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1 virtually abolished by direct inhibition of myosin light chain kinase.
2 lmodulin-binding domain of the smooth muscle myosin light chain kinase.
3 on T cell beta-integrin function, as well as myosin light chain kinase.
4 on myosin activity and regulated by RhoA and myosin light chain kinase.
5 to phosphorylation of LC20 via activation of myosin light chain kinase.
6 a2+/calmodulin pathway, a known activator of myosin light chain kinase.
7 f p21-activated kinase (Pak), caldesmon, and myosin light chain kinase.
8 istent with an activating phosphorylation by myosin light chain kinase.
9 rylation of RLC by Ca2+/calmodulin-dependent myosin light chain kinase.
10 protein kinase II but not with smooth muscle myosin light chain kinase.
11 altered with regulatory segments from either myosin light chain kinase.
12 calmodulin-binding domain from smooth muscle myosin light chain kinase.
13 (T18A/S19A) that cannot be phosphorylated by myosin light chain kinase.
14 LC20) at the same peptides phosphorylated by myosin light chain kinase.
15 )) at Ser(19) by Ca(2+)/calmodulin-dependent myosin light chain kinase.
16 mplitude and partly by a mechanism involving myosin light chain kinase.
17 ransfecting cells with constitutively active myosin light-chain kinase.
18 20), the CaM-binding domain of smooth muscle myosin light-chain kinase.
19 n observed in the complex of calmodulin with myosin light-chain kinase.
20 um channels and calcium/calmodulin-dependent myosin light-chain kinase.
21 in II heavy chain (MHC) and the long form of myosin light-chain kinase.
22 ng region closely related to the 130-150 kDa myosin light chain kinases.
23 etchin-MLCK that are analogous to vertebrate Myosin light chain kinases.
24 phorylation of its regulatory light chain by myosin light chain kinase A (MLCK-A), an unconventional
25 p-800, Arg-812, and Leu-813 in smooth muscle myosin light chain kinase abrogated calmodulin-dependent
26 ced cell invasion, but not survival requires myosin light chain kinase activation and myosin light ch
27 In turn, IL-1beta increased NF-kappaB and myosin light chain kinase activation in intestinal epith
28 with cGMP-mediated decreases in calcium and myosin light chain kinase activity, could accelerate lig
29 endent myosin light chain phosphorylation by myosin light chain kinase and actin stress fiber formati
30 act conformation adopted by CaM upon binding myosin light chain kinase and CaM-dependent protein kina
31 osphorylated by Ca(2+) /calmodulin-dependent myosin light chain kinase and dephosphorylated by myosin
32 development in ileal smooth muscle depend on myosin light chain kinase and MLCP activities without ch
33 e activities of Ca(2+) /calmodulin-dependent myosin light chain kinase and myosin light chain phospha
34 is determined by the relative activities of myosin light chain kinase and myosin light chain phospha
35 is modulated by the antagonistic activity of myosin light chain kinase and myosin light chain phospha
37 s indicate that Ca(2+)/calmodulin-stimulated myosin light chain kinase and p160 Rho-associated coiled
40 lated through two myosin-signaling pathways, myosin light chain kinase and Rho-associated kinase.
