ライフサイエンスコーパス: kinesin

1 rther support non-mitotic functions for this kinesin.

2 evaluate the transport of cargo by a single kinesin.

3 ation of key steps in the catalytic cycle of kinesin.

4 B, an adaptor molecule between lysosomes and kinesins.

5 the motility of the microtubule-based motors kinesin 1 and cytoplasmic dynein 1 in vitro.

6 ns of force, we show that multiple mammalian kinesin-1 (from 2 to 8) communicate in a team by inducin

7 ve endosomes that contained the RAB7-binding Kinesin-1 adaptor FYCO1, and depletion of RAB7, FYCO1, o

8 s a minimal activation module that increases Kinesin-1 affinity for MTs.

9 At low loads, kinesin-1 almost always steps forward, toward microtubul

10 ame chemomechanical cycle as established for kinesin-1 and -2.

11 nsport behavior of cargo carried by pairs of kinesin-1 and -3 motors are determined by three properti

12 with MAP7, MAP7D3 has a higher affinity for kinesin-1 and a lower affinity for microtubules and, unl

13 Kinesin-1 and cytoplasmic dynein are microtubule (MT) mo

14 ment is an order of magnitude faster than in kinesin-1 and kinesin-2.

15 otor transport, we analyzed the complexes of kinesin-1 and kinesin-3 motors attached through protein

16 Staufen is determined by competition between kinesin-1 and myosin-V.

17 nteraction inhibits coupling of lysosomes to kinesin-1 and, consequently, lysosome movement toward th

18 Nevertheless, microtubules, dynein, and kinesin-1 are essential for migration, and we find that

19 Myosin-V wins over kinesin-1 at the posterior pole due to low microtubule d

20 hat not only these larger backsteps, but all kinesin-1 backsteps, are slips.

21 her, we show that a specific peptide against kinesin-1 blocks triglyceride secretion without any appa

22 passive connector of lysosome-bound ARL8 to kinesin-1 but is itself subject to intra- and inter-mole

23 Here, we explored the regulation of kinesin-1 by MAP7 proteins.

24 To understand how the activation of kinesin-1 by MAP7 regulates the motility of organelles t

25 hat keratin and vimentin are nonconventional kinesin-1 cargoes because their transport did not requir

26 y expressed KIF1A construct, dimerized via a kinesin-1 coiled-coil, exhibits fast velocity and superp

27 vivo and in vitro We propose that a KBD and Kinesin-1 complex is a minimal activation module that in

28 DDB-kinesin-1 complexes, formed using a DNA adapter, moved s

29 inhibitors of molecular motors support that kinesin-1 contributes to the anterograde transport of ca

30 n protrudin and facilitating the transfer of Kinesin-1 from protrudin to LE/Lys.

31 he control of spindle length by Ensconsin is Kinesin-1 independent but centrosome separation and oocy

32 clear migration in these cells, we find that kinesin-1 inhibition accelerates neuronal migration, sug

33 Kinesin-1 is an ATP-driven molecular motor that transpor

34 Kinesin-1 is responsible for microtubule-based transport

35 the Golgi apparatus to the cell periphery by kinesin-1 KIF5B and kinesin-3 KIF13B, which determine th

36 and microtubule recruitment of the truncated kinesin-1 KIF5B-560, which contains the stalk but not th

37 f detyrosinated microtubules or knockdown of kinesin-1 leads to a decrease in the percentage of autol

38 hat axonal transport of capsids requires the kinesin-1 molecular motor.

39 t syntabulin acts as a motor adapter linking kinesin-1 motor and presynaptic cargos.

40 does not alter the force exerted by a single kinesin-1 motor, but instead increases its binding rate

41 Single human kinesin-1 motors fail to avoid obstacles, consistent wit

42 e accumulation rate of fluorescently labeled kinesin-1 motors in a 2-dimensional (2D) system where mo

43 port of 100-nm-diameter vesicles requires 35 kinesin-1 motors, suggesting that teamwork between diffe

44 t and loses its adapter capacity for binding kinesin-1 motors.

