ライフサイエンスコーパス: myosin

1 t OM stabilizes the pre-powerstroke state of myosin.

2 l formation, and extensive polymerization of myosin.

3 eavage furrow in response to the spindle and myosin.

4 way rather than through direct inhibition of myosin.

5 le phenotype induced by this HCM mutation in myosin.

6 pendent and distinct from the function of SM myosin.

7 However, myosin-1, alpha-actin and myosin-4 proteins were the bio

8 d C1q, and the expression of their receptor, myosin 18A.

9 r association with the actomyosin components myosin 1b, actin and the actin nucleation complex Arp2/3

10 revealed that a large fraction of NM-II and myosin-1c molecules fail to fold in the absence of UNC-4

11 We identified myosin-1E (MYO1E), an actin-dependent molecular motor, t

12 r activation by F-actin vary greatly between myosin-2 isoforms.

13 tionarily conserved lysine-265 (K265) of the myosin-2 motor from Dictyostelium discoideum (Dd) is pro

14 ay helix, and the lever, abolishes nonmuscle myosin-2 specific kinetic signatures.

15 However, myosin-1, alpha-actin and myosin-4 proteins were the biomarkers that underwent the

16 port involving cooperation of kinesin-1 with myosin-5 and can move away from the apex powered by dyne

17 Myosin-5B is a ubiquitous molecular motor that transport

18 Myosin-5B malfunction causes the congenital enteropathy

19 Here we describe the interaction of myosin-5B with F-actin, nucleotides, and the pyrazolopyr

20 serve reciprocal rearrangements in actin and myosin accompanying the transition between these states,

21 In many cases, folding is associated with myosin accumulation at the apical surface of epithelial

22 rea) and unloaded shortening velocity; (iii) myosin/actin ratio and myosin content in individual musc

23 YLK encodes an important kinase required for myosin activation and subsequent interaction with actin

24 motors.Omecamtiv mecarbil (OM) is a cardiac myosin activator that is currently in clinical trials fo

25 novel mechanisms of action, such as cardiac myosin activators, are under investigation for patients

26 al feedback among the actin retrograde flow, myosin activity, and substrate adhesion gives rise to va

27 y, spacing, and orientation are regulated by myosin activity.

28 racterized myosin-binding proteins, putative myosin adaptors that belong to two unrelated families, w

29 r myofibrillar integrity, and the consequent myosin aggregation.

30 Both myosin and anillin assemble into dynamic rho-dependent c

31 bil (OM) specifically targets cardiac muscle myosin and is known to enhance cardiac muscle performanc

32 tions require the molecular coupling between myosin and junctions and apical relaxation of neighborin

33 ribute to such alterations more than loss of myosin and other muscle protein content.

34 rs, as well as cytoskeletal cross-linking by myosins and nonmotor cross-linkers, are thought to promo

35 ring including filamentous actin (F-actin), myosin, and septins and in forming the subsequent midbod

36 how that BS inhibits contractility and actin-myosin ATPase by stabilizing the OFF state of the thick

37 alcium concentration by disrupting the actin-myosin ATPase pathway.

38 Further complicating the process, myosin binding accelerates the attachment rate of neighb

39 shift away from the blocked state, allowing myosin binding and activity in the absence of Ca(2+).

40 eparately determined the distance over which myosin binding increases the attachment rate of neighbor

41 thm missed a pathogenic 18 bp duplication in myosin binding protein C (MYBPC3) because of low coverag

42 mooth muscle contains significant amounts of myosin binding subunit 85 (MBS85), another myosin phosph

43 Mavacamten also decreased the rate of myosin binding to actin in the ADP-bound state and the A

44 with augmented steric-interference of actin-myosin binding.

45 Cardiac myosin-binding protein C (cMyC) is a cardiac-restricted

46 MYBPC3, encoding cMyBP-C (cardiac myosin-binding protein C), is the most frequently mutate

47 MYBPC3, encoding beta-myosin heavy chain and myosin-binding protein C, respectively, are the 2 most c

48 drugs and in cells expressing low levels of myosin-binding protein C.

49 We identify previously uncharacterized myosin-binding proteins, putative myosin adaptors that b

50 ly stimulates local recruitment of actin and myosin but also increased traction forces that rapidly p

51 ompressing force generated by a tissue-level myosin cable contributes to SG invagination.

52 at mavacamten acts on multiple stages of the myosin chemomechanical cycle.