43 lated these recombinant species with cardiac myosin light chain kinase and zipper-interacting protein
44 atalytic cores of skeletal and smooth muscle myosin light chain kinases and Ca2+/calmodulin-dependent
45 contraction of actin filaments by activating myosin light-chain kinase and myosin II behind the leadi
46 relaxation of smooth muscle are regulated by myosin light-chain kinase and myosin phosphatase through
47 to elevated Rho activity, phosphorylation of myosin light chain kinase, and enhanced tensile stress f
48 in kinase C, phosphatidyl inositol-3-kinase, myosin light chain kinase, and intracellular protein tyr
49 RT-PCR analysis of tight junction proteins, myosin light chain kinase, and proinflammatory cytokine
50 nase A, Ca2+/calmodulin-dependent kinase II, myosin light chain kinase, and protein kinase G inhibito
51 iven that inhibition of nonmuscle myosin II, myosin light chain kinase, and Rho kinase all abrogate i
52 density and progressed independently of Rac, myosin light chain kinase, and Rho kinase, suggesting a
53 including methionine sulfoxide reductase A, myosin light chain kinase, and Runt-related transcriptio
55 in action, including Mal2, Akap12, gelsolin, myosin light chain kinase, annexin-2, and Hsp70, manifes
56 e calmodulin-binding domain of smooth muscle myosin light chain kinase are also compared with the CaM
57 y shown that residues 1-142 of smooth muscle myosin light chain kinase are necessary for high-affinit
58 measuring the stabilization of calmodulin by myosin light chain kinase at dramatically higher unfoldi
59 h of these mutations significantly decreased myosin light chain kinase binding to myofilaments in vit
64 The initial rise in contractility required myosin light chain kinase but not Rho-kinase, but both s
65 calmodulin-binding peptide of smooth muscle myosin light chain kinase but not with the calmodulin ki
66 dependent on tumor necrosis factor alpha and myosin light-chain kinase but not interleukin-1beta.
69 The full-length and the C-terminal truncated myosin light chain kinases, but not myosin light chain k
71 nship expected for competitive inhibition of myosin light chain kinase by these drugs and is seen at
72 from IP(3)R that displaces CaM from Trp3, a myosin light chain kinase Ca(2+)/CaM binding peptide tha
73 a peptide corresponding to the smooth muscle myosin light chain kinase calmodulin-binding domain (smM
74 Inhibitors of the classical CAM effectors myosin light chain kinase, CAM-dependent protein kinases
75 dependent on myosin in that an inhibitor of myosin light chain kinase can arrest DRM reorganization
76 ynaptic terminals, I show that inhibitors of myosin light chain kinase can block mobilization of the
78 site to 0.45 mol of phosphate/mol by cardiac myosin light chain kinase (cMLCK) increases Ca(2+) sensi
79 sphorylates MLC2v in cardiomyocytes, cardiac myosin light-chain kinase (cMLCK), yet the role(s) playe
82 is obtained by using a constitutively active Myosin Light Chain Kinase (ctMLCK) to selectively elevat
83 ced by coexpression of constitutively active myosin light chain kinase (ctMLCK), which increases myos
84 elial architecture require a Rho kinase- and myosin light chain kinase-dependent increase in the phos
86 release of both fatty acids was calcium- and myosin light chain kinase-dependent, suggesting that bot
88 Pharmacologic inhibition of myosin II or myosin light chain kinase dramatically reduced spreading
94 terminal regulatory segment of smooth muscle myosin light chain kinase folds back on its catalytic co
95 iac light chain phosphorylation, we cloned a myosin light chain kinase from a human heart and have id
97 econd-messenger protein calmodulin (CaM) and myosin light chain kinase from skeletal muscle (skMLCK)
99 se results define a new and specific role of myosin light chain kinase in cardiac myocytes, which may
100 osphorylated by a dedicated Ca(2+)-dependent myosin light chain kinase in fast skeletal muscle, where
101 very after photobleaching of the full-length myosin light chain kinase in saponin-permeable cells sho
102 n of myosin phosphatase or inhibition of the myosin light-chain kinase in nonmalignant cells could re
103 arization and motility, but treatment with a myosin light chain kinase inhibitor (ML-7) or the actin-
106 Concordantly, treatment of cells with the myosin light chain kinase inhibitor ML-7 or the myosin I
107 in conditioned medium, including serotonin, myosin light chain kinase inhibitor, and phorbol ester.
