戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 d centrosome positioning requires its direct microtubule binding.
2 tail, work together to promote high-affinity microtubule binding.
3 dues within the FH2 domain are important for microtubule binding.
4 activating domain functions independently of microtubule binding.
5 n the GKNDG motif, which participates in the microtubule binding.
6 nd is not essential for complex formation or microtubule binding.
7 gen synthase kinase 3 (GSK3), independent of microtubule binding.
8 inding to soluble tubulin but do not prevent microtubule binding.
9 h full phosphorylation severely compromising microtubule binding.
10 on and that its function is mediated through microtubule binding.
11 n filaments in vitro, its actin assembly and microtubule binding activities likely require spatial an
12 or the KLCs in regulating both the head- and microtubule-binding activities of the kinesin-1 tail.
13 re likely to be mediated by the tubulin- and microtubule-binding activities that we describe.
14 s checkpoint signaling, harbors two distinct microtubule-binding activities: the load-bearing activit
15 strophin/utrophin chimera completely lacking microtubule binding activity are surprisingly rescued fo
16                       Hice1 possesses direct microtubule binding activity at its N-terminal region an
17 tly, the phospho-mimic 17-21E mutant reduced microtubule binding activity in vitro and diminished loc
18 eficient Dam1 complex that retains wild-type microtubule binding activity is primarily defective in c
19 hemically compared the previously documented microtubule binding activity of dystrophin with utrophin
20  results suggest that Aurora-A modulates the microtubule binding activity of Hice1 in a spatiotempora
21                             However, whether microtubule binding activity of Hice1 is modulated by mi
22                                           No microtubule binding activity was detected for the analog
23 of Smc5 and generated a mutant with impaired microtubule binding activity.
24  able to form an intact complex that retains microtubule binding activity.
25 he regulatory mechanism of the tau protein's microtubule binding activity.
26                                Loss of tau's microtubule-binding activity facilitates an inappropriat
27                      However, separase lacks microtubule-binding activity, raising questions about me
28 f the KMN network generates graded levels of microtubule-binding activity, with full phosphorylation
29  endocytosis apparently independently of its microtubule-binding activity.
30 icacy of each ligand was consistent with the microtubule binding affinity, as was the trend in cytoto
31 that an individual MIND complex enhances the microtubule-binding affinity of a single Ndc80 complex b
32 t simulate the experimental data, unless the microtubule-binding affinity of kinesins on the endosome
33                                  The ATPase, microtubule-binding affinity, and processivity are uncha
34   We find that She1 affects the ATPase rate, microtubule-binding affinity, and stepping behavior of d
35 3A axon growth defects could be rescued with microtubule-binding agents, emphasizing the importance o
36 of key functional elements, most notably the microtubule binding alpha4-alpha5, loop8 subdomain and a
37 esin-14 Ncd motor alters both nucleotide and microtubule binding, although the mutated residue is not
38 couple cycles of ATP hydrolysis to cycles of microtubule binding and conformational changes that resu
39                          The balance between microtubule binding and error correction (e.g., release
40 uced by simulations of assembly with tighter microtubule binding and faster sliding.
41 motif in MDM1 that is required for efficient microtubule binding and found that these repeats are als
42 o, FTDP-17 mutant versions of tau can reduce microtubule binding and increase the aggregation of tau,
43                 These results show that both microtubule binding and interaction with Eg5 contribute
44 inhibitory site, leading to increased GEF-H1 microtubule binding and loss of RhoA stimulation.
45                                              Microtubule binding and mitotic ER clearance from chromo
46 ion and the WD40 domain, potentially linking microtubule binding and neurodegeneration.
47                         Perturbation of both microtubule binding and protein phosphatase 1 docking at
48 - and C-terminal domains that is involved in microtubule binding and regulation of the spindle checkp
49 mbly of centromere and kinetochore proteins, microtubule binding and stabilization, and mitotic check
50 fusions retain the TACC domain that mediates microtubule binding and the BAIAP2L1 fusion retains the
51     Dynein motility involves the coupling of microtubule binding and unbinding to a change in the con
52            In this paper, we show that KNL-1 microtubule-binding and -bundling activity resides in it
53 ng element--it transmits changes between the microtubule-binding and active sites, and can switch the
54 uct release to conformational changes in the microtubule-binding and force-generating elements of the
55                        Thus, KIF21B combines microtubule-binding and regulatory activities that toget
56 t dynamics is not simply because of weakened microtubule binding, as an N-terminally truncated comple
57  to microtubules as demonstrated by in vitro microtubule-binding assay.
