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1 ownstream effectors (phospholipase Cbeta and myosin light chain).
2 cells to injured cardiomyocytes (expressing myosin light chain.
3 in light chain phosphatase and subsequently, myosin light chain.
4 ting Rho kinase activity and phosphorylating myosin light chain.
5 including glycogen synthase kinase-3beta and myosin light chain.
6 um as judged by increased phosphorylation of myosin light chain.
7 he activation of RhoA and phosphorylation of myosin light chain.
9 repression of troponin T3, troponin I2, and myosin light chain 1 between cardiac and slow-twitch ske
10 the actin-tropomyosin and myosin heavy chain-myosin light chain 1 interactions independently correlat
11 ns of OGA with alpha-actin, tropomyosin, and myosin light chain 1, along with reduced OGT and increas
12 itoylation of proteins involved in motility (myosin light chain 1, myosin A), cell morphology (PhIL1)
15 gin: including myofibrillar proteins (titin, myosin light chain 1/3, myomesin 3 and filamin-C), glyco
18 f Mstn selectively in skeletal muscle with a myosin light chain 1f (MLC1f)-cre allele induced robust
19 ly the phosphorylation of the ROCK substrate myosin light chain 2 (MLC2) in intact human breast, lung
20 for PKM2's localization and interaction with myosin light chain 2 (MLC2) in the contractile ring regi
25 myosin heavy chain, myosin light chain, and myosin light chain 2 phosphorylation, which showed no si
26 s whereas the phosphorylation of ventricular myosin light chain 2 was significantly increased, implyi
27 signaling and by the localization of phospho-myosin light chain 2, in turn controlling the changes in
31 decreased phosphorylation of the regulatory myosin light chain-2 (MLC2), a critical cytoskeletal reg
32 by myosin regulatory proteins (for example, myosin light chain-2 [MLC2]) in cardiac muscle remain po
33 osphorylation of several proteins, including myosin light chain-2 slow and troponin T and carbonylati
35 In addition, increased phosphorylation of myosin light chain-20, a key regulator of lymphatic musc
36 ssion of cardiac alpha-actinin, connexin 43, myosin light chain 2a, alpha/beta-myosin heavy chain, an
37 sion, evidenced by reduced expression of the myosin light chain 9 (MYL9) component of myosin II compl
39 ion, which prevents dephosphorylation of the myosin light chain, allowing actomyosin contractility to
40 increased levels of F-actin, phosphorylated myosin light chain, alpha-smooth muscle actin, collagen-
41 y, which is necessary for phosphorylation of myosin light chain and actin myosin-mediated contraction
42 wever, the structural features of this novel myosin light chain and its interaction with its cognate
43 activity to downstream effectors, including myosin light chain and p38(MAPK), and is reversed upon t
44 by means of reducing the phosphorylation of myosin light chain and vascular endothelial (VE)-cadheri
45 evidence, complexes between CaM or CaM-like myosin light chains and IQ motifs are highly diverse and
46 he myofilament proteins, myosin heavy chain, myosin light chains and subunits of the Troponin complex
48 d a detailed analysis of myosin heavy chain, myosin light chain, and myosin light chain 2 phosphoryla
51 hereas F-actin, vinculin, and phosphorylated myosin light chain associated only with the peripheral a
54 ion resulted in decreased phosphorylation of myosin light chains, attenuated smooth muscle contractil
58 e, the complex included GAP40, an additional myosin light chain designated essential light chain (ELC
59 erall morphology, f-actin and phosphorylated myosin light chain distribution, and nuclear position an