108 r, blockade of MRLC phosphorylation with the myosin light chain kinase inhibitor, ML-7, or the rho ki
112 fening response was not inhibited by ML-7, a myosin light-chain kinase inhibitor, or BAPTA, an intrac
113 fonyl)-2-methyl-piperazine (H-7), a proposed myosin light-chain kinase inhibitor; and the direct acti
115 lmodulin-binding domain of the smooth muscle myosin light chain kinase is examined using 15N and 2H N
117 n catalyzed by a Ca(2+)/calmodulin-dependent myosin light chain kinase is important in the initiation
118 us, the N terminus and not the C terminus of myosin light chain kinase is necessary for high affinity
119 were mimicked in (+/+) NMJs by inhibitors of myosin light chain kinase, known to affect vesicle mobil
121 Our results also suggest that PKC and MLCK (myosin light chain kinase) may be downstream effectors o
122 at neutrophil transmigration is regulated by myosin light chain kinase-mediated endothelial cell cont
123 ion development at the leading edge requires myosin light chain kinase-mediated myosin II contractili
126 om the CaM binding domain of skeletal muscle myosin light chain kinase (MLCK(579-595)), which contain
127 he well-known, muscle-specific smooth muscle myosin light chain kinase (MLCK) (smMLCK) and skeletal m
128 hains by the catalytic COOH-terminal half of myosin light chain kinase (MLCK) activates myosin II in
129 uce barrier defects that are associated with myosin light chain kinase (MLCK) activation and increase
131 aphase-anaphase transition by Ca2+-dependent myosin light chain kinase (MLCK) activity and is maintai
132 dominantly by Rho kinase in both cell types, myosin light chain kinase (MLCK) also appeared to contro
133 served between CaM and peptides derived from myosin light chain kinase (MLCK) and CaM-dependent kinas
134 on of myosin regulatory light chain (RLC) by myosin light chain kinase (MLCK) and myosin binding prot
136 e activities of Ca(2+) /calmodulin-dependent myosin light chain kinase (MLCK) and myosin light chain
137 ve activities of Ca(2+)-calmodulin-dependent myosin light chain kinase (MLCK) and myosin light chain
139 tivation of the calcium/calmodulin-dependent myosin light chain kinase (MLCK) and regulation of non-m
140 in (RLC) phosphorylation, which is driven by myosin light chain kinase (MLCK) and Rho-associated kina
142 of transgenic mice that express a FRET-based myosin light chain kinase (MLCK) biosensor molecule, we
144 on of an embryonic Ca2+/calmodulin-dependent myosin light chain kinase (MLCK) by blocking the ATP-bin
150 the actin-binding proteins cortactin and EC myosin light chain kinase (MLCK) in mediating this respo
151 transgenic mice expressing calmodulin sensor myosin light chain kinase (MLCK) in smooth muscles, the
154 ocusing on regulatory roles of IFN-gamma and myosin light chain kinase (MLCK) in TW myosin phosphoryl
156 d in the absence or presence of the specific myosin light chain kinase (MLCK) inhibitor ML-7 under bo
157 chronized blebbing cells indicated that only myosin light chain kinase (MLCK) inhibitors decreased bl
158 ABSTRACT: Ca(2+) /calmodulin activation of myosin light chain kinase (MLCK) initiates myosin regula
159 on of myosin regulatory light chain (RLC) by myosin light chain kinase (MLCK) initiates smooth muscle
160 chains (RLC) by Ca(2+)/calmodulin-dependent myosin light chain kinase (MLCK) is a critical step in t
162 stimulated with a proapoptotic agent or when myosin light chain kinase (MLCK) is inhibited pharmacolo
163 at epithelial barrier dysfunction induced by myosin light chain kinase (MLCK) is required for the dev
164 ensor allowing simultaneous determination of myosin light chain kinase (MLCK) localization and its [C
169 , where it bound to its binding motif on the myosin light chain kinase (MLCK) promoter region, leadin
170 9 of the myosin II regulatory light chain by myosin light chain kinase (MLCK) regulates actomyosin co
171 as a module for directing sequestered CaM to myosin light chain kinase (MLCK) through Ca(2+)-dependen
172 pproach used functional genomics analysis of myosin light chain kinase (MLCK) to identify short autoi