53 ariety of coiled-coil protein fragments from myosin, chemotaxis receptor, vimentin, fibrin, and pheny

54 at if average lengths of actin filaments and myosin clusters are similar, then the proposed microscop

55 ening velocity; (iii) myosin/actin ratio and myosin content in individual muscle fibres were not alte

56 xplore minimal free-boundary models of actin-myosin contractility consisting of the force-balance and

57 dhesion strength, actin polymerization rate, myosin contractility, and the integrity of the putative

58 including F-actin flow, the contribution of myosin contraction, and actin polymerization at bundles'

59 processes: mechanical activity of the actin-myosin cortex and biochemical activity of partitioning-d

60 The NM myosin cross-bridge cycling inhibitor blebbistatin suppr

61 lic function in vivo by directly binding the myosin cross-bridges (XBs) in the sarcomere.

62 mble are determined by the average number of myosin cross-bridges.

63 ll-cell junctions links the contractile acto-myosin cytoskeletons of adjacent cells, serving as a ten

64 of Fat leads to accumulation of the atypical myosin Dachs at the apical junctional region, which in t

65 bcellular localization of the unconventional myosin Dachs on the distal side of cells (nearest the ce

66 less parameter combinations, which represent myosin-dependent contractility, a characteristic viscosi

67 ses phospho-Myosin, followed by Pkn-mediated Myosin downregulation, possibly through Rok inhibition.

68 Moreover, the phase boundary allowed myosin driven actin filament rearrangements to actively

69 on, in this issue, Simoes et al. reveal that myosin-driven anisotropic junction loss and apical const

70 We propose that OM increases the myosin duty ratio, which results in enhanced calcium sen

71 We propose that the modulation of cortical myosin dynamics is part of the cellular response trigger

72 cell elongation and demonstrate the role of myosin efflux in the second phase.

73 This myosin efflux is a novel feature of cytokinesis and its

74 en (i.e. the velocity of sliding between the myosin filament and the actin filament under zero load,

75 e NM myosin regulatory light chain (RLC), NM myosin filament assembly and contraction, although it di

76 1943A, in SM tissues inhibits ACh-induced NM myosin filament assembly and SM contraction, and also in

77 myosin heavy chain on Ser1943 and causes NM myosin filament assembly at the SM cell cortex.

78 Stimulation with ACh caused NM myosin filament assembly, as assessed by a Triton solubi

79 ting NM myosin Ser1943 phosphorylation or NM myosin filament assembly.

80 of the actin filament is maximal, while the myosin filament is in the OFF state characterized by mos

81 ms after the start of stimulation, when the myosin filament is still in the OFF state.

82 we propose that spatiotemporally controlled Myosin flows in conjunction with spindle positioning and

83 gest that apical Rok first increases phospho-Myosin, followed by Pkn-mediated Myosin downregulation,

84 Sequence similarities with tropomyosin and myosin from mollusks were detected.

85 nts that allows the head or motor domains of myosin from the thick filaments to bind to them and indu

86 arches of the spine suggesting that loss of myosin function in these muscles contribute to the disea

87 ense mutant myo2-E1 [4], concluded that each myosin has distinct functions and proposed that Myp2p pl

88 the OFF state of the thick filament in which myosin head domains are more parallel to the filament ax

89 racterized by helical packing of most of the myosin head or motor domains on the thick filament surfa

90 hydrolysis, although a small fraction of the myosin heads are constitutively ON.

91 availability of the majority fraction of the myosin heads for contraction is controlled in part by th

92 However, OM also traps a population of myosin heads in a weak actin affinity state with slow pr

93 ally due to drag forces from weakly attached myosin heads.

94 where Tpm shields actin from the binding of myosin heads.

95 he interaction between CBFbeta-smooth muscle myosin heavy chain (SMMHC; encoded by CBFB-MYH11) and RU

96 s markers such as alpha smooth muscle actin, myosin heavy chain 11, and smooth muscle 22 alpha.

97 In parallel, mRNA expression of myosin heavy chain 7 and natriuretic peptide B is up-reg

98 Elevated myosin heavy chain 7 mRNA expression is detected in left

99 increased heart-to-body weight ratios, alpha myosin heavy chain and cardiac isoprostane levels, sugge

100 MYH7 and MYBPC3, encoding beta-myosin heavy chain and myosin-binding protein C, respect

101 tone marks and did not show up-regulation of myosin heavy chain and myotube formation when grown in d

102 entiation was confirmed by uniform NCAM1 and myosin heavy chain expression.

