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1 ownstream effectors (phospholipase Cbeta and myosin light chain).
2 ction and lower expression of phosphorylated myosin light chain.
3 he activation of RhoA and phosphorylation of myosin light chain.
4 cells to injured cardiomyocytes (expressing myosin light chain.
5 in light chain phosphatase and subsequently, myosin light chain.
6 ting Rho kinase activity and phosphorylating myosin light chain.
7 including glycogen synthase kinase-3beta and myosin light chain.
8 um as judged by increased phosphorylation of myosin light chain.
9 e substrates via reduction of phosphorylated myosin light chain.
11 repression of troponin T3, troponin I2, and myosin light chain 1 between cardiac and slow-twitch ske
12 the actin-tropomyosin and myosin heavy chain-myosin light chain 1 interactions independently correlat
13 ns of OGA with alpha-actin, tropomyosin, and myosin light chain 1, along with reduced OGT and increas
14 3-kDa IgE-reactive protein was identified as myosin light chain 1, designated Gallus domesticus 7 (Ga
15 itoylation of proteins involved in motility (myosin light chain 1, myosin A), cell morphology (PhIL1)
18 gin: including myofibrillar proteins (titin, myosin light chain 1/3, myomesin 3 and filamin-C), glyco
22 tractility is enhanced by phosphorylation of myosin light chain 2 (MLC2) by cardiac-specific MLC kina
23 ly the phosphorylation of the ROCK substrate myosin light chain 2 (MLC2) in intact human breast, lung
24 for PKM2's localization and interaction with myosin light chain 2 (MLC2) in the contractile ring regi
29 ction and permeability via the Rho-dependent myosin light chain 2 and vascular endothelial (VE)-cadhe
31 s whereas the phosphorylation of ventricular myosin light chain 2 was significantly increased, implyi
32 signaling and by the localization of phospho-myosin light chain 2, in turn controlling the changes in
34 decreased phosphorylation of the regulatory myosin light chain-2 (MLC2), a critical cytoskeletal reg
35 by myosin regulatory proteins (for example, myosin light chain-2 [MLC2]) in cardiac muscle remain po
36 osphorylation of several proteins, including myosin light chain-2 slow and troponin T and carbonylati
38 antly decreased in MetSyn lymphatic vessels, myosin light chain 20, MLC(20) phosphorylation was incre
39 In addition, increased phosphorylation of myosin light chain-20, a key regulator of lymphatic musc
40 ctural proteins myosin heavy chain alpha and myosin light chain 2a in real-time during early differen
41 ssion of cardiac alpha-actinin, connexin 43, myosin light chain 2a, alpha/beta-myosin heavy chain, an
42 Here we investigate one of these proteins, myosin light chain 4 (MYL4), which is important for cont
44 sion, evidenced by reduced expression of the myosin light chain 9 (MYL9) component of myosin II compl
46 ion, which prevents dephosphorylation of the myosin light chain, allowing actomyosin contractility to
47 increased levels of F-actin, phosphorylated myosin light chain, alpha-smooth muscle actin, collagen-
48 y, which is necessary for phosphorylation of myosin light chain and actin myosin-mediated contraction
49 wever, the structural features of this novel myosin light chain and its interaction with its cognate
50 activity to downstream effectors, including myosin light chain and p38(MAPK), and is reversed upon t
51 rease in permeability via phosphorylation of myosin light chain and subsequent shrinkage of human bra
52 by means of reducing the phosphorylation of myosin light chain and vascular endothelial (VE)-cadheri
53 he myofilament proteins, myosin heavy chain, myosin light chains and subunits of the Troponin complex
54 he R403Q myosin mutation, phosphorylation of myosin light chains, and an increased ADP:ATP ratio, des
