ライフサイエンスコーパス: kinesin

1 is independent of its known interaction with kinesin.

2 PE, a centromere binding protein and mitotic kinesin.

3 which significantly reduces the velocity of kinesin.

4 igin of the weak susceptibility for a single kinesin.

5 ets of its mechanism are distinct from other kinesins.

6 ty) and size ( 40% larger) compared to other kinesins.

7 A from binding to the MT lattice like motile kinesins.

8 e activity of MT-associated proteins such as kinesins.

9 Kinesin 1 transports dynactin to the oocyte posterior, c

10 Kinesin 1 transports oskar mRNA to the oocyte posterior

11 Furthermore, we revealed that kinesin 1 was displaced in fibers of nesprin 1alpha2-kno

12 s in null and rigor mutants of kinesin-3 and kinesin-1 (UncA and KinA, respectively), we demonstrate

13 We further provide evidence that kinesin-1 affects MT detyrosination not through changes

14 to directly observe the stepping behavior of kinesin-1 and -2 family motors with different length nec

15 ilt in the same spirit of our early work for kinesin-1 and Ncd towards physical understanding of its

16 Underlining the importance of the kinesin-1 association, neurons expressing APC lacking ki

17 It concludes by presenting a consensus kinesin-1 chemomechanical that incorporates recent work,

18 Here we show that the heavy chain of kinesin-1 directly interacts with the APC C-terminus, co

19 equires interactions with both kinesin-2 and kinesin-1 for this localisation.

20 pendent trafficking and establish a distinct kinesin-1 function in which a motor is exploited to crea

21 cell bodies into axons, and then Unc-104 and kinesin-1 function together to support fast, highly proc

22 Recently, we have shown that kinesin-1 heavy chain (KHC) can transport one microtubul

23 uced this mutation into the genomic locus of kinesin-1 heavy chain (KHC), generating the Khc(mutA) al

24 ore, a small molecule that in vitro inhibits kinesin-1 interactions with short linear peptide motifs

25 The microtubule motor kinesin-1 interacts via its cargo-binding domain with bo

26 These results demonstrate that MT sliding by kinesin-1 is an essential biological phenomenon required

27 The specific use of kinesin-1 is due to its unique ability to select posttra

28 The plus-end microtubule (MT) motor kinesin-1 is essential for normal development, with key

29 In the absence of cargo, kinesin-1 is found in an autoinhibited conformation.

30 We find that the microtubule-based motor kinesin-1 is recruited to the ER membrane by binding to

31 scovered that propofol inhibits conventional kinesin-1 KIF5B and kinesin-2 KIF3AB and KIF3AC, causing

32 We found that the protein abundance of the kinesin-1 light chain (KLC1) was reduced selectively in

33 ular means of regulating Tau's inhibition of kinesin-1 motility remains unknown.

34 otubule dynamics, and preferentially inhibit kinesin-1 motility.

35 tyrosine 18 reduces 3RS-Tau's inhibition of kinesin-1 motility.

36 understanding control of Tau's inhibition of kinesin-1 motility.

37 n acetylation alone does not directly affect kinesin-1 motility.

38 le of PLD2-generated PA in the regulation of kinesin-1 motor functions and breast cancer metastasis a

39 her nucleocapsids interact with lepidopteran kinesin-1 motor molecules and are potentially carried as

40 icrotubule (MT) motility by surface-tethered kinesin-1 motor proteins has been widely studied, as wel

41 lated and experimental data from GFP-labeled kinesin-1 motors stepping along immobilized microtubules

42 n, force, and torque generated by individual kinesin-1 motors.

43 This is mediated by recruitment of kinesin-1 mRNA and protein within FUS inclusions, leadin

44 Kinesin-1 recruitment to the Slp3/Rab27b effector comple

45 Together, we propose that kinesin-1 slides free cytoplasmic microtubules against c

46 the KASH protein UNC-83, recruits dynein and kinesin-1 to the nuclear surface.

47 For example, kinesin-1 transports cargo in a step-wise manner along m

48 ansfer (smFRET) analyses indicate the NIS of kinesin-1 undergoes similar conformational changes under

49 transport by modifying its interaction with kinesin-1 whereas mitochondrial damage induces Phosphata

50 terograde transport involving cooperation of kinesin-1 with myosin-5 and can move away from the apex

51 cargo engagement affects the balance between kinesin-1's active and inactive conformations and roles

52 nelle-specific cargo adaptors, yet activates kinesin-1's function of controlling microtubule dynamics

53 that mice lacking Kif5b (the heavy chain of kinesin-1) in hematopoietic cells are less sensitive to

54 ires the well-known mitochondrial motor Khc (kinesin-1).

