ライフサイエンスコーパス: myosin VI

1 toinhibition, promoting its interaction with myosin VI.

2 of coordination between the heads of dimeric myosin VI.

3 ctural plasticity during force generation by myosin VI.

4 o binding normally regulates dimerization of myosin VI.

5 al dimerization sequences within full-length myosin VI.

6 m generates an extension of the lever arm of myosin VI.

7 l or apical cargo, however, does not involve myosin VI.

8 on that hinders binding of both PlexinD1 and myosin VI.

9 e of the presumed poststroke conformation of myosin VI.

10 a testis-specific light chain of Drosophila myosin VI.

11 h differs from Kinesin-1 and is more akin to myosin VI.

12 P hydrolysis mechanism and motor function of myosin VI.

13 s waltzer mutant mice, which fail to express myosin VI.

14 ver dynamics and the monomer/dimer nature of myosin VI.

15 identify the binding partners of Drosophila myosin VI.

16 the extension by altering the strain path in myosin VI.

17 tor of 2,500 for a bipartite binding site on myosin-VI.

18 ated by binding of the coiled-coil domain to myosin-VI.

19 the light-chain domain of individual dimeric myosin VIs.

20 We apply our nanospring to human myosin VI, a mechanosensory motor protein, and demonstra

21 In this study, we found that myosin VI, a motor protein that regulates border cell mi

22 Myosin VI, a ubiquitously expressed unconventional myosi

23 er development, have consistently shown that myosin VI, a unique actin-based motor, is upregulated in

24 abundantly expressed in the testis and like myosin VI, accumulates on these cones.

25 New work shows that the motor protein myosin VI, acting through vinculin, plays a key role in

26 native targeting and activation mechanism of myosin VI, allowing direct inferences on myosin VI funct

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

28 RF) microscopy during processive motility of myosin VI along actin.

29 Myosin VI, an actin-dependent, minus-end directed mechan

30 Further, myosin VI and Acam co-immunoprecipitate from the testis

31 ation), as demonstrated by the colabeling of myosin VI and BrdU.

32 her supporting the model demonstrate that 1) myosin VI and GIPC1 interactions do not require a mediat

33 mation is characteristic of the single IQ of myosin VI and is common throughout the myosin superfamil

34 This study examined the changes of myosin VI and myosin VIIa, two unconventional myosins th

35 We show that myosin VI and Rab8 colocalize around the Golgi complex a

36 for intracellular interactions of GIPC1 with myosin VI and recruitment of overexpressed myosin VI to

37 artner Dab2 and is identical for full-length myosin VI and the cargo-binding tail region.

38 We identified a novel interaction between myosin VI and the GLUT1 transporter binding protein GLUT

39 CFTR co-localized with alpha-AP-2, Dab2, and myosin VI and was identified in a complex with all three

40 o the place where a large insert is found in myosin VI and where several cardiomyopathy mutations hav

41 Single molecule experiments indicate that myosin-VI and myosin-V are processive molecular motors,

42 After 48 h, those SCs expressed myosins VI and VIIA, and by 72 h, they developed hair bu

43 , as a force transducer in the mechanoenzyme myosin VI, and as a flexible spacer in the Kelch-motif-c

44 icrotubule-associated protein Cornetto bound myosin VI, and we demonstrated a role for both in secret

45 alternative clathrin-adaptor Dab2, dynamin, myosin-VI, and actin are involved in the internalization

46 in VEGFR2 intracellular trafficking requires myosin-VI, and myosin-VI knockout in mice or knockdown i

47 We also found that AP-2 interacts with myosin VI, another otoferlin binding partner important f

48 The contractile and enzymatic activities of myosin VI are regulated by calcium binding to associated

49 Mutations in the reverse-direction myosin, myosin VI, are associated with deafness in humans and mi

50 ography, the authors identified Munc18-1 and myosin VI as interacting partners for CaBP5.