45 aintain microtubule organization by opposing kinesin-1 powered microtubule sliding.

46 NBs, illustrating the importance of adapting Kinesin-1 recruitment to different biological contexts.

47 While kinesin-1 removes osk/Staufen from the cortex along micr

48 lation by Ensconsin is essential for optimal Kinesin-1 targeting to MTs in oocytes, but not in NBs, i

49 Interestingly, the KBD can stimulate Kinesin-1 targeting to MTs in vivo and in vitro We propo

50 occur directly on the MT and triggers higher Kinesin-1 targeting.

51 microtubule landing rate and processivity of kinesin-1 through transient association with the motor.

52 MAP7 proteins promote binding of kinesin-1 to microtubules both directly, through the N-t

53 on and oocyte transport require targeting of Kinesin-1 to microtubules by Ensconsin.

54 MAP7 also recruits kinesin-1 to microtubules.

55 low microtubule density at this site, while kinesin-1 wins at anterior and lateral positions because

56 otubule lattice (as exemplified by the motor kinesin-1).

57 o directly compare dimeric motors across the kinesin-1, -2, and -3 families to their minimal monomeri

58 ilaments, together with a microtubule motor, kinesin-1, and an actin motor, myosin-V, are essential f

59 the three main classes of transport motors: kinesin-1, kinesin-3, and cytoplasmic dynein.

60 with both microtubules and the motor protein kinesin-1, plays a key role at branch junctions.

61 oop 12 of kinesin-3 was swapped with that of kinesin-1, the landing rates reversed, indicating that t

62 h the N-terminal region comprising ARL8- and kinesin-1-binding sites.

63 Lysosome enrichment is mediated through a kinesin-1-dependent mechanism, since knocking down this

64 MAP7D1, and MAP7D3 act redundantly to enable kinesin-1-dependent transport and microtubule recruitmen

65 protein kinectin-1, controls the anterograde kinesin-1-dependent transport of the ER required for the

66 also relieves SKIP autoinhibition, promoting kinesin-1-driven, anterograde lysosome transport.

67 iation enhances the interaction of SKIP with kinesin-1.

68 sosomes to the anterograde microtubule motor kinesin-1.

69 and had threefold higher landing rates than kinesin-1.

70 f IFs, are transported along microtubules by kinesin-1.

71 l four mammalian MAP7 family members bind to kinesin-1.

72 on active turbulent gels of microtubules and kinesin [12, 13], we explore the kinematics of this in v

73 RNAs in tandem to simultaneously knock down kinesin-13 and MBP, we created a stable dual knockdown s

74 fically, CRISPRi knockdown of kinesin-2a and kinesin-13 causes severe flagellar length defects that m

75 radient of a depolymerizing protein, such as kinesin-13 in Giardia, along the length of the flagellum

76 strongly exacerbated by the depletion of the kinesin-13 KLP-7/MCAK, resulting in incomplete centrosom

77 Mitotic error correction relies on the kinesin-13 MCAK, a microtubule depolymerase whose activi

78 llenged by a known microtubule depolymerase, kinesin-13 MCAK.

79 gellar transport (IFT)-mediated assembly and kinesin-13-mediated disassembly in different flagellar p

80 we show that key functions of budding yeast Kinesin-14 Cik1-Kar3 are accomplished in a complex with

81 r results reveal the contributions of an EB1-Kinesin-14 complex for spindle formation as a prerequisi

82 ences, recruit their own novel and divergent kinesin-14 family members to form neocentromeres.

83 In addition, we adopted moss kinesin-14 for efficient retrograde transport with minim

84 re we examine how the Ran gradient regulates Kinesin-14 function to control spindle organization.