58 otubule-binding protein that participates in microtubule binding at kinetochores and in the mitotic r
59        The motor head of kinesin carries out microtubule binding, ATP hydrolysis, and force generatio
60 CDK1 phosphorylation site located within its microtubule-binding basic patch.
61  N-terminal portion of mPar3 exhibits strong microtubule binding, bundling, and stabilization activit
62 al dissipates automatically upon kinetochore-microtubule binding, but it has been shown that under co
63          We also show that KLCs inhibit tail-microtubule binding by a separate mechanism.
64 ted actin-microtubule cross-talk, we studied microtubule binding by Cappuccino (Capu), a formin invol
65 at 2.4 mum(-1) s(-1) through Vik1, promoting microtubule binding by Kar3 followed by ADP release at 1
66                              We propose that microtubule binding by KNL-1 functions in checkpoint sil
67 y, and stepping behavior of dynein, and that microtubule binding by She1 is required for its effects
68                                              Microtubule binding by Ska, rather than acting in force
69  depend on the coupling of ATP hydrolysis to microtubule binding by the motor.
70 itial lateral microtubule capture, inhibited microtubule binding by the Ndc80 complex, which ultimate
71 Ska3-Ska1 interactions negatively influences microtubule binding by the Ska complex in vitro and affe
72 the Ska3 subunit is required to modulate the microtubule binding capability of the Ska complex (i) by
73        We further show that Ska requires its microtubule-binding capability to promote Aurora B activ
74                                    While the microtubule-binding capacity of the protein tau has been
75                                          The microtubule-binding capacity of the SAH domain is import
76 our results argue that sustained exposure of microtubule-binding chemotherapeutic agents in periphera
77      This suggests that mud, which encodes a microtubule-binding coiled-coil protein homologous to Nu
78  The conserved Ndc80 complex is an essential microtubule-binding component of the kinetochore.
79 omponents, Mif2 and COMA, with the principal microtubule-binding component, the Ndc80 complex (Ndc80C
80    The Dam1 and Ndc80 complexes are the main microtubule binding components of the Saccharomyces cere
81 jacent microtubule protofilaments in a novel microtubule binding configuration and uses an ATP-promot
82 hain (Khc) subunits that alternate cycles of microtubule binding, conformational change, and ATP hydr
83           p150(glued) contains an N-terminal microtubule-binding cytoskeleton-associated protein glyc
84                          Overexpression of a microtubule binding-defective CEP120-K76A mutant signifi
85                                  First, upon microtubule binding, dimeric Eg5 releases both bound ADP
86 lectrostatic funnel that guides the dynein's microtubule binding domain (MTBD) as it finally docks to
87 markable flexibility at a hinge close to the microtubule binding domain (the stalkhead) producing a w
88 ts that the Mn modules represent each a full microtubule binding domain and that MAP6 proteins may st
89 both at the catalytic site as well as at the microtubule binding domain and the neck linker.
90  helix sliding in the stalk which causes the microtubule binding domain at its tip to release from th
91 ubules, suggesting the existence of a second microtubule binding domain at the C terminus of ARK1.
92 ike structures, we demonstrate that the Ska1 microtubule binding domain can associate with soluble tu
93 d proline residues in repeats 2 and 3 of the microtubule binding domain have differential effects on
94              Thus, crowding by either dynein microtubule binding domain or Klp2, a kinesin-14, conver
95 d mutations on distinct surfaces of the Ska1 microtubule binding domain that disrupt binding to solub
96 ral constraints limit the motion of the free microtubule binding domain to one dimension, increasing
97 of adult-specific exon 10, which codes for a microtubule binding domain, results in expression of abn
98 d the tubulin-binding properties of the Ska1 microtubule binding domain.
99 contacts and a concomitant compaction of the microtubule binding domain.
100  two coiled coils that create a base for the microtubule binding domain.
101  sites exist in repeats two and three of the microtubule binding domain.
102 a intermediary proteins and directly via its microtubule-binding domain (MBD).
103 nown glutamylase activity utilize a cationic microtubule-binding domain analogous to that of TTLL7.
