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1 in a process depending on Ca binding to CaM (calmodulin).
2 ctivation of Ca2+ -sensitive enzymes such as calmodulin.
3 ssium channels that are activated by calcium-calmodulin.
4 ated Na channels, also potently regulated by calmodulin.
5 interaction of the RS20 peptide and calcium-calmodulin.
6 on and its potential regulators, CAMK IV and calmodulin.
7 mbrane via a peripheral protein complex with calmodulin.
8 e and reveal that the enzyme is regulated by calmodulin.
9 inase A (PKA)-independent CFTR activation by calmodulin.
10 ted at the interface between the channel and calmodulin.
11 teins are instead shielded in the cytosol by calmodulin.
14 e target proteins: an alpha-helical protein (calmodulin), a protein with internal cysteines (rubredox
15 nctional roles enhanced by interactions with calmodulin, accessory proteins, or CaMKII that modulate
19 tic spine, we show that SK-channels regulate calmodulin activation specifically during neuron-firing
22 Furthermore, the modulation of UBE3B via calmodulin and calcium implicates a role for calcium sig
23 tegy to characterize the interaction between calmodulin and creatine kinase, which we identify as a n
24 onpalmitoylated state 1, like K-Ras4B, binds calmodulin and is associated with colorectal and other a
26 rmine that the T3SS effector, HopE1, targets calmodulin and the microtubule-associated protein MAP65-
27 A subset of mammalian N-BAR domains bound calmodulin, and co-expression of calmodulin with endophi
28 intracellular calcium, protein kinase C, and calmodulin, and downstream signaling regulated the relea
34 ng of ATP (betaK43R and alphaK42M) or Ca(2+)/calmodulin (betaA303R) had no effect on the interaction
35 motif (amino acids 29-58) results in loss of calmodulin binding and a significant increase in the in
39 , we identified the eNOS peptide as the only calmodulin binding peptide and S peptide as the only rib
40 inding transcription activators (CAMTA)3 and calmodulin binding protein 60g (CBP60g) together amplify
41 rinciple to the long-standing controversy of calmodulin binding to ion channels, we find a surprising
42 domain toward cytochrome c; (v) response to calmodulin binding; and (vi) the rates of interflavin ET
43 lmodulin (CaM) molecules associated with the calmodulin-binding domain (CaM-BD) of these channels.
44 domains, the autoinhibitory domain (AID) and calmodulin-binding domain (CBD), which block the catalyt
45 ion of the carboxy-lobe of calmodulin with a calmodulin-binding domain in the C-terminus of TRPA1.
46 us for a 2 base pair (bp) deletion within IQ calmodulin-binding motif-containing protein-1 (IQCB1), t
52 ansient membrane-interactions, it contains a calmodulin-binding region, suggesting that in vivo FaEO
54 RSRE induction via the transcription factor CALMODULIN-BINDING TRANSCRIPTION ACTIVATOR 3 (CAMTA3), i
57 dulin stoichiometry with Ca(2+) channels-one calmodulin binds at basal cytosolic Ca(2+) levels while
58 eceptor and the combined effect of the rapid calmodulin buffer and the frequency-dependent increase i
59 AFM and then measuring the stabilization of calmodulin by myosin light chain kinase at dramatically
60 demonstrate that upon Ca(2+) influx, Ca(2+)/calmodulin (Ca(2+)/CaM) binding to the N-terminus of PSD
62 strictly depends on Ca(2+) and Ca(2+)-bound calmodulin (Ca(2+)/CaM) to relieve autoinhibition of the
63 s revealed that extinction recruited calcium/calmodulin (Ca(2+)/CaMK)-dependent protein kinase II (Ca
64 HR), the SOX11 transcription factor (SOX11), calmodulin (CALM), and estrogen receptor 2 (ESR2A), all
66 represent cellular Ca(2+) sensors, including calmodulin (CaM) 3, CaM7 and several CaM-like proteins,
67 ing of calcium to its intracellular receptor calmodulin (CaM) activates a family of Ca(2+)/CaM-depend
68 results in an order of magnitude decrease in calmodulin (CaM) activation, providing a mechanism for t
73 The proximal Kv7.1 C terminus (CT) binds calmodulin (CaM) and phosphatidylinositol-4,5-bisphospha
74 t requires binding of the incoming Ca(2+) to calmodulin (CaM) and subsequent binding of CaM to the pr
75 in the intracellular Ca(2+)-sensing protein calmodulin (CaM) are arrhythmogenic, yet their underlyin
77 functional calcium-binding messenger protein Calmodulin (CaM) as a function of temperature and Ca(2+)
79 dothelial NO synthase (eNOS) is triggered by calmodulin (CaM) binding and is often further regulated
80 segment of the channel important for Ca(2+)/calmodulin (CaM) binding as evidenced by bio-layer inter
82 d in a case study, where we synthesize human calmodulin (CaM) by using a CFPS kit and prove the struc
85 C activates TRPC6 channels is not known, but calmodulin (CaM) contributes to the regulation of TRPC c
86 ypothesis that S100A1 directly competes with calmodulin (CaM) for binding to intact, functional ryano