57 hereas F-actin, vinculin, and phosphorylated myosin light chain associated only with the peripheral a
60 ion resulted in decreased phosphorylation of myosin light chains, attenuated smooth muscle contractil
65 e, the complex included GAP40, an additional myosin light chain designated essential light chain (ELC
68 the 2.3-A-resolution crystal structure of a myosin light chain domain, corresponding to one type fou
70 pomethylation was also found in promoters of myosin light chain, dystrophin, actin polymerization, PA
71 ble-green-fluorescent-protein (PAGFP)-tagged myosin light chain expressed in zebrafish skeletal muscl
73 alpha-smooth muscle actin and phosphorylated myosin light chain in cortical patches, decreased abunda
77 site to 0.45 mol of phosphate/mol by cardiac myosin light chain kinase (cMLCK) increases Ca(2+) sensi
78 tro and in vivo, the precise role of cardiac myosin light chain kinase (cMLCK), the primary kinase ac
79 he well-known, muscle-specific smooth muscle myosin light chain kinase (MLCK) (smMLCK) and skeletal m
80 on of myosin regulatory light chain (RLC) by myosin light chain kinase (MLCK) and myosin binding prot
82 ve activities of Ca(2+)-calmodulin-dependent myosin light chain kinase (MLCK) and myosin light chain
83 e activities of Ca(2+) /calmodulin-dependent myosin light chain kinase (MLCK) and myosin light chain
84 in (RLC) phosphorylation, which is driven by myosin light chain kinase (MLCK) and Rho-associated kina
87 testinal TJ permeability and the increase in myosin light chain kinase (MLCK) expression, confirming
89 transgenic mice expressing calmodulin sensor myosin light chain kinase (MLCK) in smooth muscles, the
91 ocusing on regulatory roles of IFN-gamma and myosin light chain kinase (MLCK) in TW myosin phosphoryl
92 d in the absence or presence of the specific myosin light chain kinase (MLCK) inhibitor ML-7 under bo
93 ABSTRACT: Ca(2+) /calmodulin activation of myosin light chain kinase (MLCK) initiates myosin regula
97 , where it bound to its binding motif on the myosin light chain kinase (MLCK) promoter region, leadin
98 ulin-dependent protein kinase II (CaMKII) to myosin light chain kinase (MLCK) to myosin light chain,
99 myosin II, Rho-associated kinase (ROCK), and myosin light chain kinase (MLCK) were also recruited to
100 ted by arp2/3 and contractility regulated by myosin light chain kinase (MLCK) were responsible for th
101 The mylk1 gene encodes a 220-kDa nonmuscle myosin light chain kinase (MLCK), a 130-kDa smooth muscl
102 reduction in the expression and activity of myosin light chain kinase (MLCK), a primary regulator of
103 lity pathway involving Rho kinase (ROCK) and myosin light chain kinase (MLCK), culminating in the act
105 erijunctional actomyosin ring contributes to myosin light chain kinase (MLCK)-dependent tight junctio
109 ght junction (TJ) permeability by activating myosin light chain kinase (MLCK; official name MYLK3) ge
111 d by TRPC6, in turn, activates the nonmuscle myosin light chain kinase (MYLK), which not only increas
112 nied by an increase in protein expression of myosin light chain kinase (P<0.05) and casein kinase II-
116 ene that encodes nonmuscle and smooth muscle myosin light chain kinase (smMLCK) isoforms and regulate
117 riation in a gene of major effect, Stretchin Myosin light chain kinase (Strn-Mlck), which we validate
118 In turn, IL-1beta increased NF-kappaB and myosin light chain kinase activation in intestinal epith
119 osphorylated by Ca(2+) /calmodulin-dependent myosin light chain kinase and dephosphorylated by myosin
120 development in ileal smooth muscle depend on myosin light chain kinase and MLCP activities without ch
121 e activities of Ca(2+) /calmodulin-dependent myosin light chain kinase and myosin light chain phospha
124 lated through two myosin-signaling pathways, myosin light chain kinase and Rho-associated kinase.