62 the 2.3-A-resolution crystal structure of a myosin light chain domain, corresponding to one type fou
64 ble-green-fluorescent-protein (PAGFP)-tagged myosin light chain expressed in zebrafish skeletal muscl
66 alpha-smooth muscle actin and phosphorylated myosin light chain in cortical patches, decreased abunda
70 site to 0.45 mol of phosphate/mol by cardiac myosin light chain kinase (cMLCK) increases Ca(2+) sensi
71 he well-known, muscle-specific smooth muscle myosin light chain kinase (MLCK) (smMLCK) and skeletal m
72 uce barrier defects that are associated with myosin light chain kinase (MLCK) activation and increase
74 dominantly by Rho kinase in both cell types, myosin light chain kinase (MLCK) also appeared to contro
75 on of myosin regulatory light chain (RLC) by myosin light chain kinase (MLCK) and myosin binding prot
77 ve activities of Ca(2+)-calmodulin-dependent myosin light chain kinase (MLCK) and myosin light chain
78 e activities of Ca(2+) /calmodulin-dependent myosin light chain kinase (MLCK) and myosin light chain
79 in (RLC) phosphorylation, which is driven by myosin light chain kinase (MLCK) and Rho-associated kina
83 transgenic mice expressing calmodulin sensor myosin light chain kinase (MLCK) in smooth muscles, the
85 ocusing on regulatory roles of IFN-gamma and myosin light chain kinase (MLCK) in TW myosin phosphoryl
86 d in the absence or presence of the specific myosin light chain kinase (MLCK) inhibitor ML-7 under bo
87 ABSTRACT: Ca(2+) /calmodulin activation of myosin light chain kinase (MLCK) initiates myosin regula
90 , where it bound to its binding motif on the myosin light chain kinase (MLCK) promoter region, leadin
91 ulin-dependent protein kinase II (CaMKII) to myosin light chain kinase (MLCK) to myosin light chain,
92 myosin II, Rho-associated kinase (ROCK), and myosin light chain kinase (MLCK) were also recruited to
93 ted by arp2/3 and contractility regulated by myosin light chain kinase (MLCK) were responsible for th
94 The mylk1 gene encodes a 220-kDa nonmuscle myosin light chain kinase (MLCK), a 130-kDa smooth muscl
95 iated response that leads to upregulation of myosin light chain kinase (MLCK), a hallmark of the path
96 reduction in the expression and activity of myosin light chain kinase (MLCK), a primary regulator of
97 lity pathway involving Rho kinase (ROCK) and myosin light chain kinase (MLCK), culminating in the act
99 erijunctional actomyosin ring contributes to myosin light chain kinase (MLCK)-dependent tight junctio
102 ght junction (TJ) permeability by activating myosin light chain kinase (MLCK; official name MYLK3) ge
105 d by TRPC6, in turn, activates the nonmuscle myosin light chain kinase (MYLK), which not only increas
107 nied by an increase in protein expression of myosin light chain kinase (P<0.05) and casein kinase II-
111 ene that encodes nonmuscle and smooth muscle myosin light chain kinase (smMLCK) isoforms and regulate
112 nase that controls SMC contractile function (myosin light chain kinase [MYLK]) cause FTAAD, we sequen
113 In turn, IL-1beta increased NF-kappaB and myosin light chain kinase activation in intestinal epith
114 endent myosin light chain phosphorylation by myosin light chain kinase and actin stress fiber formati
115 osphorylated by Ca(2+) /calmodulin-dependent myosin light chain kinase and dephosphorylated by myosin
116 development in ileal smooth muscle depend on myosin light chain kinase and MLCP activities without ch
117 e activities of Ca(2+) /calmodulin-dependent myosin light chain kinase and myosin light chain phospha
120 lated through two myosin-signaling pathways, myosin light chain kinase and Rho-associated kinase.