92 (+) channels are gated by calcium binding to calmodulin (CaM) molecules associated with the calmoduli
96 ular rearrangements and its interaction with Calmodulin (CaM) under activation by chemical agonists a
100 with the calcium-binding messenger protein, calmodulin (CaM), and phosphorylation of the CaM-binding
101 be negatively regulated by the Ca(2+) sensor calmodulin (CaM), and previous work has focused on a C-t
102 n, and fragments of the beta-tubulin (BenA), calmodulin (CaM), and RNA polymerase II second largest s
103 HopE1 effector uses the host calcium sensor, calmodulin (CaM), as a co-factor to target the microtubu
104 rectly regulates AKAP79 through its effector calmodulin (CaM), but the molecular basis of this regula
105 ction of Syt-7 on SG recruitment may involve calmodulin (CaM), pretreatment of islets with CaM blocke
107 meric and tetradecameric forms, and that the calmodulin (CaM)-binding element of CaMKII can bind to t
108 this form of LQTS is a disruption of Ca(2+)/calmodulin (CaM)-dependent inactivation of L-type Ca(2+)
110 longation factor 2 kinase (eEF-2K), the only calmodulin (CaM)-dependent member of the unique alpha-ki
111 citatory synapse strength require the Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) an
112 lly composed of one or two subunits, calcium-calmodulin (CaM)-dependent protein kinase II (CaMKII) is
122 atase calcineurin (CN) by stabilizing the CN-calmodulin complex, relieving enzymatic autoinhibition a
123 lcium, which results in formation of calcium-calmodulin complexes, followed by recruitment of eNOS fr
124 A protein with similarities to the Ca(2+)/ calmodulin dependent protein kinase II_association domai
127 er, they were associated with reduced Ca(2+)/calmodulin-dependent auto-phosphorylation of eEF2 kinase
128 autophosphorylation (activation) of calcium/calmodulin-dependent kinase 2 (CaMKII) and also that inh
129 The Ca(2+) and redox-sensing enzyme Ca(2+) /calmodulin-dependent kinase 2 (CaMKII) is a crucial and
131 dynamin-related protein 1 (Drp1), by Ca(2+)/calmodulin-dependent kinase II (CaMKII) at a serine 616
132 glucagon-induced calcium signaling, calcium/calmodulin-dependent kinase II (CaMKII) phosphorylates O
134 NK1 in vitro Inhibiting PKC, JNK, or calcium/calmodulin-dependent kinase II activity prevented the ef
135 y-dependent phosphorylation event on calcium-calmodulin-dependent kinase II alpha (CaMKIIalpha) at se
136 horylation directly through JNK1 and calcium/calmodulin-dependent kinase II and also by inducing expr
137 FIP2 expression also increases alpha-calcium/calmodulin-dependent kinase II protein expression, and t
138 ude local synthesis of APP and alpha-calcium/calmodulin-dependent kinase II, a kinase that can phosph
140 utophagy via a pathway that included calcium/calmodulin-dependent kinase kinase beta (CaMKKbeta), AMP
142 endent on the relative activities of Ca(2+) /calmodulin-dependent myosin light chain kinase (MLCK) an
143 ght chain (RLC) is phosphorylated by Ca(2+) /calmodulin-dependent myosin light chain kinase and depho
144 ends on the respective activities of Ca(2+) /calmodulin-dependent myosin light chain kinase and myosi
146 BAA signaling by calcineurin, a calcium- and calmodulin-dependent phosphatase, enables homeostatic ba
147 Psi Here, we characterize a role for calcium/calmodulin-dependent protein kinase (CaMK) I in the regu
148 +)-dependent binding of S100B to the calcium/calmodulin-dependent protein kinase (CaMK)-type domain o
149 ore than 20 years, we have known that Ca(2+)/calmodulin-dependent protein kinase (CaMKII) activation
151 prevent the arrhythmias induced by a Ca(2+) -calmodulin-dependent protein kinase (CaMKII)-dependent l
152 cannabinoid type 1 (CB1) receptor and Ca(2+)/calmodulin-dependent protein kinase beta, activates AMP-
157 tate (NMDA) receptor activation, and Calcium/calmodulin-dependent protein kinase II (CaMKII) activati
158 y (SOCE) and sequential activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and Ca(2
160 phorylated at serine 409 (Ser-409) by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and prot
163 Here we show that the activity of calcium/calmodulin-dependent protein kinase II (CaMKII) is incre
164 Considerable evidence suggests that calcium/calmodulin-dependent protein kinase II (CaMKII) overacti
165 nhanced [(3) H]ryanodine binding and Ca(2+) /calmodulin-dependent protein kinase II (CaMKII) phosphor
166 treated wild-type C57BL/6 mice with calcium/calmodulin-dependent protein kinase II (CaMKII) specific
169 which in turn requires binding of the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) to the N
172 CaMK2N2 are endogenous inhibitors of calcium/calmodulin-dependent protein kinase II (CaMKII), a key s
173 triggers the exchange of subunits in Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), an olig