104 stead, MIND binds Ndc80 complex far from the microtubule-binding domain and confers increased microtu
105 a C-terminal region outside NuMA's canonical microtubule-binding domain and is independent of minus-e
106 les requires two hexapeptides located in its microtubule-binding domain and is modulated by its proje
107          We map ACF7's GSK3beta sites to the microtubule-binding domain and show that phosphorylation
108 y requires the interaction between the FHDC1 microtubule-binding domain and the Golgi-derived microtu
109 c isoforms through a region encompassing the microtubule-binding domain and upstream proline-rich reg
110  motor domain at its N-terminus and a second microtubule-binding domain at its C-terminus of unknown
111 ubnanometer-resolution structure of dynein's microtubule-binding domain bound to microtubules by cryo
112     Mutations within the p150(Glued) CAP-Gly microtubule-binding domain cause neurodegenerative disea
113         HookA contains a putative N-terminal microtubule-binding domain followed by coiled-coil domai
114                            Disruption of the microtubule-binding domain in a mouse model of LCA was s
115                                     The Ska1 microtubule-binding domain interacts with tubulins using
116 ver, we find that She1 directly contacts the microtubule-binding domain of dynein, and that their int
117 -repeat region of tau, which flanks the core microtubule-binding domain of tau, contributes largely t
118 en receptor deletion mutants to identify the microtubule-binding domain of the androgen receptor, whi
119  with green fluorescent protein fused to the microtubule-binding domain of the mammalian microtubule-
120 ity or the tubulin contact sites of the Ska1 microtubule-binding domain perturbs normal mitotic progr
121  of the Kif5b motor domain fused to the MAP7 microtubule-binding domain rescues nuclear positioning d
122  Finally, we present a structure of the Ska1 microtubule-binding domain that reveals its interaction
123                           BuGZ also uses its microtubule-binding domain to enhance the loading of Bub
124 isoform 1B lacks 20 amino acids in the basic microtubule-binding domain).
125 e, CEP120 was found to contain an N-terminal microtubule-binding domain, a C-terminal dimerization do
126 ich autoinhibits the NLS and the neighboring microtubule-binding domain, and RhoA-GTP binding may rel
127 letion of dynein from plus ends requires its microtubule-binding domain, suggesting that motility is
128 direction of the linker stroke is toward the microtubule-binding domain.
129  assembly-promoting region of the C-terminal microtubule-binding domain.
130 ssociated with deletion of a majority of its microtubule-binding domain.
131 bule dynamics through a separable, non-motor microtubule-binding domain.
132 dence that microtubule binding of nonkinesin microtubule binding domains may be affected by adociasul
133 tains separable kinetochore localization and microtubule binding domains.
134 achment and, similar to CENP-E, contains two microtubule-binding domains at its termini.
135           This property depends on non-motor microtubule-binding domains located in the stalk region
136 ause variations in the hematologic target of microtubule-binding drugs might alter their myelosuppres
137                           At their MTDs, the microtubule-binding drugs paclitaxel and ixabepilone ind
138 hat may affect the myelosuppresive action of microtubule-binding drugs.
139 suppression that occurs after treatment with microtubule-binding drugs.
140 ence, and the presence of both ESCRT-III and microtubule binding elements may underlie the recent fin
141            The Ska complex contains multiple microtubule-binding elements and promotes kinetochore-mi
142 formed stronger attachments and carried more microtubule-binding elements than kinetochores isolated
143 n of a conserved Ser residue adjacent to the microtubule-binding exon released Drp1-x01 from microtub
144    The Ndc80 and Ska complexes are the major microtubule-binding factors of the kinetochore responsib
145                             Furthermore, the microtubule binding FH2 domain of mDia3 is phosphorylate
146 otubule, which suggests a precise balance of microtubule binding forces is required.
147 f the Ndc80 tail, which compromises in vitro microtubule binding, has no effect on kinetochore-microt
148              Selective perturbation of KNL-1 microtubule binding in Caenorhabditis elegans embryos re
149 ogy (CH) domains, which are known to mediate microtubule binding in certain proteins.
150 l tail of Ndc80 is essential for kinetochore-microtubule binding in human cells but is not required f
151 ersion from lattice diffusion to end-coupled microtubule binding in vitro.