103 bridge kinetics bat and songbird SFM express myosin heavy chain genes that are evolutionarily and ont

104 sitive lipase, glutathione peroxidase-1, and myosin heavy chain IIa in quadriceps of control mice but

105 tissues stimulates phosphorylation of the NM myosin heavy chain on Ser1943 and causes NM myosin filam

106 h driven by the cardiomyocyte-specific alpha-myosin heavy chain promoter.

107 ons in the beta-cardiac/slow skeletal muscle myosin heavy chain rod.

108 ated NM myosin RLC phosphorylation and by NM myosin heavy chain Ser1943 phosphorylation.

109 des could lower the denaturation of crayfish myosin heavy chain when compared to the control.

110 eversed end-diastolic flow contained reduced myosin heavy chain, smooth muscle actin, and desmin, and

111 with actin and its C-terminal lobe with the myosin heavy chain.

112 n-2 slow and troponin T and carbonylation of myosin heavy chains.

113 Remarkably, we discovered that the myosin I protein in fission yeast, Myo1, which is requir

114 on promoting factors Wsp1p (WASp) and Myo1p (myosin-I) define two independent pathways that recruit A

115 alysis highlights that the strong binding of myosin Ic to actin is dominated by the ADP state for sma

116 ize to anisotropic features under non-muscle myosin II (MII) inhibition, despite MII ordinarily being

117 odelling requires the activity of non-muscle myosin II (MyoII) in the interphasic cells neighbouring

118 formation has been correlated with nonmuscle myosin II (NM-II) activity.

119 Nonmuscle myosin II (NM-II) is an important motor protein involved

120 However, the mechanisms by which nonmuscle myosin II (NM-II) is recruited to those structures and a

121 Nonmuscle myosin II (NMII) is uniquely responsible for cell contra

122 ll shape changes are controlled by nonmuscle myosin II (NMII) motor proteins, which are tightly regul

123 we have investigated the role of non-muscle myosin II (nmy-2) in these asymmetric divisions.

124 le in cell division among protists that lack myosin II and additionally implicate the broad use of me

125 These MTs suppress Rho activation, nonmuscle myosin II bipolar filament assembly, and actin retrograd

126 ue of Science, Shyer et al. (2017) show that myosin II contractility drives the smooth dermal mesench

127 copy indicated that within the CR, actin and myosin II filaments were organized into tightly packed l

128 ation of Rab35 compartments does not require Myosin II function.

129 n affects the upper 50 kDa sub-domain of the myosin II heavy chain, and cells carrying this lethal mu

130 ular function of non-muscle (NM) isoforms of myosin II in smooth muscle (SM) tissues and their possib

131 results were mimicked by treatment with the myosin II inhibitor blebbistatin.

132 Myosin II is a key component of the actomyosin ring, alt

133 clude that the assembly and activation of NM myosin II is regulated during contractile stimulation of

134 sphorylation of eNOS(pThr497) and the 20 kDa myosin II light chains.

135 stiffness by simultaneous drug inhibition of myosin II motors and integrin-mediated adhesions.

136 ng shear stress and inhibition of non-muscle myosin II motors, respectively.

137 NM myosin II plays a critical role in airway SM contraction

138 are periodic pulses of junctional and medial myosin II that result in progressively stronger cortical

139 ends on the correct regulation of non-muscle Myosin II, but how this motor protein is spatiotemporall

140 changes are accompanied by reorganization of Myosin II, PIP3, adhesion and active Cdc42.

141 align the Fn matrix by increasing nonmuscle myosin II- and platelet-derived growth factor receptor a

142 s, and the lamellipodium buckles upward in a myosin II-independent manner.

143 intercalation within the cochlea all require myosin II.

144 nase (ROCK) controlled excessive contractile myosin-II activity and not to elevated F-actin polymeriz

145 uclear stiffness resulting from increases in myosin-II and lamin-A,C.

146 formation of podosomes by inhibition of RhoA/myosin-II and promotion of actin core assembly.

147 on compliant 3D ECMs, and these effects are myosin-II dependent.

148 in response to matrix elasticity, knockdown, myosin-II inhibition, and even constricted migration tha

149 and contractions, but this can be blocked by myosin-II inhibition.

150 mbly via the formin FMNL2 and Arp2/3, active myosin-II localization, and integrin-based adhesion dyna

151 ntal data and analytical modelling show that myosin-II-dependent force anisotropy within the lateral

152 d regulation of MT growth dynamics through a myosin-II-dependent signaling pathway.