55 This movement is driven by kinesin-1, a major microtubule motor.

56 Kinesin-1, a robust axonal motor, moves cargo less effic

57 Kinesin-1, AC141, and microtubules colocalized predomina

58 KIF5B, the heavy chain of the motor protein kinesin-1, as a new PA-binding protein.

59 We have previously demonstrated that kinesin-1, in addition to its well-established role in o

60 ow that an ensemble of BORC, Arl8, SKIP, and kinesin-1, previously shown to mediate centrifugal trans

61 d Hsp104 disaggregases, or overexpression of kinesin-1, reverses these effects.

62 The identification of this novel kinesin-1-APC interaction highlights the complexity and

63 association, neurons expressing APC lacking kinesin-1-binding domain have shorter axons.

64 w axonal transport speeds; inhibition of the kinesin-1-dynein interaction effectively blocks this pro

65 les are transported throughout the embryo by kinesin-1.

66 monstrate that PI3K-dependent formation of a kinesin-1/Slp3/Rab27b complex is critical for the microt

67 We propose that KLP-18/kinesin-12 and MESP-1 form a complex that functions to s

68 ociated protein, TPX2, targets kinesin-5 and kinesin-12 motors to spindle microtubules.

69 t is not known whether this domain regulates kinesin-12, Kif15.

70 deletion constructs we conclude that 1) the Kinesin-13 class specific neck domain and loop-2 help or

71 TZ components and microtubule elongation by kinesin-13 is required for axoneme formation in male ger

72 s oocyte, we provide novel evidence that the kinesin-13 KLP-7 promotes destabilization of the whole c

73 from the well-described catastrophe factors kinesin-13 MCAK and kinesin-8 Kip3/KIF18A.

74 Misregulation of one target, a kinesin-13 microtubule depolymerase, underlies a major p

75 ur results highlight the general function of kinesin-13 microtubule depolymerases in preventing ectop

76 Kif2a is a member of the Kinesin-13 microtubule depolymerases.

77 duced, the absence of KLP-7 or the mammalian kinesin-13 protein MCAK (KIF2C) also resulted in ectopic

78 Kinesins-13s are members of the kinesin superfamily of m

79 flection fluorescence microscopy that KlpA-a kinesin-14 from Aspergillus nidulans-is a context-depend

80 Human kinesin-14 KIFC1 is unique in that cancer cells with amp

81 eric Kif25, a microtubule minus-end-directed kinesin-14 motor, in preventing premature centrosome sep

82 to antagonize the inward pulling forces from kinesin-14 or dynein.

83 nce is restored when both kinesin-5 Cut7 and kinesin-14 Pkl1 are deleted, restoring spindle bipolarit

84 e with new structures of two closely related kinesin-14 proteins, Ncd and KIFC3, to determine the pot

85 dynein microtubule binding domain or Klp2, a kinesin-14, converts Cut7 from net minus end-directed to

86 tering of disengaged centrioles requires the kinesin-14, HSET.

87 Kinesin-14s are commonly known as nonprocessive minus en

88 icrotubules of the assembling flagellum by a kinesin-15 family member.

89 escribe a novel interaction between KIF17, a kinesin 2 family motor, and septin 9 (SEPT9).

90 ate that APC requires interactions with both kinesin-2 and kinesin-1 for this localisation.

91 17 and heterotrimeric KIF3AB are processive, kinesin-2 family motors that act jointly to carry out an

92 ol inhibits conventional kinesin-1 KIF5B and kinesin-2 KIF3AB and KIF3AC, causing a significant reduc

93 subunit of the functional microtubule-based kinesin-2 KIF3AC motor, an anterograde cargo transporter

94 d NPHP5 interact with the axoneme-associated kinesin-2 motor KIF17 and thus spatially map to the inne

95 By characterizing the motility properties of kinesin-2 motors as a function of load we find that the

96 nd cargoes of intraflagellar transport (IFT) kinesin-2 motors kinesin-II and OSM-3/KIF17 without affe

97 glutamylation to control the velocity of the kinesin-2 OSM-3/KIF17 and kinesin-3 KLP-6 without affect

98 and the kinesin-3 KLP-6, and velocity of the kinesin-2 OSM-3/KIF17, whereas a cell-specific alpha-tub

99 Neither kinesin-2, kinesin-3 nor kinesin-5 promotes foci formati

100 of SVs and EEs in null and rigor mutants of kinesin-3 and kinesin-1 (UncA and KinA, respectively), w

101 Our results highlight the importance of kinesin-3 based axonal transport in synaptic transmissio

102 The kinesin-3 family member KIF1A has been shown to be impor

103 KIF16B is a highly processive kinesin-3 family member that participates in the traffic

104 The kinesin-3 family member Unc-104/KIF1A is required for ax

105 kinesin-II and OSM-3/KIF17 without affecting kinesin-3 KLP-6 motility.