152                  Mutants show weak-ADP/tight-microtubule binding, instead of tight-ADP/weak-microtubu
153 thogenic effect of tau did not depend on its microtubule binding, interactions with Fyn, or potential
154 namic communication between the active site, microtubule-binding interface and neck-linker via loop7
155 80 complex (KMN) network acts as the primary microtubule-binding interface at kinetochores [3] and pr
156                We discuss how such a complex microtubule-binding interface may facilitate the couplin
157 sembly because it links centromeres with the microtubule-binding interface of kinetochores.
158 a novel mechanism for regulating kinetochore-microtubule binding involving NDC80 complex oligomerizat
159        Using an in vitro assay, we show that microtubule binding is direct and identify a novel micro
160                          We find that PRC1's microtubule binding is mediated by a structured domain w
161 ved kinase Aurora B phosphorylates the major microtubule-binding kinetochore subcomplexes, Ndc80 and
162 DNA-binding complex that associates with the microtubule-binding KMN network via a short Mtw1 recruit
163 ltiple kinetochore components, including the microtubule-binding KMN network, the presence of microtu
164 crotubule binding, instead of tight-ADP/weak-microtubule binding like wild type--they hydrolyze ATP f
165 ting the large, class-specific insert in the microtubule-binding loop 8 reverts Cin8 to one motor per
166                                         TOG5-microtubule binding maintained mitotic spindle formation
167              KLC-mediated inhibition of tail-microtubule binding may also influence diffusional movem
168 ified FHDC1 (also known as INF1) as a unique microtubule-binding member of the formin family of cytos
169                                    The novel microtubule-binding mode of Cin8 identified here provide
170 dues, including lysine 280 (K280) within the microtubule-binding motif as the major sites of tau acet
171 ubule binding is direct and identify a novel microtubule-binding motif encompassed within amino acids
172                 Finally, the ATP-independent microtubule-binding motif is required for cargo localiza
173 ly the auto-inhibitory IAK and the auxiliary microtubule-binding motifs, are crucial for transport by
174 nkages between centromeric chromatin and the microtubule-binding Ndc80 complex at the human kinetocho
175 iously unidentified mechanism for regulating microtubule binding of an outer kinetochore component by
176                 We also report evidence that microtubule binding of nonkinesin microtubule binding do
177 e of Drosophila Pins (LGN), which blocks the microtubule binding of NuMA and competes with Astrin for
178 with different HSP mutations, independent of microtubule-binding or severing activity.
179 han generating exclusively binary changes in microtubule binding, our results suggest a mechanism for
180 the chromatin-associated inner domain to the microtubule-binding outer domain has eluded researchers.
181    This preference is mediated by dynactin's microtubule-binding p150 subunit rather than dynein itse
182  Our results show that RASSF1A uses a unique microtubule-binding pattern to promote site-specific mic
183                              In both motors, microtubule binding promotes ordered conformations of co
184 ontains a motor homology domain that retains microtubule binding properties but lacks a nucleotide bi
185 esidue-wise determinants of distinct kinesin-microtubule binding properties.
186                                Combining the microtubule-binding properties of TAU with the Cre-loxP
187 hemically and structurally characterized the microtubule-binding properties of the amino- and carboxy
188 unit in turn caused a dramatic change in the microtubule-binding properties of the N-terminal domain
189 t asymmetric Rac activity both localizes the microtubule binding protein Apc2 to orient one GSC centr
190 lopmental Cell, Ambrose et al. show that the microtubule binding protein CLASP regulates PIN2 auxin t
191 e have found that 14-3-3epsilon binds to the microtubule binding protein doublecortin preventing its
192 were fused to the C-terminal helix bundle of microtubule binding protein EB1.
193 reviously unreported interaction between the microtubule binding protein end-binding 1 (EB1) and the
194 t of 3.1), such that Pins recruitment of the microtubule binding protein Mud (NuMA) occurs over a ver
195 -box protein FSN-1 and functions through the microtubule binding protein RAE-1.
196             Extensive phosphorylation of the microtubule binding protein tau has been implicated in n
197                                          The microtubule binding protein tau is strongly implicated i
198                                          The microtubule binding protein tau may mediate the effects
199                                     Tau is a microtubule binding protein that forms pathological aggr
200 ugh its direct downstream effector ninein, a microtubule binding protein.