121 lated these recombinant species with cardiac myosin light chain kinase and zipper-interacting protein
122 measuring the stabilization of calmodulin by myosin light chain kinase at dramatically higher unfoldi
127 osphorylated by a dedicated Ca(2+)-dependent myosin light chain kinase in fast skeletal muscle, where
128 Concordantly, treatment of cells with the myosin light chain kinase inhibitor ML-7 or the myosin I
131 he recent identification of cardiac-specific myosin light chain kinase necessary for basal RLC phosph
132 ression of contraction through inhibition of myosin light chain kinase normalized the effects of subs
133 ented cytoskeletal defects, while inhibiting myosin light chain kinase or phosphorylation of focal ad
134 hidden and unphosphorylated; on activation, myosin light chain kinase phosphorylates the monophospho
135 inal extension (Dmlc2(Delta2-46)), disrupted myosin light chain kinase phosphorylation sites (Dmlc2(S
137 rough RhoA GTPase, Rho-associated kinase, or myosin light chain kinase restored stiffness-dependent s
139 m1a), expressed specifically in the MHB, and myosin light chain kinase together mediate MHBC cell len
141 nhibition of actin polymerization as well as myosin light chain kinase with the drug ML7 limited both
142 RT-PCR analysis of tight junction proteins, myosin light chain kinase, and proinflammatory cytokine
143 density and progressed independently of Rac, myosin light chain kinase, and Rho kinase, suggesting a
144 including methionine sulfoxide reductase A, myosin light chain kinase, and Runt-related transcriptio
145 in action, including Mal2, Akap12, gelsolin, myosin light chain kinase, annexin-2, and Hsp70, manifes
146 in), regulators of the contractile response (myosin light chain kinase, myosin phosphatase target sub
147 ytosis, and localized phosphorylation of the myosin light chain kinase, thereby impinging on the acto
148 titutively active mutants of RhoA GTPase and myosin light chain kinase, we show that varying the expr
150 at neutrophil transmigration is regulated by myosin light chain kinase-mediated endothelial cell cont
151 ion development at the leading edge requires myosin light chain kinase-mediated myosin II contractili
154 sphorylates MLC2v in cardiomyocytes, cardiac myosin light-chain kinase (cMLCK), yet the role(s) playe
156 egulated the downstream nuclear factor-B and myosin light-chain kinase (MLCK) signalling, and these c
158 mbers, we demonstrated the role of nonmuscle myosin light-chain kinase (nmMYLK) in Tat(1)(-)(7)(2) (1
159 contraction of actin filaments by activating myosin light-chain kinase and myosin II behind the leadi
161 n of myosin phosphatase or inhibition of the myosin light-chain kinase in nonmalignant cells could re
164 s, including phosphatidylinositol 3-kinases, myosin light-chain kinase, Ras-related C3 botulinum toxi
169 yosin phosphatase (MP) is a key regulator of myosin light chain (LC20) phosphorylation, a process ess
171 IPF, using phosphorylation of the regulatory myosin light chain (MLC(20)) as a biomarker of in vivo c
172 2 demonstrates no requirement for regulatory myosin light chain (MLC(20)) phosphorylation for maximum
173 nd CXCR4, and inhibited Ca(2+) mobilization, myosin light chain (MLC) 2 phosphorylation, and contract
174 ), which modifies the activity of regulatory myosin light chain (MLC) and cofilin by altering their p
175 ive manner and suppressed phosphorylation of myosin light chain (MLC) and CPI-17, but not myosin targ
176 phosphorylation of intracellular epithelial myosin light chain (MLC) and screened using Caco-2 monol
177 we demonstrate that the non-muscle ~214-kDa myosin light chain (MLC) kinase (nmMLCK) modulates the i
178 part, to a Ca(2+)-independent activation of myosin light chain (MLC) phosphatase by protein kinase G
182 increased smooth muscle stress and decreased myosin light chain (MLC) phosphorylation in vivo, provid
183 of MRP4 expression on cAMP and cGMP levels, myosin light chain (MLC) phosphorylation, actin filament
184 nges in gene expression, actin cytoskeleton, myosin light chain (MLC) phosphorylation, and extracellu
186 gonist-evoked intracellular calcium flux and myosin light chain (MLC) phosphorylation, which are prer
187 ell (VSMC) tone is regulated by the state of myosin light chain (MLC) phosphorylation, which is in tu
190 mulus requires phosphorylation of the 20 kDa myosin light chain (MLC), which activates crossbridge cy
192 hat Git2a is required for phosphorylation of myosin light chain (MLC), which regulates myosin II-medi
196 ed using FRET probes, and phosphorylation of myosin light chain (MLC-p), a downstream target of RhoA,
199 esponsible for phosphorylation of regulatory myosin light chain (MLC20), resulting in actin-myosin cr
200 n several cytoskeletal/contractile proteins (myosin light chain MLY2, myosin heavy chain 6, myosin-bi
201 increased expression of Myogenin (MYOG) and Myosin Light Chain (MYL1) in RMS cell lines representati
202 target subunit (MYPT1) and the expression of myosin light chain of myosin II (MLC2), which was identi
204 et subunit of myosin phosphatase with either myosin light chain or HDAC6, a microtubule deacetylase.