153 ted regulation of MT growth persistence from myosin-II-mediated regulation of growth persistence spec

154 branching and shape change largely through a myosin-II-mediated reorganization of the actin and micro

155 proposed convergence measure correlates with myosin IIa immuno-localization and is capable to resolve

156 Myosin IIA is also required for this mitochondrial calci

157 a disruption of podosome rosettes caused by myosin-IIA overassembly, and a myosin-independent increa

158 e polarized localization of MCAM, actin, and myosin IIB in a Wnt5a-induced manner.

159 kinase C, a negative regulator of non-muscle myosin IIB.

160 Comparison to the myosin IIC-F-actin rigor complex reveals an almost compl

161 persistent postnatal expression of embryonic myosin in the small muscles joining the neural arches of

162 g, revealing a regulatory role for embryonic myosin in the TGFbeta signaling pathway.

163 that converge to increase phosphorylation of myosin in vascular smooth muscle (VSM) cells, causing pe

164 dentified in the MyTH4-FERM tandems of these myosins in patients suffering visual and hearing impairm

165 ter the predicted mechanical response of the myosin independent of other factors present in a sarcome

166 Disassembly of anillin patches was myosin independent, suggesting that CSNK-1 prevents expu

167 tes caused by myosin-IIA overassembly, and a myosin-independent increase in microtubule acetylation,

168 gs support PIP2's role in modulating a fast, myosin-independent, and Ca(2+)-independent adaptation pr

169 ans zygote, feedback between active RhoA and myosin induces a contractile instability in the cortex.

170 d the inhibitory potential of the allosteric myosin inhibitor pentabromopseudilin (PBP).

171 ack of conservation of residues at the actin-myosin interface despite preservation of the primary seq

172 t a systems level by combining slow and fast myosin isoforms heterogeneously.

173 [1], Zambon et al. reinvestigated how three myosin isoforms participate in the formation and constri

174 Myosin VI (MYO6) is the only myosin known to move toward the minus end of actin filam

175 Moreover, planar polarization of myosin leads to the loss of anterior-posterior junctions

176 h our findings, this suggests that tuning of myosin levels is a conserved mechanism for the stabiliza

177 Myosin light chain (MLC) phosphorylation and MLC kinase

178 Phosphorylated myosin light chain colocalization with actin stress fibe

179 in (RLC) phosphorylation, which is driven by myosin light chain kinase (MLCK) and Rho-associated kina

180 ted by arp2/3 and contractility regulated by myosin light chain kinase (MLCK) were responsible for th

181 Smooth muscle myosin light chain kinase (smMLCK) is a member of a dive

182 lated through two myosin-signaling pathways, myosin light chain kinase and Rho-associated kinase.

183 measuring the stabilization of calmodulin by myosin light chain kinase at dramatically higher unfoldi

184 Intestinal myosin light chain kinase expression decreased in Cd14-d

185 ented cytoskeletal defects, while inhibiting myosin light chain kinase or phosphorylation of focal ad

186 m1a), expressed specifically in the MHB, and myosin light chain kinase together mediate MHBC cell len

187 RT-PCR analysis of tight junction proteins, myosin light chain kinase, and proinflammatory cytokine

188 ssociated with changes in phosphorylation of myosin light chain or of myosin light chain phosphatase

189 phosphorylation of myosin light chain or of myosin light chain phosphatase regulatory subunit.

190 oA, reduced RhoA GTP-loading and reversal of myosin light chain phosphorylation.

191 nuclear reprogramming of the muscle-specific myosin light chain promoter did occur.

192 ted contraction (via ROCK phosphorylation of myosin light chain), which are coupled to ECM signaling

193 , invertebrate tropomyosin, arginine kinase, myosin light chain, sarcoplasmic calcium-binding protein

194 Species-specific peptides derived from myosin light chain-1 and 2 were identified for authentic

195 osphorylation of several proteins, including myosin light chain-2 slow and troponin T and carbonylati

196 In addition, increased phosphorylation of myosin light chain-20, a key regulator of lymphatic musc

197 adjacent to the MTIP-binding site, and both myosin light chains co-located to the glideosome.