201  identified microtubule-associated protein 4 microtubule-binding protein as a novel SKAP-binding part
202                         Here we identify the microtubule-binding protein centriole and spindle-associ
203 tes centrosome maturation by stabilizing the microtubule-binding protein ch-TOG, defining a novel rol
204    We identify a novel function for both the microtubule-binding protein CLAMP and members of the mic
205         Miller et al. find that a TOG domain microtubule-binding protein imparts intrinsic tension se
206 r and spindle-associated protein NUSAP1 is a microtubule-binding protein implicated in spindle stabil
207  centromere-associated network proteins, the microtubule-binding protein NDC80, and the formation of
208 ns and that the phosphorylation state of the microtubule-binding protein Tau can be altered by RNA in
209                                Recently, the microtubule-binding protein tau has been implicated in t
210                          Accumulation of the microtubule-binding protein tau is a key event in severa
211             The abnormal accumulation of the microtubule-binding protein tau is associated with a num
212                         CENP-F is a nonmotor microtubule-binding protein that participates in microtu
213 rtin on the X-chromosome (DCX) is a neuronal microtubule-binding protein with a multitude of roles in
214                                     DCX is a microtubule-binding protein, and much work has focused o
215 ation factor like-2 (Arl2) and Msps, a known microtubule-binding protein, control cell polarity and s
216                                          The microtubule-binding protein, tau, is the major component
217 e repeats are also present in CCSAP, another microtubule-binding protein.
218  for X-linked lissencephaly, which encodes a microtubule-binding protein.
219 ce-based assay for measuring the affinity of microtubule binding proteins for microtubules.
220                                      Several microtubule binding proteins, including end-binding prot
221  microtubules, microtubule motors, and other microtubule binding proteins.
222 ons of the mechanisms of action of different microtubule-binding proteins and drugs, thereby enabling
223 ificant gaps in our knowledge concerning how microtubule-binding proteins bind to microtubules, how d
224 al proteins to axons and dendrites relies on microtubule-binding proteins such as CRMP, directed moto
225                    Septins are membrane- and microtubule-binding proteins that assemble into filament
226 TAN1) and AUXIN-INDUCED-IN-ROOTS9 (AIR9) are microtubule-binding proteins that localize to the divisi
227 mplex that connects the inner kinetochore to microtubule-binding proteins.
228 n are believed to regulate interactions with microtubule-binding proteins.
229  version of the CPC lacking the INCENP/Sli15 microtubule binding region (residues Glu-91 to Ile-631)
230 over, phosphorylation of INCENP/Sli15 on its microtubule binding region also negatively regulates CPC
231 -range contacts between both termini and the microtubule binding region that characterize its compact
232  Moreover, the individual repeats within the microtubule binding region that directly interface with
233 rons is C-terminally truncated and lacks the microtubule-binding region (MTBR) thought necessary for
234                                We mapped the microtubule-binding region of Smc5 and generated a mutan
235     The phosphorylation site is located in a microtubule-binding region that is variable for two isof
236                                          The microtubule-binding region, spanning residues 244-372, r
237 gregation-competent tau (i.e., contained the microtubule-binding regions) and this material appears t
238 ease, whereby the N terminus (exons 2/3) and microtubule binding repeat length contribute to Tau rele
239 nteraction with cyanine was localized to the microtubule binding repeat region.
240 ndent on the presence or absence of a fourth microtubule binding repeat.
241 auopathy characterised by deposition of four microtubule-binding repeat (4R) tau with minimal Abeta p
242 d residues include motifs located within the microtubule-binding repeat domain on tau (Ser-262, Ser-3
243 tations are primarily located in or near the microtubule-binding repeat regions of tau and can have v
244 rming region to a hexapeptide from the third microtubule-binding repeat resulted in a peptide that ra
245             Self-assembly is mediated by the microtubule binding repeats in tau.
246 ptide corresponding to the first of the four microtubule binding repeats of Tau.
247 -length tau or truncated tau containing four microtubule binding repeats resulted in rapid induction
248 ncation mutant, K18, which contains all four microtubule binding repeats, and isolate the monomeric f
249 hat contain either three (3-R) or four (4-R) microtubule binding repeats.
250 he presence or absence of the second of four microtubule binding repeats.
251 10 generates tau isoforms with three or four microtubule-binding repeats, 3R-tau and 4R-tau, which is
252  isoforms containing three (3R) or four (4R) microtubule-binding repeats.