85 Here we describe a second kinesin-14 gene, TR-1 kinesin (Trkin), that is required

86 To date, no Ncd-type kinesin-14 has been found to naturally exhibit long-dist

87 our results show that the minus-end-directed kinesin-14 HSET/KIFC1 suppresses tubulin off-rate to spe

88 In mammals, there are three kinesin-14 members, KIFC1, KIFC2, and KIFC3.

89 ral stalk as a key mechanical determinant of kinesin-14 motility [3].

90 Here, we found that the kinesin-14 motor KIFC3 is important for organizing dendr

91 The kinesin-14 motor proteins (Drosophila melanogaster Ncd,

92 Ncd-type kinesin-14s are a subset of kinesin-14 motors that exist as homodimers with an N-ter

93 s of the Ran pathway are critical to promote Kinesin-14 parallel microtubule cross-linking to help fo

94 ene Kinesin driver (Kindr) on Ab10 encodes a kinesin-14 required to mobilize neocentromeres made up o

95 testinalis [2] is an unconventional Ncd-type kinesin-14 that uses its N-terminal microtubule-binding

96 We show that Xenopus Kinesin-14, XCTK2, and importin alpha/beta form an effec

97 KIFC1 (also called HSET or kinesin-14a) is best known as a multifunctional motor pr

98 Ncd-type kinesin-14s are a subset of kinesin-14 motors that exist

99 Kinesin-14s are conserved molecular motors required for

100 Kinesin-14s are microtubule-based motor proteins that pl

101 and diffusion coefficient for the return of kinesin-2 affect flagellar growth kinetics.

102 Here, we show that the heterodimeric FLA8/10 kinesin-2 alone is responsible for the atypically fast I

103 Kinesin-2 enables ciliary assembly and maintenance as an

104 We propose that Kinesin-2 engages with a polarised microtubule network w

105 KIF3AC is an intriguing member of the kinesin-2 family because the intrinsic kinetics of KIF3A

106 Strikingly, monomeric versions of the kinesin-2 family motors KIF3A and KIF3B are able to driv

107 ly, we linked fast FLA8/10 and slow KLP11/20 kinesin-2 from C. reinhardtii and C. elegans through a D

108 KIF3AC is a mammalian neuron-specific kinesin-2 implicated in intracellular cargo transport.

109 ants mediating trafficking of heterotrimeric kinesin-2 itself are poorly understood.

110 h to generate an inhibitable KIF3A/KIF3B/KAP kinesin-2 motor (i3A/i3B) that is capable of rescuing wi

111 he green alga C. reinhardtii, on average, 10 kinesin-2 motors "line up" in a tight assembly on the tr

112 These findings highlight differences in how kinesin-2 motors were adapted for cilium assembly and IF

113 pective of phylogeny and kinetic properties, kinesin-2 motors work mostly alone without sacrificing e

114 Heterodimeric KIF3AC is a mammalian kinesin-2 that is highly expressed in the central nervou

115 kinesin family member KIF3AC is a mammalian kinesin-2 that is highly expressed in the central nervou

116 axon and exclusion from dendrites depend on Kinesin-2, a plus-end-associated motor that guides growi

117 The heterotrimeric kinesin-2, consisting of the heterodimeric motor subunit

118 er of magnitude faster than in kinesin-1 and kinesin-2.

119 king of KAP3, a key component for functional kinesin-2.

120 Specifically, CRISPRi knockdown of kinesin-2a and kinesin-13 causes severe flagellar length

121 The kinesin-3 family contains the fastest and most processiv

122 The kinesin-3 family member KIF1A plays a critical role in s

123 to the cell periphery by kinesin-1 KIF5B and kinesin-3 KIF13B, which determine the location of secret

124 104 is the Caenorhabditis elegans homolog of kinesin-3 KIF1A known for its fast shuffling of synaptic

125 The kinesin-3 KIF1C is a fast organelle transporter implicat

126 ic dynein-1 activating adaptor Hook3 and the kinesin-3 KIF1C.