198 The small phosphoprotein pCPI-17 inhibits myosin light-chain phosphatase (MLCP).

199 lex and allow reevaluation of the role(s) of myosin light-chain phosphatase partner polypeptides in r

200 ational approach models variations in single myosin molecular structure, system organization, and for

201 Ca(++) on the rate of attachment of a single myosin molecule to a single regulated actin thin filamen

202 In this context myosin molecules operate neither as filaments, as occurs

203 celerates the attachment rate of neighboring myosin molecules, adding a cooperative element to the ac

204 We now show that the differences in myosin monomer concentration of RLC-unphosphorylated and

205 ay aiming to measure interactions between NM myosin monomers.

206 characterize the trajectories of actin in a myosin motility assay, and develop order parameters to m

207 Instead, myosin motor activity was required for the formation of

208 vide insights into structural changes in the myosin motor domain that are triggered upon F-actin bind

209 performance, yet its impact on human cardiac myosin motor function is unclear.

210 he selective release of ADP from a postrigor myosin motor head promotes highly selective and processi

211 e mitochondrial transport is mediated by the myosin motor, Myo2.

212 the rat to measure the axial movement of the myosin motors during the diastole-systole cycle under sa

213 We find that the number of myosin motors leaving the off, ATP hydrolysis-unavailabl

214 n the OFF state characterized by most of the myosin motors lying on helical tracks on the filament su

215 rmal process of intracellular trafficking by myosin motors to forcibly pull fluorescently tagged prot

216 s simulation of networks of actin filaments, myosin motors, and cross-linking proteins at biologicall

217 Specifically, both filament sliding by myosin motors, as well as cytoskeletal cross-linking by

218 cross-linked networks of actin filaments and myosin motors, in which active stress produced by motor

219 Expression of a non-phosphorylatable NM myosin mutant, NM myosin S1943A, in SM tissues inhibits

220 des that include the molecular motor type-II myosin Myo2 and the actin assembly factor formin Cdc12.

221 recursor nodes that include formin Cdc12 and myosin Myo2.

222 sion yeast, cytokinesis involves the type II myosins Myo2p and Myp2p and the type V myosin Myo51p [2]

223 pe II myosins Myo2p and Myp2p and the type V myosin Myo51p [2].

224 nt to regulation of cell cycle genes, muscle myosins, NotchR and Wnt pathway genes, and connective ti

225 CSNK-1 was required for disassembly of both myosin patches and anillin patches.

226 This study identifies myosin phosphatase (MP) holoenzyme consisting of protein

227 f myosin binding subunit 85 (MBS85), another myosin phosphatase targeting subunit (MYPT) family membe

228 One Cyclin A/Cdk1 substrate is myosin phosphatase targeting subunit 1 (MYPT1), and we s

229 Myosins play countless critical roles in the cell, each

230 Glu-469, which affects the mechanics of the myosin power stroke.

231 Myosin-powered force generation and contraction in nonmu

232 ally, and shows that tension is generated by myosin pulling on barbed-end-anchored actin filaments in

233 hat formin Cdc12 is a mechanosensor, whereby myosin pulling on formin-bound actin filaments inhibits

234 of actomyosin stress fibers (SFs) depend on myosin regulatory light chain (RLC) phosphorylation, whi

235 ectively inhibited phosphorylation of the NM myosin regulatory light chain (RLC), NM myosin filament

236 nges of troponin C in the thin filaments and myosin regulatory light chain in the thick filaments all

237 via the phosphorylation of their associated myosin regulatory light chains (MRLCs).

238 particularly for understanding and treating myosin-related diseases and developing approaches for mo

239 with the C-terminal MF domain (CMF) of these myosins remains poorly understood.

240 ion of airway SM tissues by RhoA-mediated NM myosin RLC phosphorylation and by NM myosin heavy chain

241 residues in the heptad repeat of the mutant myosin rods likely alters interactions that stabilize co

242 d phosphate release, the biochemical step in myosin's ATPase cycle associated with force generation a

243 Changing the binding probabilities and myosin's stiffness under a constant force results in a m

244 xercise was repeated for human alpha-cardiac myosin S1 and rabbit fast skeletal muscle S1.

245 DP-bound state and the ADP-release rate from myosin-S1 alone.

246 e release), mavacamten reduced the number of myosin-S1 heads that can interact with the actin thin fi

247 he rate of phosphate release of beta-cardiac myosin-S1, but the molecular mechanism of action of mava

248 Here, using human beta-cardiac myosin-S1, we combine published data from transient and

249 a non-phosphorylatable NM myosin mutant, NM myosin S1943A, in SM tissues inhibits ACh-induced NM myo

250 bly and SM contraction without inhibiting NM myosin Ser1943 phosphorylation or NM myosin filament ass

251 shown to be spatially regulated through two myosin-signaling pathways, myosin light chain kinase and

252 Myosin storage myopathy (MSM) is a congenital skeletal m

253 ge the motor mechanism nor does it influence myosin structure.