173 ulin-dependent protein kinase II (CaMKII) to myosin light chain kinase (MLCK) to myosin light chain,
174 Ca(2+)/calmodulin-dependent endothelial cell myosin light chain kinase (MLCK) triggers actomyosin con
175 ed enhanced activation of the ERK2 substrate myosin light chain kinase (MLCK) upon adhering to fibrin
177 myosin II, Rho-associated kinase (ROCK), and myosin light chain kinase (MLCK) were also recruited to
179 ted by arp2/3 and contractility regulated by myosin light chain kinase (MLCK) were responsible for th
180 The mylk1 gene encodes a 220-kDa nonmuscle myosin light chain kinase (MLCK), a 130-kDa smooth muscl
181 iated response that leads to upregulation of myosin light chain kinase (MLCK), a hallmark of the path
182 reduction in the expression and activity of myosin light chain kinase (MLCK), a primary regulator of
183 , we found that inhibition of myosin ATPase, myosin light chain kinase (MLCK), and the knockout of my
184 between calmodulin (CaM) and skeletal muscle myosin light chain kinase (MLCK), as well as the conform
185 eptide of 26 amino acids derived from muscle myosin light chain kinase (MLCK), binds to calmodulin wi
186 lity pathway involving Rho kinase (ROCK) and myosin light chain kinase (MLCK), culminating in the act
187 aM for its ability to activate smooth muscle myosin light chain kinase (MLCK), one of the best unders
189 increased activity of intestinal epithelial myosin light chain kinase (MLCK), which is the primary m
190 CaM to transiently bind approximately 60% of myosin light chain kinase (MLCK), while a 1.8 ms hw ACT
191 Also, integrin engagement and v-Src induced myosin light chain kinase (MLCK)-dependent phosphorylati
193 erijunctional actomyosin ring contributes to myosin light chain kinase (MLCK)-dependent tight junctio
194 nse to neutrophil activation with a focus on myosin light chain kinase (MLCK)-mediated myosin light c
195 of actin and myosin II that are regulated by myosin light chain kinase (MLCK)-mediated phosphorylatio
206 ght junction (TJ) permeability by activating myosin light chain kinase (MLCK; official name MYLK3) ge
209 osin II (MLC20) by Ca2+/calmodulin-dependent myosin light-chain kinase (MLCK) is essential for initia
210 phorylation of smooth muscle myosin (SMM) by myosin light-chain kinase (MLCK) proposes that MLCK is b
211 egulated the downstream nuclear factor-B and myosin light-chain kinase (MLCK) signalling, and these c
212 rom the amino acid sequence of smooth-muscle myosin light-chain kinase (MLCK) were characterized as i
221 d by TRPC6, in turn, activates the nonmuscle myosin light chain kinase (MYLK), which not only increas
223 nase that controls SMC contractile function (myosin light chain kinase [MYLK]) cause FTAAD, we sequen
224 pression of vinculin, focal adhesion kinase, myosin light chain kinase, myosin heavy chain or myosin
225 in), regulators of the contractile response (myosin light chain kinase, myosin phosphatase target sub
226 he recent identification of cardiac-specific myosin light chain kinase necessary for basal RLC phosph
227 eat consensus sequences in the N terminus of myosin light chain kinase necessary for high-affinity bi
230 mbers, we demonstrated the role of nonmuscle myosin light-chain kinase (nmMYLK) in Tat(1)(-)(7)(2) (1
232 ression of contraction through inhibition of myosin light chain kinase normalized the effects of subs
233 his gene, which has been designated Obscurin-myosin light chain kinase (Obscurin-MLCK), would be pred
234 een (Ca(2+))4-calmodulin and skeletal muscle myosin light chain kinase or a peptide containing its co
236 st, exposure to ML-9 or KN-62, inhibitors of myosin light chain kinase or Ca2+-calmodulin-dependent p
237 either the catalytic core of skeletal muscle myosin light chain kinase or Ca2+/calmodulin-dependent p
238 proteins similar to recombinant full-length myosin light chain kinase or enzyme purified from smooth
239 ented cytoskeletal defects, while inhibiting myosin light chain kinase or phosphorylation of focal ad
240 nied by an increase in protein expression of myosin light chain kinase (P<0.05) and casein kinase II-