127 lso supported previous work, suggesting that kinesin-3 microtubule detachment is very sensitive to lo

128 s and unveil MAP9 as a positive modulator of kinesin-3 motility.

129 The kinesin-3 motor KIF1A is involved in long-ranged axonal

130 induced, accelerated degradation of KIF1A, a kinesin-3 motor promoting the sorting and transport of P

131 PNS) neurons have demonstrated that KIF1A, a kinesin-3 motor, mediates the efficient axonal sorting a

132 , we analyzed the complexes of kinesin-1 and kinesin-3 motors attached through protein scaffolds movi

133 In single-molecule experiments, isolated kinesin-3 motors moved twofold faster and had threefold

134 When the positively charged loop 12 of kinesin-3 was swapped with that of kinesin-1, the landin

135 main classes of transport motors: kinesin-1, kinesin-3, and cytoplasmic dynein.

136 o delineate the chemomechanical cycle of the kinesin-3, KIF1A.

137 tion modules and engineered a photosensitive kinesin-3, which is activated upon blue light-sensitive

138 ght into this process through studies of the kinesin-4 family member Kif4 in mouse oocytes.

139 Here, we show that the knockout of KIF21B, a kinesin-4 linked to autoimmune disorders, causes microtu

140 Human Kinesin-5 (Eg5) has a large number of known allosteric i

141 e turbulence is driven by the homotetrameric kinesin-5 Eg5, and that acute Eg5 inhibition in turbulen

142 Members of the evolutionarily conserved kinesin-5 family of motor proteins have been shown to pl

143 2, a protein that enriches the cross-linking kinesin-5 motor Eg5 at spindle poles [3].

144 The primary spindle force generators are kinesin-5 motors and crosslinkers in early mitosis, whil

145 ns regulate the localization and activity of kinesin-5 motors in cells.

146 Kinesin-5 motors organize mitotic spindles by sliding ap

147 Kinesin-5 tails decrease microtubule-stimulated ATP-hydr

148 revised microtubule-sliding model, in which kinesin-5 tails stabilize motor domains in the microtubu

149 bules during spindle elongation, the mitotic kinesin-5, Eg5, promotes microtubule polymerization, emp

150 ontributes to the control of spindle length, kinesin-5/Klp61F is crucial for maintaining a bipolar sp

151 cross-linking kinesins, MKlp1/Pavarotti and kinesin-5/Klp61F, accumulate to the spindle equator in l

152 Kinesin-5s are microtubule-dependent motors that drive s

153 have recently demonstrated that a 'mitotic' kinesin-6 (Pavarotti in Drosophila) effectively inhibits

154 gulated: coupled to cell size, the amount of kinesin-6 Klp9 molecules increases, resulting in an acce

155 entralspindlin complex, composed of CYK4 and kinesin-6.

156 However, it is still unclear how kinesin-8 depolymerizes microtubules.

157 Motor proteins from the kinesin-8 family depolymerize microtubules by interactin

158 Understanding the mechanics of kinesin-8's microtubule end activity will provide import

159 he microtubule end-binding activity of yeast kinesin-8, Kip3, under varying loads and nucleotide cond

160 For ensembles of kinesin, a greater number of kinesin motors are simultan

161 Consequently, multiple kinesins acting as a team may play a significant role in

162 Spatial and temporal regulation of kinesin activity is essential for building these local e

163 s interact with Nesprin-2 through the dynein/kinesin "adaptor" BicD2, both in neurons and in non-mito

164 changes could regulate the activity of other kinesin adaptors.

165 Kinesins adopt two distinct states, with one-third slowi

166 vities, many mutations that impact transport kinesins also impair MCAK/Kif2C's depolymerizing activit

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

168 Kinesin and dynein are microtubule (MT)-associated motor

169 In addition, MAPs alter the motility of kinesin and dynein to control trafficking along microtub

170 ifferent microtubule motor proteins (such as kinesin and dynein) to the corresponding CytVs.