106 he velocity of the kinesin-2 OSM-3/KIF17 and kinesin-3 KLP-6 without affecting the intraflagellar tra

107 ocalization of the TRP channel PKD-2 and the kinesin-3 KLP-6, and velocity of the kinesin-2 OSM-3/KIF

108 to their unique ultrastructure and accessory kinesin-3 motor, CEM cilia are specialized to produce ex

109 Neither kinesin-2, kinesin-3 nor kinesin-5 promotes foci formation or infec

110 Past work showed that Unc-104 (a kinesin-3) is a key anterograde DCV motor.

111 Here, we show that the mammalian kinesin-4 KIF21B is a processive motor that can accumula

112 New work shows that two kinesin-4 motor proteins act to shorten the domain of ov

113 Kinesin-4-mediated shortening of these overlaps at the o

114 Competition assays with human kinesin-5 (Eg5) only partially abrogated this behavior,

115 icrotubule-associated protein, TPX2, targets kinesin-5 and kinesin-12 motors to spindle microtubules.

116 ectional motility mechanism of fission yeast kinesin-5 and provide insight into the function of this

117 ces that ensembles of purified budding yeast kinesin-5 Cin8 produce in microtubule gliding assays in

118 n yeast, force balance is restored when both kinesin-5 Cut7 and kinesin-14 Pkl1 are deleted, restorin

119 During cell division, the mitotic kinesin-5 Eg5 generates most of the force required to se

120 The force production of a bidirectional kinesin-5 has not yet been measured.

121 Accordingly, Kinesin-5 inactivation results in force imbalance leadin

122 Unlike most other kinesins, Cin8, a kinesin-5 motor in Saccharomyces cerevisiae, can move bi

123 However, some fungal kinesin-5 motors are bidirectional.

124 Like other yeast kinesin-5 motors, Cut7 can reverse its stepping directio

125 assembly requires a balance of forces where kinesin-5 produces outward pushing forces to antagonize

126 Neither kinesin-2, kinesin-3 nor kinesin-5 promotes foci formation or infection.

127 hin measured ranges for kinesins (especially kinesin-5 proteins), approximately four motors can bind

128 Members of the kinesin-5 subfamily were initially described as unidirec

129 properties appear to be conserved within the kinesin-5 subfamily.

130 utes to the localization and motility of the kinesin-5, Eg5, but it is not known whether this domain

131 roposals for the reversal mechanism of yeast kinesins-5.

132 ytokinesis, at sites distinct from the other Kinesin-6 family members.

133 called MPHOSPH1 or MPP1) is a member of the Kinesin-6 family, which also includes the better-known m

134 independently of motor activity, except for kinesin-6 Klp9, which is required for anaphase spindle e

135 Here we report the crystal structure of kinesin-6 Zen4 in a nucleotide-free, apo state, with the

136 MKLP2, a kinesin-6, has critical roles during the metaphase-anaph

137 compared to motile kinesins, and enhanced by kinesin-6-specific sequences.

138 on to the central spindle is mediated by Pav/kinesin-6.

139 ndlin is seven times higher than that of Pav/kinesin-6.

140 y extended loop6 insertion characteristic of kinesin-6s is nucleotide-independent and does not contac

141 Despite extensive study, the kinesin-8 depolymerase mechanism remains under debate.

142 ibed catastrophe factors kinesin-13 MCAK and kinesin-8 Kip3/KIF18A.

143 Kinesin-8 motors regulate the size of microtubule struct

144 To better understand the role of kinesin-8 proteins in mitosis, we studied the effects of

145 the effects of deletion of the fission yeast kinesin-8 proteins Klp5 and Klp6 on chromosome movements

146 tubule depolymerization by the budding yeast kinesin-8, Kip3.