174 tream effector of WNT/Ca(2+) pathway, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), led to
175 scular smooth muscle (VSM) expresses calcium/calmodulin-dependent protein kinase II (CaMKII)-delta an
176 ators of myocardial excitability, and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)-dependen
177 he hypotheses that (1) inhibition of Ca(2+) /calmodulin-dependent protein kinase II (CAMKII)-mediated
178 o the model reveal that inclusion of Ca(2+) /calmodulin-dependent protein kinase II (CAMKII)-mediated
181 increase in oxidation-dependent calcium and calmodulin-dependent protein kinase II activity, which c
183 Alcohol-sensitive proteins included calcium/calmodulin-dependent protein kinase II alpha (CaMKIIalph
184 rrhythmic manifestations, related to Ca(2+) /calmodulin-dependent protein kinase II and ryanodine rec
190 A null mutation of the Drosophila calcium/calmodulin-dependent protein kinase II gene (CaMKII) was
191 ion and subsequent activation of calcium and calmodulin-dependent protein kinase II has a causal role
192 eam signaling protein, PKC-alpha, and Ca(2+)/calmodulin-dependent protein kinase II in endothelial ce
193 2B, also referred to as Pyk2) and of calcium/calmodulin-dependent protein kinase II in wild-type brai
194 Development of organ-specific calcium and calmodulin-dependent protein kinase II inhibitors may re
195 rom transgenic mice expressing a calcium and calmodulin-dependent protein kinase II inhibitory peptid
196 as phosphorylation of substrates for calcium/calmodulin-dependent protein kinase II was unchanged.
197 Pharmacologic inhibition of calcium and calmodulin-dependent protein kinase II with 2.5 microM o
198 stabilization of postsynaptic CaMKII (Ca(2+)/calmodulin-dependent protein kinase II) at inhibitory sy
199 mitochondrial recruitment of CaMKII (Ca(2+)/calmodulin-dependent protein kinase II), which decreases
200 ng protein, but not the activation of Ca(2+)/calmodulin-dependent protein kinase II, Akt or mitogen-a
201 ellular protein mediators Homer1b/c, calcium/calmodulin-dependent protein kinase II, and the Alzheime
202 a(2+) must first mobilize actin-bound Ca(2+)/calmodulin-dependent protein kinase II, freeing it for s
204 turn, led to the phosphorylation of calcium/calmodulin-dependent protein kinase II, which promoted b
205 at have the ryanodine receptor 2 calcium and calmodulin-dependent protein kinase II-dependent phospho
206 used 1 Hz optogenetic stimulation of calcium/calmodulin-dependent protein kinase II-positive principa
210 is study, we investigated the role of Ca(2+)/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha
211 d cardiomyocyte apoptosis, fibrosis, calcium/calmodulin-dependent protein kinase IIdelta phosphorylat
212 as a direct inhibitor of CaMKIIdelta (Ca(2+)/calmodulin-dependent protein kinase IIdelta) activity, a
213 ive oxygen species (ROS) production, calcium/calmodulin-dependent protein kinase IV (CaMKIV) activati
214 ally reduced by the application of a calcium/calmodulin-dependent protein kinase kinase 2 inhibitor (
215 istic target of rapamycin complex 1, calcium/calmodulin-dependent protein kinase kinase 2, and protei
216 PK kinases liver kinase B1 (LKB1) and Ca(2+)/calmodulin-dependent protein kinase kinase beta (CaMKKbe
217 AMPK activation by aa is mediated by Ca(2+)/calmodulin-dependent protein kinase kinase beta (CaMKKbe
219 alcineurin, Akt/protein kinase B, and Ca(2+)/calmodulin-dependent protein kinase signaling pathways i
220 ger, phospholamban, calcineurin, and calcium/calmodulin-dependent protein kinase type II (CaMKII) wer
221 to remodeling pathways (e.g., Akt and Ca(2+)/calmodulin-dependent protein kinase type II) and develop
226 or somatostatin-positive interneurons and of calmodulin-dependent, protein kinase-positive, principal
227 Furthermore, our simulations showed that the calmodulin domain binding to the linker region was impor
228 associated Bak interacts with the kinase and calmodulin domains of DAPk1 to increase the contact site
230 Using a 3-dimensional model of Ca2+ and calmodulin dynamics within an idealised, but biophysical
233 This gene family, with a proposed new name, Calmodulin Fused Kinase (CFK), had expanded and diverged
235 ty, such as protein inhibitor of NOS1 (PIN), calmodulin, heat shock protein 90, and NOS interacting p
236 pe was rescued by co-expression of TCF4 plus calmodulin in a calcium-dependent manner and by dampenin
237 These studies reveal a conserved role for calmodulin in regulating the intrinsic membrane-sculptin
245 tained reduction of intracellular Ca(2+) and calmodulin kinase activity, ranolazine prevented the dev
246 ted increase in calcium (Ca(2+)) levels, via calmodulin kinase II (CaMKII) phosphorylation, inhibits
247 k-out mice (C3KO), Ca(2+) release and Ca(2+)/calmodulin kinase II (CaMKII) signaling are attenuated.