51 Using expression microarrays, we identified myosin VI as one of the top genes that demonstrated canc

52 , a population of supporting cells expressed myosin VI at 78 hours after gentamicin treatment and myo

53 entified optineurin as a binding partner for myosin VI at the Golgi complex and confirmed this intera

54 e phosphatase receptor Q, normally linked to myosin VI at the tapered base of stereocilia, was maldis

55 Furthermore, we show that knockdown of myosin VI attenuates activation of p53 and impairs Golgi

56 s do not require a mediating protein; 2) the myosin VI binding domain in GIPC1 is necessary for intra

57 s study refines the model by identifying two myosin VI binding domains in the GIPC1 C terminus, assig

58 us, assigning respective oligomerization and myosin VI binding functions to separate N- and C-termina

59 This half-life is shared by the myosin VI-binding partner Dab2 and is identical for full

60 f Disabled-2 (Dab2), a tumour suppressor and myosin VI-binding partner, inhibits recruitment of myosi

61 or protein of myosin VI, optineurin, and the myosin VI-binding segment from a monomeric cargo adaptor

62 This is the first demonstration that myosin VI binds lipid membranes.

63 Our data also demonstrate that myosin VI binds to the cone front using its motor domain

64 stological features continued to overexpress myosin VI but to a lesser extent.

65 f the interactions among PlexinD1, GIPCs and myosin VI by a series of crystal structures of these pro

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

67 We propose that myosin VI, by removing key molecules from developing hai

68 erse directionality and large powerstroke of myosin VI can be attributed to unusual properties of a s

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

70 n) minus end-directed unconventional myosin, myosin VI, cause hereditary deafness in mice (Snell's wa

71 Myosin VI challenges the prevailing theory of how myosin

72 Dab2 (Disabled 2) is the binding partner for myosin VI, clathrin, and alpha-AP-2 and directs endocyto

73 away from the plasma membrane via a synectin-myosin-VI complex.

74 tion of GIPC1 with such structures; 3) GIPC1/myosin VI complexes coordinately move within cellular ex

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

76 large (-)-end-directed stroke of a monomeric myosin VI construct.

77 arm, we have generated a series of truncated myosin VI constructs and characterized the size and dire

78 TP concentration-dependent processivities of myosin VI constructs containing either native or artific

79 In this study we investigate whether myosin VI contributes to mechano-electrical transduction

80 The underlying motion of the myosin VI converter domain must therefore differ substan

81 an unexpected change in conformation of the myosin VI converter domain, essential for twisting the l

82 d to determine whether the actin-based motor myosin VI coordinately retracts with NHE3 in response to

83 ibed kinetics, this allows us to explain how myosin VI coordinates its heads processively while maint

84 ation of p53, and consequently, knockdown of myosin VI de-sensitizes MCF7 cells to DNA damage-induced

85 A myosin VI deafness mutation, D179Y, which is in the tran

86 In acute hypertension, myosin VI decreased in z1 (from 20.6 +/- 1.9 to 10.5 +/-

87 of myosin VI enhances, whereas knockdown of myosin VI decreases, DNA damage-induced stabilization of

88 impairs Golgi complex integrity, which makes myosin VI-deficient cells susceptible to apoptosis upon

89 The findings support alpha-AP-2 in directing myosin VI-dependent endocytosis of CFTR and a requiremen

90 genes in resting Th1 cells and released in a myosin VI-dependent manner following activation.

91 Myosin VI depletion increased the same movement paramete

92 Recent experimental work proposed that myosin VI dimerization triggers the unfolding of the pro

93 Maternally provided myosin VI does not account for the survival of myosin VI

94 in-coated structures suggests that wild type myosin VI does not function as a stable dimer, but eithe

95 ching (FRAP) to examine the turnover rate of myosin VI during endocytosis.

96 Finally, we showed that overexpression of myosin VI enhances, whereas knockdown of myosin VI decre

97 o function optimally as a dimer, full-length myosin VI exists as a monomer in isolation.