147 Kinesin-8/Kip3 uses ATP hydrolysis, like other kinesins,

148 Accounting for the rotational work makes kinesin a highly efficient machine.

149 ighlight compartment-specific differences in kinesin activity that likely reflect specialized tuning

150 led basis of walking by dimeric molecules of kinesin along microtubules has remained unclear, partly

151 explains how structural differences between kinesins alter kinetic rates in the ATPase cycle to prod

152 on of many pre-synaptic components (bassoon, kinesin, among others) is relatively undisturbed althoug

153 cargos are transported along microtubules by kinesin and dynein molecular motors, but how transport i

154 The motor proteins kinesin and dynein transport organelles, mRNA, proteins,

155 the events are necessary in the motility of kinesin and for the maintenance of processivity.

156 However, the identity of the kinesin and mechanism of cargo binding were not known.

157 interaction between septins and a nonmitotic kinesin and suggest that SEPT9 modulates the interaction

158 recruits Akap450 to the NE independently of kinesin and that Akap450, but not other centrosomal prot

159 the MT surface is altered compared to motile kinesins, and enhanced by kinesin-6-specific sequences.

160 In fed state, ARF1 and kinesin appear on LDs, consequently transporting LDs to

161 Cytoplasmic dynein and kinesin are both microtubule-based molecular motors but

162 Furthermore, we show that two load-bearing kinesins are incapable of equally sharing the load unles

163 es a framework for understanding how diverse kinesins are tuned for their specific cellular roles.

164 We found that electrostatics help guide kinesins as they walk: N-kinesins towards the plus-end,

165 lengths and stabilize microtubules, inhibit kinesin-based axonal transport, but not dynein-based tra

166 We found that microtubule defects influence kinesin-based transport in vitro.

167 st mechanistic insight to how defects impact kinesin-based transport.

168 s and provides a greater number of available kinesin binding sites.

169 structures of microtubule-attached, dimeric kinesin bound to an ATP analog.

170 idence has emerged that multiple anterograde kinesins can contribute to some transport processes.

171 ction in the distances that these processive kinesins can travel.

172 However, Kif15, another mitotic kinesin, can replace Eg5 function, permitting mammalian

173 al importance to the diversity of tasks that kinesins carry out in cells, no existing quantitative mo

174 Unlike most other kinesins, Cin8, a kinesin-5 motor in Saccharomyces cerev

175 by creating a coarse-grained model of the MT-kinesin complex, which reproduces the measured stall for

176 The former structure reveals a novel kinesin conformation that revises the current understand

177 studies provide new insight into how diverse kinesins contribute to spatial microtubule organization

178 These results reveal a novel kinesin-dependent mechanism controlling the MT cytoskele

179 es to redirect Rab7-containing vesicles to a kinesin-dependent trafficking mode promoting virion secr

180 cell-permeable, 23-amino acid peptide termed kinesin-derived angiogenesis inhibitor (KAI) not only pr

181 Kinesin-derived angiogenesis inhibitor also inhibits VEG

182 We find that under these conditions, the kinesin dimer can attach to the microtubule with either

183 ines, and our findings have implications for kinesin-driven cellular processes.

184 ganelles, or melanosomes, are transported by kinesin, dynein, and myosin motors.

185 pendent of microtubules and presumably their kinesin/dynein motors.

186 ase kinetics fell within measured ranges for kinesins (especially kinesin-5 proteins), approximately

187 red for the localization and function of two kinesins essential for cytokinesis, Mklp2 and Kif14.

188 nce of the weak susceptibility, the trailing kinesin faces the challenge of catching up to the leadin

189 the opposite side, a kinetoplastid-specific kinesin facilitates attachment of the junction to the mi

190 subjects, EoE associated strongly with IL-4/kinesin family member 3A (IL4/KIF3A) (P = 2.8 x 10(-6);

191 cible Cre/Lox recombination system to delete kinesin family member 3A (Kif3a), a gene that is essenti

192 KIF3A, the gene encoding kinesin family member 3A, is a susceptibility gene locus

193 Missense mutations in kinesin family member 5A (KIF5A) cause spastic paraplegi

194 The kinesin family plus-end motor KIF13B transports VEGFR2 t

195 ctivates UNC-104/KIF1A, the axonal-transport kinesin for SVPs in C. elegans.

196 nesin-8/Kip3 uses ATP hydrolysis, like other kinesins, for stepping on the microtubule lattice, but a

197 sting, insulin is lowered to remove ARF1 and kinesin from LDs, thus down-regulating LD transport and

198 direct link between microtubule defects and kinesin function.

