMKIV) signaling cascade, resulting in downregulation o
148 Ca2+-calmodulin-dependent protein kinase IV (CaMKIV), a nuclear enzyme that can phosphorylate and act
149 cium/calmodulin-dependent protein kinase IV (CaMKIV), calcineurin A (CnA), and the transcriptional co
151 (2+)/calmodulin-dependent protein kinase IV (CaMKIV), the maintenance of cerebellar LTD is abolished.
152 cium/calmodulin-dependent protein kinase IV (CaMKIV), through inhibitory serine phosphorylation of GS
153 lation recruits a fast calmodulin kinase IV (CaMKIV)-dependent pathway that dominates early signaling
154 lear calmodulin-dependent protein kinase IV (CaMKIV)-mediated phosphorylation and activation of the t
155 by a calcium/calmodulin-dependent kinase IV (CaMKIV)-regulated pathway that is activated by the relea
161 calmodulin-dependent protein kinase type IV (CaMKIV) is a key sensory/effector in excitatory synaptic
162 calmodulin-dependent protein kinase type IV (CaMKIV) is highly expressed in cerebellar cortical granu
163 calmodulin-dependent protein kinase type IV (CaMKIV), which translocates to the nucleus upon engageme
164 impaired activation of the downstream kinase CaMKIV/Gr and its substrate, the transcription factor cy
165 e Ca(2+)/calmodulin-dependent protein kinase CaMKIV was first identified in the cerebellum and has be
167 m whereby a protein serine-threonine kinase (CaMKIV) is regulated by a tightly associated protein ser
168 )/calmodulin-dependent protein kinase kinase/CaMKIV/CREB pathway appears to be involved in regulating
170 ue of Neuron, Boyden et al. use mice lacking CaMKIV and Hansel et al. use mice lacking alphaCaMKII to
171 ively-active (ca) forms of nuclear-localized CaMKIV and measured the induction of all three forms of
175 gration and trafficking require ROS-mediated CaMKIV activation leading to formation of NFATc3 and Fos
176 ta justify the development of small-molecule CaMKIV inhibitors for the treatment of patients with SLE
178 alyzing the behavior of wild-type and mutant CaMKIV proteins in biochemical experiments and cellular
180 f cytosolic CaMKI, but not CaMKII or nuclear CaMKIV, dramatically decreases axonal outgrowth and bran
184 hese results indicate that the activation of CaMKIV and CREB are necessary to establish a late phase
187 lso been repeatedly noted that activation of CaMKIV is accompanied by the generation of Ca(2+)/CaM-in
189 unt of CaMK kinase (an upstream activator of CaMKIV) protein and mRNA was significantly reduced.
190 ase-kinase (CAMKK), an upstream activator of CaMKIV, suggesting a role for CaMKIV in signaling though
192 We have recently shown that deletion of CaMKIV has no effect on calspermin expression but does i
193 Ca(2+)/CaM binding-autoinhibitory domain of CaMKIV is required for association of the kinase with PP
197 he expression of a dominant-negative form of CaMKIV (dnCaMKIV) is restricted to the postnatal forebra
198 xpression of a constitutively active form of CaMKIV that also has increased endogenous CaMKII activit
200 expression of constitutively active forms of CaMKIV and CREB on synaptic function in the rodent hippo
201 We further demonstrate that a fraction of CaMKIV in spermatids is hyperphosphorylated and specific
209 plied lentivius-mediated RNA interference of CaMKIV to human T cells and found that knockdown of CaMK
210 s shown by the effect of RNA interference of CaMKIV to markedly accelerate RA-dependent up-regulation
211 to human T cells and found that knockdown of CaMKIV abrogates T-cell receptor-mediated transcription
214 l means and by a dominant negative mutant of CaMKIV impairs the ionomycin-induced activity of all thr
215 m by which catalytically inactive mutants of CaMKIV exert their "dominant-negative" functions within
216 sigmoid kinetics, rate-limited by paucity of CaMKIV, protecting against saturation of phospho-CREB in
222 dification participates in the regulation of CaMKIV activation and function, possibly coordinating nu
223 tion and Ca(2+)-dependent down-regulation of CaMKIV were associated with significant alterations in o
224 ablishes nuclear m-calpain as a regulator of CaMKIV and associated signaling molecules under conditio
230 is required for the transcriptional roles of CaMKIV, these data suggest that CaMKK phosphorylation of
231 cylation sites located in the active site of CaMKIV can modulate its phosphorylation at Thr-200 and i
236 uced activation and nuclear translocation of CaMKIV, which preceded HMGB1 nucleocytoplasmic shuttling
237 nctions downstream of CaMKII but upstream of CaMKIV in a pathway that restricts dendritic complexity.
241 n vitro that the absence of either CaMKK2 or CaMKIV disrupts the ability of developing cerebellar gra
244 CaMKIV in granule cells that lack CaMKK2 or CaMKIV, respectively, restores pCREB and BDNF to wild-ty
249 However, Mphi treated with KN93, STO609, or CaMKIV RNAi before LPS showed reduced nucleocytoplasmic
251 nase 4 (gene and transcript: CaMK4; protein: CaMKIV) is the nuclear effector of the Ca(2+) /calmoduli
255 vation of HEK293 cells, hemagglutinin-tagged CaMKIV GlcNAcylation rapidly decreases, in a manner dire
256 esponses in cardiomyocytes in vitro and that CaMKIV overexpressing mice develop cardiac hypertrophy w
257 transcriptional assays, we demonstrate that CaMKIV autonomous activity is necessary and sufficient f
260 Together, these findings demonstrate that CaMKIV plays key roles in the function and development o
261 Collectively, our results demonstrate that CaMKIV promotes the nucleocytoplasmic shuttling of HMGB1
262 studies in rat testes have demonstrated that CaMKIV mRNA is localized to pachytene spermatocytes, whi
264 n in mouse testis and unexpectedly find that CaMKIV is expressed in spermatogonia and spermatids but
265 KIV in CREB activation, we hypothesized that CaMKIV might be a crucial molecular component in the dev
270 CaMKIV in nicotine reward, and suggest that CaMKIV has opposing roles in nicotine and cocaine reward
274 tion analysis and found that variants in the CaMKIV gene are associated with a protective effect agai
277 3)), fits the expected consensus whereas the CaMKIV site, Ser(24) ((19)SSPALSASAS(28)), is novel.
278 ous ribonucleoprotein L interaction with the CaMKIV-responsive RNA element 1 of stress axis-regulated
280 re coregulated in individual neurons through CaMKIV signaling, which is tightly controlled by neurona
284 ns do not inhibit nuclear entry of wild-type CaMKIV but do inhibit the ability of the wild-type prote
286 IV, respectively, suggesting that uncoupling CaMKIV activation from activity generates an error signa
289 lates Ca(2+)-dependent NFATc1 expression via CaMKIV/CREB during inflammatory osteoclastogenesis in th
293 inhibitor), or we utilized cells from which CaMKIV was depleted by RNA interference (RNAi) before st
294 actors by an NFAT-dependent mechanism, while CaMKIV/Gr selectively and independently activates MEF2D.
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