98 l interfering RNA-mediated downregulation of myosin VI expression results in a significant reduction

99 Depletion of myosin VI expression was also accompanied by global gene

100 ations uncover a novel mechanism mediated by myosin VI for stabilizing long-lived actin structures in

101 h of which can be co-immunoprecipitated with myosin VI from LNCaP cells.

102 Interfering with myosin VI function in PC12 cells reduced the density of

103 of myosin VI, allowing direct inferences on myosin VI function.

104 lmodulin and provide a basis for specialized myosin VI function.

105 The actin-based molecular motor myosin VI functions in the endocytic uptake pathway, bot

106 Here, we demonstrate that myosin VI gating is achieved instead by blocking ATP bin

107 binds to, and activates, the promoter of the myosin VI gene.

108 about how myosin VI is regulated and whether myosin VI has a function in the DNA damage response.

109 In addition, myosin VI has a number of other specialized structural a

110 sence of these adaptor proteins, full-length myosin VI has ATPase properties of a dimer, appears as a

111 Because myosin VI has been shown to facilitate secretory traffic

112 protein secretion, but the overexpression of myosin VI has no major impact on clathrin-mediated endoc

113 Although myosin VI has properties that would allow it to function

114 lever arm hypothesis needs modification, or myosin VI has some unique form of extension of its lever

115 Myosin VI has two light chain binding sites that can bot

116 d-coil sequences, and reports on full-length myosin VI have failed to demonstrate the existence of di

117 We observe force-induced transitions of myosin VI heads from non-adjacent to adjacent binding, w

118 We considered an alternative model in which myosin VI heads sequentially take 60 nm steps whereas th

119 LOVDab also activates myosin VI in an in vitro gliding filament assay.

120 a p53-dependent manner such that the pool of myosin VI in endocytic vesicles, membrane ruffles, and c

121 The absence of myosin VI in fibroblasts derived from the Snell's waltze

122 re binding partners for CFTR and the role of myosin VI in localizing endocytic adaptors in the intest

123 nt endocytosis of CFTR and a requirement for myosin VI in membrane invagination and coated pit format

124 Thus, to understand the role of myosin VI in prostate cancer development, we have charac

125 intenance of Golgi complex integrity and for myosin VI in the p53-dependent prosurvival pathway.

126 pected to produce the pre-powerstroke state, myosin VI in their presence was most similar to the trun

127 othesize that it may alter the regulation of myosin VI in this tissue.

128 y in some tumors, differential regulation of myosin VI in various tumor cells by topoisomerase inhibi

129 hich load may regulate the dual functions of myosin VI in vivo.

130 caused by a mutation in MYO6 (which encodes myosin VI) in one and by noise exposure, suggesting that

131 ase inhibitors dictates whether knockdown of myosin VI inhibits, rather than enhances, the susceptibi

132 GIPCs and myosin VI interact through two distinct interfaces and f

133 Intracellular targeting seems to involve two myosin VI-interacting proteins, GIPC and LMTK2, both of

134 with these peptides, we cannot detect a CaM/myosin VI interaction in the testis.

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

136 sity of both myosins and a redistribution of myosin VI into the stereocilia bundle, concurrent with e

137 Our results suggest that myosin VI is a crucial component in the AP-1B-dependent

138 Myosin VI is a molecular motor implicated in many proces

139 Myosin VI is a molecular motor that is thought to functi

140 Myosin VI is a motor protein that moves toward the minus

141 Myosin VI is a reverse direction actin-based motor capab

142 Myosin VI is an actin motor that moves to the minus end

143 Myosin VI is an actin-based motor that has been implicat

144 We find that myosin VI is an efficient transporter at loads of up to

145 Myosin VI is an unconventional motor protein and functio

146 Myosin VI is an unconventional motor protein with unusua

147 Myosin VI is an unconventional motor protein, and its mu

148 Herein, we demonstrate that full-length myosin VI is capable of forming stable, processive dimer

149 These results support that myosin VI is critical in maintaining the malignant prope

150 triggers dimerization, it would appear that myosin VI is designed to function as a dimer in cells.