199 -function analysis suggests that nuclear and kinesin functions are dispensable, whereas binding to CY

200 atterning, interacts with a type-14 kinesin, KINESIN G (KinG).

201 A mAb directed to TbKHC1, an orphan kinesin H chain from Trypanosoma brucei, inhibited T. mu

202 lysis in peptidergic neurons suggest the two kinesins have compartment specific influences.

203 aminyltransferase 110 kDa subunit (OGT1) and kinesin heavy chain isoform 5A and alterations in the no

204 Kinesin heavy chains move cargo along microtubules by on

205 Kinesins hydrolyse ATP to transport intracellular cargoe

206 raflagellar transport (IFT) kinesin-2 motors kinesin-II and OSM-3/KIF17 without affecting kinesin-3 K

207 Dynein-1b is carried to the tip by kinesin-II as inactive cargo on anterograde trains.

208 n of kinesin-II to the basal body, depleting kinesin-II available for anterograde transport.

209 Unlike dynein-1b, kinesin-II detaches from IFT trains at the tip and diffu

210 Our results suggest that dissociation of kinesin-II from IFT trains serves as a negative feedback

211 lum grows longer, diffusion delays return of kinesin-II to the basal body, depleting kinesin-II avail

212 affecting the intraflagellar transport (IFT) kinesin-II.

213 , we propose a novel function for the Kif13b kinesin in glial cells as a key component of the PI3K/AK

214 t utility to study the functions of specific kinesins in a dynamic manner in cells and animals.

215 Our work highlights a general mechanism of kinesin inhibition in which small-molecule binding near

216 We analyze the previously identified kinesin inhibitor binding sites and identify features of

217 erences to functional differences in diverse kinesin isoforms.

218 We show here that BLOC-1 coordinates the kinesin KIF13A-dependent pulling of endosomal tubules al

219 lly by cytoplasmic dynein and basally by the kinesin KIF1A, which has recently been implicated in hum

220 Although the anterograde motor kinesin KIF1B is involved in mbp mRNA transport in zebra

221 gh coupling to the small GTPase Arl8 and the kinesins KIF1B and KIF5B.

222 also identify a requirement for the mitotic kinesin KIF23, a key target gene of MMB, in tumorigenesi

223 Among a number of cargo transporting kinesins, KIF5A was notably upregulated during TGF-beta

224 Here we identified the ciliary tip kinesins Kif7 and Kif17 as novel interaction partners of

225 Arl3 also interact with another ciliary tip kinesin, Kif7, which is a conserved regulator of Hedgeho

226 radial patterning, interacts with a type-14 kinesin, KINESIN G (KinG).

227 2 nodes containing Blt1p, Rho-GEF Gef2p, and kinesin Klp8p remain intact throughout the cell cycle an

228 We further show that kinesin knockdown inhibits hepatitis-C virus replication

229 in-1 levels are increased concomitantly with kinesin light chain (KLC-1/2) and immunoprecipitation an

230 uster, BtubC, previously known as "bacterial kinesin light chain," binds along protofilaments every 8

231 move cargo along microtubules by one of many kinesin light chains (KLCs), which directly bind the car

232 rated high CIN by reducing expression of the kinesin-like mitotic motor protein CENP-E.

233 Human kinesin-like protein KIF14, a microtubule motor protein,

234 network, including MKK2, HY5, CaSR, STN7 and kinesin-like protein, show a remarkable difference betwe

235 es suggested that the heterotrimeric ciliary kinesin may be dispensable for certain aspects of transp

236 ng activity of mitotic centromere-associated kinesin (MCAK), thereby promoting leading-edge MT growth

237 vely), we demonstrate that KinA is the major kinesin mediating the anterograde transport of SVs.

238 Kinesin microtubule motor proteins play essential roles

239 d US9 function by tethering HSV particles to kinesin microtubule motors.

240 iginate from multiple effects not related to kinesin-microtubule binding, the prediction rate of 0.84

241 s of microtubules where it strongly inhibits kinesin motility.

242 atic component of the force acting between a kinesin motor domain and tubulin.

243 For example, phosphorylation of kinesin motor domain at the serine residue is implicated

244 non-disease-causing mutations found in human kinesin motor domains using the receiver operating chara

245 in mitosis through regulation of the mitotic kinesin motor EG5 for proper spindle architecture and ch

246 of family-specific insertions in modulating kinesin motor function.