248 reases depend on protein kinase A (PKA)- and calmodulin kinase II (CaMKII)-mediated enhancement of Ca
249 )-dependent CREB/c-fos activation via Ca(2+)-calmodulin kinase IV (CaMKIV) induces transcriptional re
251 aining permutated GFP and the calcium sensor calmodulin (Lck-GCaMP3 and GCaMP3), we demonstrated enri
252 e the differential calcium ion dependence of calmodulin ligand-binding affinities, a system at the fo
255 signalling mediated by Calmodulin (CaM) and calmodulin-like (CML) proteins is critical to plant immu
257 Ser/Thr and Tyr) kinase domain tethered to a calmodulin-like domain (CLD) via an autoinhibitory junct
260 cting proteins in Arabidopsis, we identified calmodulin-like protein 38 (CML38) as an AtRALF1-interac
264 for FS, rs1067327 within CAMKMT encoding the calmodulin-lysine N-methyltransferase on chromosomal ban
266 re involved in pathogen recognition, calcium/calmodulin-mediated defense signaling, jasmonic acid (JA
269 ion of this region promotes the occupancy of calmodulin on the channel, thus increasing channel open
270 r, we suggest that because only KRas4B binds calmodulin, only KRas can fully activate PI3Kalpha/Akt s
271 Kojak and the popular pLink algorithms on a calmodulin-plectin complex data set, as well as three ad
273 arrhythmias produced by exacerbated Ca(2+) /calmodulin-protein kinase (CaMKII) activity, ryanodine r
275 form in vivo and, as frequently observed for calmodulin-regulated proteins, it may be expressed in di
276 Furthermore, the MAPKKK YDA and two calcium/calmodulin-regulated receptor-like kinases, CRLK1 and CR
277 -D-aspartate (NMDA) receptors activates Ca2+/calmodulin signal transduction networks that either incr
278 e find a surprising Ca(2+)-induced switch in calmodulin stoichiometry with Ca(2+) channels-one calmod
279 the neuronal calcium sensor subclass of the calmodulin superfamily, confers Ca(2+)-sensitive activat
280 e lack of motility at high calcium is due to calmodulin switching to a higher affinity binding site,
282 on between the regulatory region of CFTR and calmodulin, the major calcium signaling molecule, and re
283 b interface, away from the kinase domain and calmodulin, thus unlocking the ability of activated CaMK
284 cture and position of the S4-S5 linker allow calmodulin to bind to the intracellular domains and to c
286 ediates calcium influx in LECs and activates calmodulin to facilitate a physical interaction between
287 vealed that FGF13 potentiates the binding of calmodulin to NaV1.5 and that phosphomimetic mutations a
289 ich a pathogen effector is activated by host calmodulin to target MAP65 and the microtubule network,
290 calcium (Ca(2+) i) through binding of Ca(2+)-calmodulin to three sites adjacent to the eagD and cNBHD
291 d by the absence from olfactory axons of the calmodulin transcript Calm1, which is highly expressed i
293 er's biological utility by first resolving a calmodulin unfolding intermediate previously undetected
294 g activation of CsGAD1 enzymatic activity by calmodulin upon the onset of the stress and accumulation
295 We also discovered that UBE3B interacts with calmodulin via its N-terminal isoleucine-glutamine (IQ)
296 he BRET assay, based on the interaction with Calmodulin, was successfully extended to TRPV3 and TRPV4
297 we show that Ca(2+) regulates TRPA1 through calmodulin, which binds to TRPA1 in a Ca(2+)-dependent m
298 pting the interaction of the carboxy-lobe of calmodulin with a calmodulin-binding domain in the C-ter
299 mains bound calmodulin, and co-expression of calmodulin with endophilin A2 potentiated tubulation in
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