151 In the sensory hair cells of the cochlea, myosin VI is expressed in the cell bodies and along the

152 Myosin VI is found in distinct intracellular locations a

153 Myosin VI is found to play a key role in the protein tra

154 In the Drosophila testis, myosin VI is important for maintenance of moving actin s

155 Specifically, we show that myosin VI is induced by p53 and DNA damage in a p53-depe

156 depleted from cells using RNA interference, myosin VI is lost from the Golgi complex, the Golgi is f

157 the leading edge of the actin cones and that myosin VI is necessary for this Acam localization.

158 We show here that complete loss of myosin VI is not lethal in flies and that the previously

159 Myosin VI is proposed to act as both a molecular transpo

160 However, very little is known about how myosin VI is regulated and whether myosin VI has a funct

161 Here, we found that myosin VI is regulated by DNA damage in a p53-dependent

162 show that the intracellular localization of myosin VI is substantially altered by p53 and DNA damage

163 Myosin VI is the only type of myosin motor known to move

164 Myosin VI is thought to function as both a transporter a

165 e, but the endocytic adaptor linking CFTR to myosin VI is unknown.

166 Previously, we found that myosin VI is up-regulated in RKO, LS174T, and H1299 cell

167 Myosin-VI is a dimeric isoform of unconventional myosins

168 Our results suggest that myosin VI kinetics are tuned such that the motor maintai

169 asts derived from the Snell's waltzer mouse (myosin VI knock-out) gives rise to defective clathrin-me

170 Small interference RNA-mediated myosin VI knockdown in the LNCaP human prostate cancer c

171 Myosin VI knockdown selectively impaired a late phase of

172 ificantly recovers arterial morphogenesis in myosin-VI(-/-) knockdown zebrafish and synectin(-/-) mic

173 cellular trafficking requires myosin-VI, and myosin-VI knockout in mice or knockdown in zebrafish phe

174 Using both dimeric myosin V- and myosin VI-labelled nanotubes, we find that neither myosi

175 ing cone movement, whereas overexpression of myosin VI leads to bigger cones with more F-actin.

176 placing calmodulin at Insert 2 will increase myosin VI lever arm flexibility, which may favor the com

177 Swapping the flexible myosin VI lever arm for the relatively rigid myosin V le

178 ecifically, intramolecular strain causes the myosin VI lever arm of the lead head to uncouple from th

179 th high affinity to peptide versions of both myosin VI light chain binding sites.

180 We conclude that Acam and not CaM acts as a myosin VI light chain in the Drosophila testis and hypot

181 cam replaces calmodulin as a tissue-specific myosin VI light chain on the actin cones that mediate D.

182 However in Drosophila, myosin VI loss of function has been thought to be lethal

183 Myosin VI (M6) is specialized for processive motion towa

184 VI redistribution and support the idea that myosin VI may serve as the molecular motor for NHE3 retr

185 We propose that homologous pairing and myosin VI-mediated transcriptional pause release account

186 and simulation to demonstrate that multiple myosin VI molecules can coordinate to efficiently transp

187 However, all dimeric myosin VI molecules so far examined have included non-na

188 rs and initiates dimerization of full-length myosin VI molecules.

189 asure the interhead distance of nearly rigor myosin VI molecules.

190 Based on the ability of myosin VI monomers to dimerize when held in close proxim

191 this bundle unfolds upon dimerization of two myosin VI monomers.

192 he Ca(2)(+)- and CaM-dependent regulation of myosin VI motility and ATP utilization.

193 This supports a model of myosin VI motility in which the lever arm is either mech

194 a and the lamellar edge in S2 cells, whereas myosin VI motility is excluded from the same regions.

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

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

197 m Spudich, on the mechanism of the enigmatic myosin VI motor; and Joe Goldstein, on the function of t

198 alters the conformation and activity of the myosin-VI motor implicated in pivotal steps of these pro

199 We report that tethering multiple myosin VI motors, but not myosin V motors, modifies thei

200 In contrast, tethering myosin VI motors, but not myosin V motors, progressively

201 function to couple vesicle-bound proteins to myosin VI movement.