125 lated these recombinant species with cardiac myosin light chain kinase and zipper-interacting protein
126 measuring the stabilization of calmodulin by myosin light chain kinase at dramatically higher unfoldi
129 osphorylated by a dedicated Ca(2+)-dependent myosin light chain kinase in fast skeletal muscle, where
130 nges, as determined by increased activity of myosin light chain kinase in the cytoplasm and enhanced
133 he recent identification of cardiac-specific myosin light chain kinase necessary for basal RLC phosph
134 ression of contraction through inhibition of myosin light chain kinase normalized the effects of subs
135 ented cytoskeletal defects, while inhibiting myosin light chain kinase or phosphorylation of focal ad
137 hidden and unphosphorylated; on activation, myosin light chain kinase phosphorylates the monophospho
138 inal extension (Dmlc2(Delta2-46)), disrupted myosin light chain kinase phosphorylation sites (Dmlc2(S
140 rough RhoA GTPase, Rho-associated kinase, or myosin light chain kinase restored stiffness-dependent s
142 m1a), expressed specifically in the MHB, and myosin light chain kinase together mediate MHBC cell len
144 nhibition of actin polymerization as well as myosin light chain kinase with the drug ML7 limited both
145 RT-PCR analysis of tight junction proteins, myosin light chain kinase, and proinflammatory cytokine
146 density and progressed independently of Rac, myosin light chain kinase, and Rho kinase, suggesting a
147 including methionine sulfoxide reductase A, myosin light chain kinase, and Runt-related transcriptio
148 in action, including Mal2, Akap12, gelsolin, myosin light chain kinase, annexin-2, and Hsp70, manifes
149 ts the CaM binding domain of skeletal muscle myosin light chain kinase, forms a complex with CaM in t
150 in), regulators of the contractile response (myosin light chain kinase, myosin phosphatase target sub
151 ytosis, and localized phosphorylation of the myosin light chain kinase, thereby impinging on the acto
152 titutively active mutants of RhoA GTPase and myosin light chain kinase, we show that varying the expr
154 nase- and myosin II motor-dependent (but not myosin light chain kinase-dependent) epithelial barrier
155 rge molecule permeability but did not affect myosin light chain kinase-induced increases in epithelia
156 at neutrophil transmigration is regulated by myosin light chain kinase-mediated endothelial cell cont
157 on by blocking the nuclear factor-kappaB and myosin light chain kinase-mediated redistribution of the
160 sphorylates MLC2v in cardiomyocytes, cardiac myosin light-chain kinase (cMLCK), yet the role(s) playe
162 egulated the downstream nuclear factor-B and myosin light-chain kinase (MLCK) signalling, and these c
164 mbers, we demonstrated the role of nonmuscle myosin light-chain kinase (nmMYLK) in Tat(1)(-)(7)(2) (1
166 contraction of actin filaments by activating myosin light-chain kinase and myosin II behind the leadi
169 s, including phosphatidylinositol 3-kinases, myosin light-chain kinase, Ras-related C3 botulinum toxi
170 ofibrotic myofibroblast functions, including myosin light-chain kinase-mediated myofibroblast contrac
177 IPF, using phosphorylation of the regulatory myosin light chain (MLC(20)) as a biomarker of in vivo c
178 nd CXCR4, and inhibited Ca(2+) mobilization, myosin light chain (MLC) 2 phosphorylation, and contract
179 ), which modifies the activity of regulatory myosin light chain (MLC) and cofilin by altering their p
180 ive manner and suppressed phosphorylation of myosin light chain (MLC) and CPI-17, but not myosin targ
181 hearts exhibited reduced phosphorylation of myosin light chain (MLC) and focal adhesion kinase (FAK)
182 phosphorylation of intracellular epithelial myosin light chain (MLC) and screened using Caco-2 monol
183 we demonstrate that the non-muscle ~214-kDa myosin light chain (MLC) kinase (nmMLCK) modulates the i
184 part, to a Ca(2+)-independent activation of myosin light chain (MLC) phosphatase by protein kinase G
187 increased smooth muscle stress and decreased myosin light chain (MLC) phosphorylation in vivo, provid
188 of MRP4 expression on cAMP and cGMP levels, myosin light chain (MLC) phosphorylation, actin filament
189 nges in gene expression, actin cytoskeleton, myosin light chain (MLC) phosphorylation, and extracellu
190 uced MLCK1 recruitment as well as downstream myosin light chain (MLC) phosphorylation, barrier loss,
192 gonist-evoked intracellular calcium flux and myosin light chain (MLC) phosphorylation, which are prer
193 ell (VSMC) tone is regulated by the state of myosin light chain (MLC) phosphorylation, which is in tu
195 mulus requires phosphorylation of the 20 kDa myosin light chain (MLC), which activates crossbridge cy
203 esponsible for phosphorylation of regulatory myosin light chain (MLC20), resulting in actin-myosin cr
204 n several cytoskeletal/contractile proteins (myosin light chain MLY2, myosin heavy chain 6, myosin-bi
206 increased expression of Myogenin (MYOG) and Myosin Light Chain (MYL1) in RMS cell lines representati
207 target subunit (MYPT1) and the expression of myosin light chain of myosin II (MLC2), which was identi
209 et subunit of myosin phosphatase with either myosin light chain or HDAC6, a microtubule deacetylase.