254 ubstituted it for the VELC of bovine cardiac myosin subfragment 1.

255 sin VI (MVI) is the only known member of the myosin superfamily that, upon dimerization, walks proces

256 The actin-myosin system, responsible for muscle contraction, is al

257 Myosin systems are shown to have highly nonlinear behavi

258 e motility and includes the MyoA light chain myosin tail domain-interacting protein (MTIP) and severa

259 In addition to the known light chain myosin tail interacting protein (MTIP), we identified an

260 acterized by subsarcolemmal accumulations of myosin that have a hyaline appearance.

261 lective, small-molecule activator of cardiac myosin that is being developed as a potential treatment

262 ed novel small-molecule modulator of cardiac myosin that targets the underlying sarcomere hypercontra

263 termediate filaments, SH3-containing class I myosins, the dual-GEF Trio, and other adaptors and signa

264 ng that the diminished ability of the mutant myosin to form stable thick filaments contributes to the

265 actility consisting of the force-balance and myosin transport equations.

266 of chemical energy to directional motion in myosin V is examined by careful simulations that include

267 In Saccharomyces cerevisiae, the myosin V motor Myo2 binds the vacuole-specific adapter V

268 ead promotes highly selective and processive myosin V.

269 The detailed dynamics of the cycle of myosin-V are explored by simulation approaches, examinin

270 the result of the energetics of the complete myosin-V cycle and is not the source of directional moti

271 cular interactions including the motion of a myosin-V dimer "walking" on an actin fibre, RNA stem-loo

272 t is well known that the Rab27a/melanophilin/myosin Va complex mediates actin-based transport in vivo

273 Intracellular cargo transport relies on myosin Va molecular motor ensembles to travel along the

274 ivity of the actin-based Rab27a/melanophilin/myosin Va transport complex in vitro.

275 d track selection of the Rab27a/melanophilin/myosin Va transport complex.

276 Cardiac beta-myosin variants cause hypertrophic (HCM) or dilated (DCM

277 Myosin VI (MVI) has been found to be overexpressed in ov

278 Myosin VI (MVI) is the only known member of the myosin s

279 Myosin VI (MYO6) is the only myosin known to move toward

280 e created an optogenetic tool for activating myosin VI by fusing the light-sensitive Avena sativa pho

281 V2 domain to a peptide from Dab2 (LOVDab), a myosin VI cargo protein.

282 ay underlies the oligomerization of the GIPC/Myosin VI complexes in solution and cells.

283 tural mechanisms for the GIPC/cargo and GIPC/myosin VI interactions remained unclear.

284 structures of the unique minus-end directed myosin VI motor domain in rigor (4.6 A) and Mg-ADP (5.5

285 docytosis by tethering cargo proteins to the myosin VI motor.

286 es cooperate to activate myosin VI, allowing myosin VI to integrate Ca(2+), lipid, and protein cargo

287 To control myosin VI with this specificity, we created an optogenet

288 tein and lipid cargoes cooperate to activate myosin VI, allowing myosin VI to integrate Ca(2+), lipid

289 ctural plasticity during force generation by myosin VI.

290 toinhibition, promoting its interaction with myosin VI.

291 Given that wild-type mouse myosin VIIa is a slow, high-duty ratio, monomeric motor,

292 However, myosin VIIa is not required for USH2 complex assembly in

293 n the MYO7A gene, encoding the motor protein myosin VIIa, can cause Usher 1B, a deafness/blindness sy

294 stal structure of OM bound to bovine cardiac myosin, which shows that OM stabilizes the pre-powerstro

295 he single molecule movement of a full-length myosin-X construct with leucine zipper at the C-terminal

296 ll)LZ localizes at the tip of filopodia like myosin-X full-length (M10(Full)).

297 he tail (M10(Full)LZ) and the tail-truncated myosin-X without artificial dimerization motif (BAP-M10(

298 Thus, the myosin XI transport network increased in complexity and

299 We investigate the myosin XI-driven transport network in Arabidopsis using

300 wo major groups of nodes in this network are myosins XI and their membrane-anchored receptors (MyoB)