202 Myosin VI moves processively along actin with a larger s

203 Dimeric myosin VI moves processively hand-over-hand along actin

204 Unusual for this motor family, myosin VI moves toward the minus (pointed) end of actin

205 The molecular motor protein myosin VI moves toward the minus-end of actin filaments

206 Myosin VI moves toward the pointed (minus) end of actin

207 In a myosin VI mutant, the cones do not accumulate F-actin du

208 oacetamide-labeled actin with strongly bound myosin VI (MVI) and to evaluate the effect of MVI-bound

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

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

211 f network components revealed a key role for myosin VI (MYO6) in Salmonella invasion.

212 Myosin VI (Myo6) is a minus end-directed actin-based mot

213 Myosin VI (Myo6) is an actin-based motor protein implica

214 Myosin VI (myo6) is the only actin-based molecular motor

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

216 acting partners: vimentin, actin, myosin Va, myosin VI, myosin X, myosin XIV, kinesin 1, Als2cr4, and

217 Myosin Va (myoV) and myosin VI (myoVI) are processive molecular motors that t

218 In this article the effect of the loss of myosin VI no insert isoform (NoI) on endocytosis in nonp

219 osin VI does not account for the survival of myosin VI null animals.

220 e common to both the large insert isoform of myosin VI on clathrin-coated structures and the no-inser

221 fe of an artificially dimerized construct of myosin VI on clathrin-coated structures suggests that wi

222 light and electron microscopy, we identified myosin VI on Rab5-positive early endosomes, as well as o

223 of constitutively active Rab8-Q67L recruits myosin VI onto Rab8-positive structures.

224 ates that a functional complex consisting of myosin VI, optineurin, and probably the GTPase Rab8 play

225 ing a known dimeric cargo adaptor protein of myosin VI, optineurin, and the myosin VI-binding segment

226 d 4) blocking either GIPC1 interactions with myosin VI or GLUT1 interactions with GIPC1 disrupts norm

227 xpected Mendelian frequency, suggesting that myosin VI participates in processes which contribute to

228 The myosin VI PDZ (postsynaptic density 95, Disk large, Zona

229 Myosin VI plays a role in the maintenance of Golgi morph

230 We find that Acam and myosin VI precisely colocalize at the leading edge of th

231 Additionally, we found that on the myosin VI promoter, the level of acetylated histone H3 w

232 We hypothesize that myosin VI protects the actin cone structure either by cr

233 Myosin VI protein expression in cell lines positively co

234 nstrated the most consistent cancer-specific myosin VI protein overexpression, whereas prostate cance

235 Here, we showed that the levels of myosin VI protein were markedly inhibited in MCF7 and LN

236 We also found that the levels of myosin VI protein were markedly inhibited in MCF7 cells

237 During acute hypertension, myosin VI redistributed from low density apical MV-enric

238 t observation that acute hypertension causes myosin VI redistribution and support the idea that myosi

239 The actin motor myosin VI regulates endocytosis of cystic fibrosis trans

240 sults suggest that in prostate cancer cells, myosin VI regulates protein secretion, but the overexpre

241 fluorescent protein-myosin VI revealed that myosin VI remains bound to F-actin for minutes, suggesti

242 experiments using green fluorescent protein-myosin VI revealed that myosin VI remains bound to F-act

243 Single-headed myosin VI S1 constructs take nonprocessive 12 nm steps,

244 Myosin VI SI thus recruits SGs to the cortical actin net

245 These myosin VI SI-specific effects were prevented by deletion

246 However, this mechanism cannot work for myosin VI, since its lever arm positions are reversed.

247 was selectively rescued by expression of the myosin VI small insert (SI) isoform, which efficiently t

248 Thus, it may be possible to create myosin VI-specific drugs that rescue the function of dea

249 We find that myosin VI stabilizes a branched actin network in actin s

250 ly provide the source of the highly variable myosin VI step size.

251 ackbone that may account for the behavior of myosin VI stepping along actin.