210 ssociated with changes in phosphorylation of myosin light chain or of myosin light chain phosphatase
211 bsequent dephosphorylation for relaxation by myosin light chain phosphatase (MLCP) containing regulat
212 ctivation, force and phosphorylation of RLC, myosin light chain phosphatase (MLCP) targeting subunit
213 ulin-dependent myosin light chain kinase and myosin light chain phosphatase (MLCP), which contains a
219 ads to down-regulation of smooth muscle (SM) myosin light chain phosphatase activity, an increase in
220 Ca(2+) sensitivity usually is attributed to myosin light chain phosphatase activity, but findings in
223 lated, phosphorylation of the ROCK substrate myosin light chain phosphatase and subsequently, myosin
225 unts of free Ca(2+)/calmodulin combined with myosin light chain phosphatase inhibition is sufficient
227 nist-induced contractile force, RLC(20), and myosin light chain phosphatase phosphorylation in both i
230 by a GST-MYPT1(654-880) fragment inhibiting myosin light chain phosphatase were antagonized by the a
231 endogenous MYPT1 (the regulatory subunit of myosin light chain phosphatase) at Thr-696/Thr-853 or ac
232 hibitory protein of 17 kDa (CPI-17) inhibits myosin light chain phosphatase, altering the levels of m
234 eral different downstream substrates such as myosin light chain phosphatase, LIM kinase and ezrin/rad
237 and/or the leucine zipper (LZ) domain of the myosin light-chain phosphatase component, myosin-binding
238 lex and allow reevaluation of the role(s) of myosin light-chain phosphatase partner polypeptides in r
239 [p.Cys157Arg]) affecting the same residue of myosin light chain, phosphorylatable, fast skeletal musc
240 etion of either RhoC or MRK causes sustained myosin light chain phosphorylation after LPA stimulation
241 he RhoA/Rho kinase pathway via inhibition of myosin light chain phosphorylation and actin depolymeriz
243 ht chain phosphatase, altering the levels of myosin light chain phosphorylation and Ca(2+) sensitivit
244 ls regulate blood-brain barrier function via myosin light chain phosphorylation and increase in perme
245 s of connexin-50, together with decreases in myosin light chain phosphorylation and the levels of 14-
246 cells was accompanied by RhoA activation and myosin light chain phosphorylation and was reduced by th
250 increased migration was associated with high myosin light chain phosphorylation by PI3K/ERK-dependent
251 active Rho, localization of both RhoGTP and myosin light chain phosphorylation corresponds to Myo9b-
252 ractility, RhoA activation, and constitutive myosin light chain phosphorylation ex vivo compared with
253 ther, overexpression of HIF-1alpha decreased myosin light chain phosphorylation in HIF-1alpha-null SM
254 se of RhoA activity accompanied by augmented myosin light chain phosphorylation in mesenteric arterie
255 diminished Ca(2+)-independent and -dependent myosin light chain phosphorylation otherwise increased b
258 ay activates phospholipase Cbeta and induces myosin light chain phosphorylation to enhance actomyosin
261 is required for cell spreading on collagen, myosin light chain phosphorylation, and focal adhesion m
263 companied by inhibition of RhoA activity and myosin light chain phosphorylation, as well as decreased
264 lcium, and decreased actin stress fibers and myosin light chain phosphorylation, without detectable c
265 tudies showed that nmMLCK acted through both myosin light chain phosphorylation-coupled and -uncouple
278 1.38 +/- 0.072-fold (mean+/-SE) increase in myosin light-chain phosphorylation 48 h post-treatment,
280 hat the Net1A isoform predominantly controls myosin light-chain phosphorylation and is required for t
281 ding via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin
283 ivity via decreased intestinal smooth muscle myosin light-chain phosphorylation, leading to slower in
287 d that active RhoA and ROCK effector phospho-myosin light chain (pMLC) were downregulated in endothel
288 ects PIP5K1C90 and subsequent phosphorylated myosin light chain polarization, and this polarization s
290 raction force microscopy, and phosphorylated myosin light chain quantity and actin fiber colocalizati
293 t chain phosphatase activity, an increase in myosin light chain (RLC(20)) phosphorylation and force.
294 , invertebrate tropomyosin, arginine kinase, myosin light chain, sarcoplasmic calcium-binding protein
295 e inhibition studies also implicated several myosin light chain sequences located near HC796-835 as p
296 MKII) to myosin light chain kinase (MLCK) to myosin light chain, the last of which controls the contr
297 Both filamentous actin and phosphorylated myosin light chain were enriched at the apical surface o
298 ted contraction (via ROCK phosphorylation of myosin light chain), which are coupled to ECM signaling
299 f Rho kinase activity and phosphorylation of myosin light chain, which induces airway smooth muscle c
300 evels and lower expression of phosphorylated myosin light chain, which is essential for vascular smoo