205 ssociated with changes in phosphorylation of myosin light chain or of myosin light chain phosphatase
206 t analysis was used to measure the extent of myosin light chain (p-MLC) phosphorylation and ratio of
207 bsequent dephosphorylation for relaxation by myosin light chain phosphatase (MLCP) containing regulat
208 ctivation, force and phosphorylation of RLC, myosin light chain phosphatase (MLCP) targeting subunit
209 ulin-dependent myosin light chain kinase and myosin light chain phosphatase (MLCP), which contains a
216 ads to down-regulation of smooth muscle (SM) myosin light chain phosphatase activity, an increase in
217 Ca(2+) sensitivity usually is attributed to myosin light chain phosphatase activity, but findings in
220 lated, phosphorylation of the ROCK substrate myosin light chain phosphatase and subsequently, myosin
222 unts of free Ca(2+)/calmodulin combined with myosin light chain phosphatase inhibition is sufficient
224 nist-induced contractile force, RLC(20), and myosin light chain phosphatase phosphorylation in both i
228 by a GST-MYPT1(654-880) fragment inhibiting myosin light chain phosphatase were antagonized by the a
229 endogenous MYPT1 (the regulatory subunit of myosin light chain phosphatase) at Thr-696/Thr-853 or ac
230 hibitory protein of 17 kDa (CPI-17) inhibits myosin light chain phosphatase, altering the levels of m
232 eral different downstream substrates such as myosin light chain phosphatase, LIM kinase and ezrin/rad
233 selectively inhibits a specific form of PP1, myosin light chain phosphatase, which transduces multipl
236 and/or the leucine zipper (LZ) domain of the myosin light-chain phosphatase component, myosin-binding
237 lex and allow reevaluation of the role(s) of myosin light-chain phosphatase partner polypeptides in r
238 etion of either RhoC or MRK causes sustained myosin light chain phosphorylation after LPA stimulation
239 he RhoA/Rho kinase pathway via inhibition of myosin light chain phosphorylation and actin depolymeriz
241 ht chain phosphatase, altering the levels of myosin light chain phosphorylation and Ca(2+) sensitivit
242 s of connexin-50, together with decreases in myosin light chain phosphorylation and the levels of 14-
243 cells was accompanied by RhoA activation and myosin light chain phosphorylation and was reduced by th
247 ular signal-regulated kinase (ERK)-dependent myosin light chain phosphorylation by myosin light chain
248 increased migration was associated with high myosin light chain phosphorylation by PI3K/ERK-dependent
249 active Rho, localization of both RhoGTP and myosin light chain phosphorylation corresponds to Myo9b-
250 ractility, RhoA activation, and constitutive myosin light chain phosphorylation ex vivo compared with
251 ther, overexpression of HIF-1alpha decreased myosin light chain phosphorylation in HIF-1alpha-null SM
252 se of RhoA activity accompanied by augmented myosin light chain phosphorylation in mesenteric arterie
253 diminished Ca(2+)-independent and -dependent myosin light chain phosphorylation otherwise increased b
256 ugh the ROCK isoforms both regulate MLCP and myosin light chain phosphorylation through different mec
257 ay activates phospholipase Cbeta and induces myosin light chain phosphorylation to enhance actomyosin
258 ng experiments, we show that CD11b modulates myosin light chain phosphorylation to suppress lateral p
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 n polymerization; however, it did not affect myosin light chain phosphorylation, which is necessary f
265 lcium, and decreased actin stress fibers and myosin light chain phosphorylation, without detectable c
266 tudies showed that nmMLCK acted through both myosin light chain phosphorylation-coupled and -uncouple
280 1.38 +/- 0.072-fold (mean+/-SE) increase in myosin light-chain phosphorylation 48 h post-treatment,
282 hat the Net1A isoform predominantly controls myosin light-chain phosphorylation and is required for t
283 ding via downregulation of RhoA activity and myosin light-chain phosphorylation and triggered F-actin
284 n program that eventually leads to decreased myosin light-chain phosphorylation and, thus, decreased
286 ivity via decreased intestinal smooth muscle myosin light-chain phosphorylation, leading to slower in
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 m microtubules to initiate a RhoA/Rho kinase/myosin light chain signaling pathway that regulates cell
297 MKII) to myosin light chain kinase (MLCK) to myosin light chain, the last of which controls the contr
298 Both filamentous actin and phosphorylated myosin light chain were enriched at the apical surface o
299 ted contraction (via ROCK phosphorylation of myosin light chain), which are coupled to ECM signaling
300 f Rho kinase activity and phosphorylation of myosin light chain, which induces airway smooth muscle c
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