252 he androcam structure and its binding to the myosin VI structural (Insert 2) and regulatory (IQ) ligh

253 lish a Ca(2+)-regulated, calmodulin-mediated myosin VI structural change.

254 The myosin VI structure demonstrates that a unique insert at

255 Recent experiments suggest that the myosin VI structure has an unfolded and flexible region

256 Myosin VI supports movement toward the (-) end of actin

257 We propose that myosin VI supports the acquisition of adaptation by remo

258 d in expansion of the terminal web region in myosin VI((sv/sv)) enterocytes.

259 umulated in this location in Snell's Waltzer myosin VI((sv/sv)) intestine.

260 ing induces a large structural change in the myosin VI tail (31% increase in helicity) and when assoc

261 However, the myosin VI tail fragment had no effect on the recycling o

262 omains, and defining a central region in the myosin VI tail that binds GIPC1.

263 the 36-nm step-size observed in myosin V and myosin VI that corresponds to the actin pseudohelical re

264 hich may favor the compact monomeric form of myosin VI that functions on the actin cones by facilitat

265 We found that in the absence of myosin VI the MET current fails to acquire its character

266 We have studied the shape of myosin VI, the actin minus-end directed motor, by negati

267 n the motor domain and lever arm that allows myosin VI to accommodate the helical position of binding

268 In vivo targeting and recruitment of myosin VI to clathrin-coated structures (CCSs) at the pl

269 nstead, we propose that for the two heads of myosin VI to coordinate their processive movement, the l

270 VI-binding partner, inhibits recruitment of myosin VI to endocytic structures at the plasma membrane

271 o the lead head, which makes it possible for myosin VI to function as a processive transporter as wel

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

273 h myosin VI and recruitment of overexpressed myosin VI to membrane structures, but not for the associ

274 These results show that optineurin links myosin VI to the Golgi complex and plays a central role

275 LOVDab robustly recruits human full-length myosin VI to various organelles in vivo and hinders pero

276 U2OS cells allow for 1 motor class, myosin VI, to move along stress fiber bundles, while mot

277 Surprisingly, we found that the level of myosin VI transcript was slightly increased instead of d

278 However, the levels of myosin VI transcript were decreased only by topoisomeras

279 The results demonstrate that myosin VI turns over dynamically on endocytic structures

280 shows that CaBP5 interacts with Munc18-1 and myosin VI, two proteins involved in the synaptic vesicle

281 mine force generation by single molecules of myosin VI under physiological nucleotide concentrations.

282 Here, we demonstrate a new function of myosin VI using observations of Drosophila spermatid ind

283 Myosin VI walks in a hand-over-hand fashion with an aver

284 By confocal microscopy, myosin VI was detected over the whole length of the MV i

285 In controls, myosin VI was evenly distributed through the five MV zon

286 n assay and mass spectrometry, we found that myosin VI was recruited to SGs in a Ca(2+)-dependent man

287 Protein expression of myosin VI was subsequently analyzed in arrayed prostate

288 The shape of truncated apo myosin VI was very similar to the apo crystal structure,

289 ral model for the redirected power stroke of myosin VI, we have constructed bidirectional myosins thr

290 Furthermore, several molecules of monomeric myosin VI, which are nonprocessive in single molecule as

291 the gene encoding an unconventional myosin, myosin VI, which is present in the hair bundles.

292 Allelic pairing required a nuclear myosin, myosin VI, which is rapidly recruited to the LT/TNF locu

293 Using myosin VI, which moves toward the pointed end of actin f

294 characterization of their interactions with myosin VI will advance our understanding of the roles of

295 ures, understanding the design principles of myosin VI will help guide the study of the functions of

296 e observed that a specific splice isoform of myosin VI with no insert in the tail domain is required

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

298 tin, we compare and contrast the motility of myosin-VI with myosin-V.

299 Combining the measured kinetics of myosin-VI with the elasticity of the light chains, and t

300 core, we attached the myosin V lever arm to myosin VI, with and without the unique insert.