171 ty of organelles transported by ensembles of kinesin and dynein, we isolated organelles and reconstit

172 ansport driven by the opposing activities of kinesin and dynein-dynactin-BicD2, the dynactin p150 sub

173 median value of attachment durations between kinesin and microtubules can be up to 10-fold longer tha

174 After briefly introducing the motor proteins kinesin and myosin and their associated cytoskeletal fil

175 ts are equivalent interacting substrates for kinesin and that the median value of attachment duration

176 results address the limited actions of three kinesins and a cross-linking MAP that are known to have

177 zation of skeletal muscle nuclei mediated by kinesins and suggest that its primary role is at the out

178 esprin-2, which recruits cytoplasmic dynein, kinesin, and actin to the nuclear envelope (NE) in other

179 nd driven by motor proteins, such as myosin, kinesin, and dynein.

180 kinesins, but it is poorly understood which kinesins are present on particular cargos, what their co

181 kinesin family member 3A/3B (KIF3A/3B), and kinesin-associated protein 3 (KAP3), is highly conserved

182 -alpha2 and nesprin-1-giant co-localize with kinesin at the junctions of concatenated nuclei and at t

183 de neuronal migration through attenuation of kinesin autoinhibition leading to aberrant KIF21B motili

184 eals that the system is highly dynamic, with kinesin binding and unbinding along the length of the mi

185 through an allosteric effect exerted by the kinesin-binding C-terminal domain.

186 microtubule (MT)-binding domain (MBD) and a Kinesin-binding domain (KBD).

187 trudin's endoplasmic reticulum localization, kinesin-binding or phosphoinositide-binding properties a

188 Kinesin-binding protein (KBP) interacts with a subset of

189 Here, we demonstrate that kinesin-binding protein (KBP) reduces the activity of KI

190 3 (RAB11FIP3), ninein (NIN), and trafficking kinesin-binding protein 1 (TRAK1).

191 microtubule binding or motility of the FRA1 kinesin but differentially affected the protein levels a

192 Intracellular transport relies on multiple kinesins, but it is poorly understood which kinesins are

193 e geometry of forces across the microtubule, kinesin can switch from a fast detaching motor (median a

194 n late cytokinesis and de-phosphorylates the kinesin component MKLP1/KIF23 of the centralspindlin com

195 AMPPNP-bound Cut7 adopts a kinesin-conserved ATP-like conformation including cover

196 ight chains, which are a typical adapter for kinesin-dependent cargo transport.

197 ophila oocyte, a cell that displays distinct Kinesin-dependent streaming.

198 Kinesin-dependent transport of keratin filaments: a unif

199 olarity microtubule-based motors, dynein and kinesin, drive long-distance intracellular cargo transpo

200 at multiple KIF3B pathomechanisms can impair kinesin-driven ciliary transport in the photoreceptor.

201 We previously demonstrated that the gene Kinesin driver (Kindr) on Ab10 encodes a kinesin-14 requ

202 rough the nonselective labeling of the human kinesin Eg5 with photoconverted 3,3'-azibutan-1-ol.

203 tural similarities between VPg and the human kinesin EG5.

204 ssive motors of the three neuronal transport kinesin families, yet the sequence of states and rates o

205 Moreover, expression of the kinesin family member 1B, an Mbp mRNA transport protein,

206 ng of Intraflagellar Transport 88 (Ift88) or Kinesin Family Member 3 A (Kif3a) to inhibit the formati

207 de polymorphisms (SNPs) in the gene encoding kinesin family member 3A, KIF3A, have been associated wi

208 sisting of the heterodimeric motor subunits, kinesin family member 3A/3B (KIF3A/3B), and kinesin-asso

209 Heterodimeric kinesin family member KIF3AC is a mammalian kinesin-2 th

210 Intracellular cargo transport by kinesin family motor proteins is crucial for many cellul

211 alcineurin regulator RCAN3, and KIF1C of the kinesin family).