247 ed by heterozygous missense mutations in the kinesin motor protein KIF21A or in the beta-tubulin isot

248 with an Arabidopsis mitochondrial-localized kinesin motor protein.

249 The human genome encodes 45 kinesin motor proteins that drive cell division, cell mo

250 ntraflagellar transport (IFT) is mediated by kinesin motor proteins; however, the function of the hom

251 al dysfunction in the setting of an abnormal kinesin "motor." These results highlight the role of exp

252 Further, higher surface density of kinesin motors and shorter kinesin-surface tethers promo

253 We show that kinesin motors are recruited to triglyceride-rich lipid

254 DNF/TrkB motility, suggesting that dendritic kinesin motors may cooperate with dynein to drive the tr

255 Most kinesin motors move in only one direction along microtub

256 Kinesin motors play central roles in establishing and ma

257 Kinesin motors play diverse roles in mitosis and are tar

258 appear to be transported unidirectionally by kinesin motors towards distal egress sites.

259 efects influence cargo transport by multiple kinesin motors.

260 extension relies on anterograde transport by kinesin motors.

261 xperimentally observed weak cooperativity of kinesins motors.

262 Kinesin neck linker (NL) functions as the central mechan

263 size the need to consider factors beyond the kinesin neck-linker motif when attempting to understand

264 Here, we studied the role of kinesin on collagen-1 (Col-1) containing vesicle transpo

265 ocity reduction is that the neck linker of a kinesin only detaches from the motor head when pulled by

266 Toll-6-FoxO signaling represses the mitotic kinesin Pavarotti/MKLP1 (Pav-KLP), which itself attenuat

267 Thus, this orphan kinesin plays an important role in promoting trypanosome

268 To test the multi-kinesin possibility for a single vesicle type, we studie

269 gle-molecule results presented show that the kinesin processive stepping distance decreases 40-60% wi

270 s provide a kinetic framework for explaining kinesin processivity and for mapping structural differen

271 Kinesin processivity, defined as the average number of s

272 The trafficking kinesin proteins (TRAKs) are well characterized for thei

273 Microtubule depolymerization and kinesin-related motors contribute to copy addition.

274 Thus a kinesin-related protein can function intimately with a m

275 predominantly bundled, and bundling enhances kinesin run lengths and provides a greater number of ava

276 These results reflect the dependence of kinesin's function on motility along the microtubule, wh

277 efficiency in siRNA uptake and silencing of kinesin spindle protein at peptide:siRNA w/w ratio of 80

278 Kinesins-13s are members of the kinesin superfamily of motor proteins that depolymerize

279 urface density of kinesin motors and shorter kinesin-surface tethers promote PFB formation, whereas m

280 diffusion and minimizes the probability that kinesin takes side steps, implying that both the events

281 KinG is a calponin homology domain kinesin that directly interacts with the SHR-binding pro

282 s also been implicated as an injury-specific kinesin that is a key regulator of axonal growth and reg

283 live cells suggests that KinG is a nonmotile kinesin that promotes the pausing of SHR-associated endo

284 naphase-specific function for these effector kinesins that is controlled by specific Nek kinase signa

285 s particles tether themselves to dyneins and kinesins that motor along microtubules from axon tips to

286 shaft and diffusing into spines or through a kinesin to myosin hand-off at the base of spines.

287 rins are also involved in the recruitment of kinesin to the NE and play a role in nuclear positioning

288 nd Arl3 regulate the trafficking of specific kinesins to cilia tips and provide additional evidence t

289 udied the functional relationships of axonal kinesins to dense core vesicles (DCVs) that were filled

290 walk: N-kinesins towards the plus-end, and C-kinesins towards the minus-end of microtubules.

291 ostatics help guide kinesins as they walk: N-kinesins towards the plus-end, and C-kinesins towards th

292 step in controlling the velocity of a single kinesin under an external force is the ATP release from

293 We found that single kinesins undergo premature dissociation, but not prefere

294 For kinesin, velocity is weakly influenced by a small to mid

295 Kinesin walks processively on microtubules (MTs) in an a

296 ion of a major molecular motor, conventional kinesin, when transporting cargos along individual micro

297 asted with those observations on other known kinesins, which can bind only a single "canonical" site

298 indings reveal a key missing conformation of kinesins, which provides the structural basis of the sta

299 oskeletal remodeling, the first example of a kinesin whose function is directly tuned to neuronal act

300 , followed by the cytoskeletal regulator and kinesin ZEN-4/MKLP1 and the polarity protein PAR-6.