243 hidden and unphosphorylated; on activation, myosin light chain kinase phosphorylates the monophospho
244 inal extension (Dmlc2(Delta2-46)), disrupted myosin light chain kinase phosphorylation sites (Dmlc2(S
245 ced stress fiber assembly, and inhibitors of myosin light chain kinase prevented this response but di
246 gion also shows 29, 25 and 29% identify with myosin light-chain kinase, protein kinase C, and cAMP-de
248 tebrate smooth muscle and nonmuscle forms of myosin light chain kinase, provides insight into the str
250 s, including phosphatidylinositol 3-kinases, myosin light-chain kinase, Ras-related C3 botulinum toxi
253 rough RhoA GTPase, Rho-associated kinase, or myosin light chain kinase restored stiffness-dependent s
257 tive fragment of the monomeric smooth muscle myosin light chain kinase (smMLCK) (residues 472-972), w
258 investigated the regulation of smooth muscle myosin light chain kinase (smMLCK) by using spontaneousl
261 ene that encodes nonmuscle and smooth muscle myosin light chain kinase (smMLCK) isoforms and regulate
262 22) repeats in the promoter of smooth muscle myosin light chain kinase (smMLCK), a key regulator of v
265 modulin binding site of rabbit smooth muscle myosin light chain kinase (smMLCKp) was studied using is
266 e calmodulin-binding domain of smooth muscle myosin light chain kinase (smMLCKp) with calcium-saturat
267 tractile proteins alpha-smooth muscle actin, myosin light chain kinase, smooth muscle myosin heavy ch
268 rotein kinase inhibitor staurosporine or the myosin light chain kinase-specific inhibitor KT5926 stop
270 ted to overexpress Ca2+/calmodulin-dependent myosin light chain kinase specifically in cardiomyocytes
273 ends on cytoskeletal function; inhibition of myosin light chain kinase suppressed wave activity.
274 a peptide corresponding to the smooth muscle myosin light chain kinase target were carried out at 295
275 ytosis, and localized phosphorylation of the myosin light chain kinase, thereby impinging on the acto
276 el-bearing vesicles with the plasmalemma and myosin light chain kinase to regulate centripetal transp
277 n the sequence linking the catalytic core of myosin light chain kinase to the calmodulin-binding sequ
278 her assays: binding of fluorescently labeled myosin light chain kinases to actin-containing stress fi
279 m1a), expressed specifically in the MHB, and myosin light chain kinase together mediate MHBC cell len
280 runcated myosin light chain kinases, but not myosin light chain kinases truncated at the N terminus o
282 P-dependent protein kinase and smooth muscle myosin light chain kinase undergo interactions with the
283 tes by the catalytic core of skeletal muscle myosin light chain kinase was altered with the regulator
284 he kinase, the polypeptide backbone chain of myosin light chain kinase was cleaved by genetic means t
286 titutively active mutants of RhoA GTPase and myosin light chain kinase, we show that varying the expr
287 tyrosine kinases, protein kinase C, and the myosin light chain kinase were ineffective in blocking t
288 initiation required proliferation, Rac, and myosin light-chain kinase, whereas repolarization to a b
289 yosin II activity is regulated by the enzyme myosin light chain kinase, which activates myosin II by
290 enic process and that targeted inhibition of myosin light chain kinase, which affects this cytoskelet
291 xperiment, a calmodulin-binding peptide from myosin light chain kinase, which has no direct interacti
292 Colonic inflammation suppresses nuclear myosin light chain kinase, which increases the unphospho
293 sidues 2-8 (DeltaNCaM) binds skeletal muscle myosin light chain kinase with high affinity but fails t
296 MT movement was suppressed by inhibition of myosin light chain kinase with ML7 or by a peptide inhib
298 nhibition of actin polymerization as well as myosin light chain kinase with the drug ML7 limited both
299 transport during CR formation, we inhibited myosin light-chain kinase with ML7 and myosin II ATPase
300 hemical species that can bind actin, such as myosin light-chain kinase, with the contractile model le
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