212 ons to dissect a standing controversy in the kinesin field over the structure of a dimer in the ATP w

213 We propose that the ubiquitous kinesin fold has been repurposed in Kif7 to facilitate o

214 Kinesin force generation involves ATP-induced docking of

215 ingle-bead assay, we show that detachment of kinesin from the microtubule is likely accelerated by fo

216 om a plus-end-directed or minus-end-directed kinesin fused to streptavidin.

217 o modulate the expression of its neighboring kinesin gene unc-104 and thus plays roles in C. elegans

218 with simulations, we determine that the rear kinesin head in the ATP waiting state is unbound but not

219 In a proteomics study, kinesin heavy and light chains were the only significant

220 ermore, we found that the same domain of the kinesin heavy chain tail is involved in keratin and vime

221 g protein 1 (ZBP1, a beta-actin RBP) and the kinesin-I motor complex.

222 1 and PAT1 within granules that also contain kinesin-I.

223 the IFT-B protein IFT54 interacts with both kinesin-II and IFT dynein and regulates anterograde IFT.

224 IFT54 directly interacted with kinesin-II and this interaction was strengthened for the

225 n that Klp64D, a motor subunit of Drosophila kinesin-II, interacts with Arm for Wg signaling.

226 machinery consists of the anterograde motor kinesin-II, the retrograde motor IFT dynein, and the IFT

227 ction and more effective competition against kinesin in a tug-of-war.

228 ary sequence divergence from Kindr and other kinesins in plants.

229 factor-like protein 8B (ARL8B) and SifA- and kinesin-interacting protein/pleckstrin homology domain-c

230 Kinesin is part of the microtubule-binding motor protein

231 Furthermore, we find that in oocytes where Kinesin is unable to induce cytoplasmic streaming, the g

232 acellular activity and proper recruitment of kinesins is regulated by biochemical signaling, cargo ad

233 Da Nesprin-2 protein, which binds dynein and kinesin, is sufficient, remarkably, to support neuronal

234 re we report that KIF1A, unlike other axonal kinesins, is an intrinsically unstable protein prone to

235 One such target is the mitotic kinesin KIF11, which can be inhibited with ispinesib, a

236 diated regulation of motile cilia length via kinesin Kif19a, a regulator of cilia length.

237 isms, and uncouples its binding with ciliary kinesin Kif19a.

238 tion assays, we showed that Fignl1 binds the kinesin Kif1bbeta and the dynein/dynactin adaptor Bicaud

239 elopmental disorders linked to the mammalian kinesin Kif21A.

240 We show that one such factor is the kinesin KIF4A, which is present along the chromosome axe

241 ence of mouse PAT1 is similar to that of the kinesin light chain (KLC), and we found that PAT1 binds

242 goes because their transport did not require kinesin light chains, which are a typical adapter for ki

243 bunits, survivin and INCENP, and the mitotic kinesin-like protein 2 (MKLP2) in targeting to these dis

244 rotti, the Drosophila MKLP1 orthologue, is a kinesin-like protein that works with Tumbleweed (MgcRacG

245 Here, we employed deletions of kinesin-like proteins to perturb microtubule dynamics an

246 icrotubule plus-end directed transport, both kinesins localize to the vesicle front and can be engage

247 nd that the effect of opposing forces on the kinesin-microtubule attachment duration depends strongly

248 Among them, microtubule cross-linking kinesins, MKlp1/Pavarotti and kinesin-5/Klp61F, accumula

249 s, both leading to deregulation of canonical kinesin motor activity.

250 olecular "traffic signals" helping to direct kinesin motor cargo delivery, and include C-terminal tai

251 to reveal the structure of KBP and of a KBP-kinesin motor domain complex.

252 c.748G>C (p.Glu250Gln) variant affecting the kinesin motor domain encoded by KIF3B.