253                             Eliminating SKAP microtubule binding results in severe chromosome segrega
254            Spastin also displays an adjacent microtubule binding sequence, and the presence of both E
255 d elements of the tail - the ATP-independent microtubule-binding sequence and the IAK autoinhibitory
256 of the mitotic spindle through a chromosomal microtubule binding site called the kinetochore.
257  motor domain, kinesin-5 also has a nonmotor microtubule binding site in its C terminus [6].
258 combinase-mediated removal in oocytes of the microtubule binding site of nuclear mitotic apparatus pr
259 persistent hydrogen bond with D26 within the microtubule binding site.
260 structure of the TcpB TIR domain reveals the microtubule-binding site encompassing the BB loop as wel
261 -terminal head domain and an ATP-independent microtubule-binding site in its C-terminal tail domain.
262 -1 molecular motor contains an ATP-dependent microtubule-binding site in its N-terminal head domain a
263 es in vitro and provides Kif2b with a second microtubule-binding site to target it to the spindle.
264 imately utilize its free energy, such as the microtubule-binding site, drug-binding loop 5, and neckl
265 for the conserved active site or disrupt the microtubule-binding site.
266  motor domain, which contains nucleotide and microtubule binding sites and mechanical elements to gen
267 oadblocks to permanently obstruct individual microtubule binding sites and studied the movement of in
268  combination of four motor and four nonmotor microtubule binding sites for its microtubule organizing
269          Rather, kinesin-5 utilizes nonmotor microtubule binding sites to tune its microtubule attach
270 ficient and accurate assembly of kinetochore-microtubule binding sites.
271 the phosphomimetic mutation S262E within tau microtubule-binding sites impairs EB/tau interaction and
272 lex via the C-terminal region of EBs and the microtubule-binding sites of tau.
273                  Tau residues in between the microtubule-binding sites remain flexible when Tau is bo
274 c24, and Spc25), constitutes one of the core microtubule-binding sites within the kinetochore.
275 tment of the NDC80 complex to form efficient microtubule-binding sites.
276 emature stabilization requires the conserved microtubule-binding Ska complex, which enriches at attac
277 au displays a strong functional overlap with microtubule-binding spectraplakins, establishing new lin
278 ATPase site within dynein's AAA+ ring or its microtubule-binding stalk directly, Lis1 engages the int
279 inds to its motor domain and induces a tight microtubule-binding state in dynein.
280 ransitions that interconvert weak and strong microtubule binding states.
281                                          How microtubule binding stimulates their ATPase and controls
282                        This unique bipartite microtubule-binding structure may mediate the spindle-po
283               Both interactions involved the microtubule-binding surfaces of Ndc80C and were directly
284                  We found that the non-motor microtubule-binding tail domain interacts with the micro
285 rotubules depends on its N-terminal nonmotor microtubule-binding tail, as KlpA without the tail is no
286                    By conjugating a specific microtubule-binding taxoid core to the tetrazole/alkene
287  addition to Aurora B regulating kinetochore-microtubule binding, the kinetochore also controls Auror
288 from multiple effects not related to kinesin-microtubule binding, the prediction rate of 0.843 area u
289 el in which L5 regulates both nucleotide and microtubule binding through a set of reversible interact
290  in growth cone filopodia via binding to the microtubule-binding +TIP protein EB3 and organizes F-act
291 ties such as autoinhibition of the motor and microtubule binding to arise through convergent evolutio
292 bonds may play an important role in coupling microtubule binding to ATPase activities in kinesin.
293 e-mapped the dystrophin domain necessary for microtubule binding to spectrin-like repeats 20-22.
294 ndle assembly checkpoint triggered when TOG5-microtubule binding was compromised, indicating that TOG
295 iation constant of approximately 200 nm, and microtubule binding was not dependent on the C-terminal
296  the C-terminal doublecortin domain affected microtubule binding, whereas a monoclonal mouse antibody
297 racterized Kif11 inhibitors that block tight microtubule binding, whereas BTB-1 traps Kif18A on the m
298 olution and is displaced allosterically upon microtubule binding, which allows its robust accumulatio
299 The INCENP SAH domain also mediates INCENP's microtubule binding, which is negatively regulated by Cy
300 Remarkably, this domain enhances kinesin-5's microtubule binding without substantially reducing motor

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。
 
Page Top