253 ht-handed alpha-solenoid that sequesters the kinesin motor domain's tubulin-binding surface, structur

254 noid concave face and edge loops to bind the kinesin motor domain, and selected structure-guided muta

255 a show that the load-bearing capacity of the kinesin motor is highly variable and can be dramatically

256 During mitosis, Kif11, a kinesin motor protein, promotes bipolar spindle formatio

257 ly proposed that the diffusive return of the kinesin motor that powers intraflagellar transport can p

258 in the cell body are actively transported by kinesin motors along axonal microtubules to presynaptic

259 s work, we demonstrate that a 3D solution of kinesin motors and microtubule filaments spontaneously f

260 Kinesin motors and their associated filaments, microtubu

261 Kinesin motors and their associated microtubule tracks a

262 or ensembles of kinesin, a greater number of kinesin motors are simultaneously engaged and generating

263 es of the system, such as the spacing of the kinesin motors bound to the microtubule and the dynamics

264 , these results suggest that dimerization of kinesin motors is not required for intracellular transpo

265 Dimerization of kinesin motors is thus critical for cellular events that

266 Kinesin motors provide the molecular forces at the kinet

267 heral mucosal tissues, a process mediated by kinesin motors.

268 Mitotic kinesins must be regulated to ensure a precise balance o

269 mination of Drosophila oocytes is defined by kinesin-myosin competition, whose outcome is primarily d

270 Kinesins overcome this limitation when working in teams,

271 the Arabidopsis (Arabidopsis thaliana) FRA1 kinesin physically interacts with cellulose synthase-mic

272 This opto-kinesin prevented motor activation before experimental o

273 ued detachment pathway is key to maintaining kinesin processivity under load.

274 KIF21B is a kinesin protein that promotes intracellular transport an

275 EWD sequence, implicated in nuclear envelope kinesin recruitment in other systems, interferes with Bi

276 ing yeast, the myosin-V Myo2 is aided by the kinesin-related protein Smy1 in carrying out the essenti

277 Recently, Kif19a, a kinesin residing at the cilia tip, was identified to be

278 trong asymmetry in the sensitivity of single-kinesin run length to load direction, raising the intrig

279 argo diffusion significantly shortens single-kinesin runs.

280 interacting kinesins, suggesting a basis for kinesin selectivity.

281 therapeutically actionable targets including kinesin spindle protein (KSP).

282 83, (Janus kinase 2/3 inhibitor), ispinesib (kinesin spindle protein inhibitor), gedatolisib (PKI-587

283 that, in each cycle of ATP turnover, forward kinesin steps can only occur before Pi release, whereas

284 and this insert is not present in any other kinesin, suggesting that it confers specific properties

285 ifs exclusively conserved in KBP-interacting kinesins, suggesting a basis for kinesin selectivity.

286 ve toward the plus-end ~80% of the time, and kinesin teams generate more force.

287 KIF11 is a homotetrameric kinesin that peaks in protein expression during mitosis.

288 rkin encodes a functional minus end-directed kinesin that specifically colocalizes with TR-1 in meios

289 cific cargo is carried out by two classes of kinesins that move at different speeds and thus compete

290 ch contrasts with microtubule-depolymerizing kinesins that preferentially bind free tubulin over micr

291 be transported by the FRAGILE FIBER1 (FRA1) kinesin to facilitate their secretion along cortical mic

292 flow speeds to counteract the recruitment of Kinesin to MTs.

293 Dimerization allows kinesins to be processive motors, taking many steps alon

294 e-guided mutations disrupt KBP inhibition of kinesin transport in cells.

295 e we describe a second kinesin-14 gene, TR-1 kinesin (Trkin), that is required to mobilize neocentrom

296 the median value of attachment durations of kinesin varies by more than 10-fold, depending on the re

297 ing protein (KBP) interacts with a subset of kinesins via their motor domains, inhibits their microtu

298 We show first that kinesin waits before forward steps for less time than be

299 ksteps and detachments; second, we show that kinesin waits for the same amount of time before backste

300 e behavior of KIF3C mirrors prior studies of kinesins with increased interhead compliance.