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1 ts based on PDB chains are newly included in ASTRAL.
2 ROs data were collected from participants of ASTRAL-2 and ASTRAL-3 studies before, during, and after
3  collected from participants of ASTRAL-2 and ASTRAL-3 studies before, during, and after treatment usi
4 d in a randomised, open-label phase 3 trial (ASTRAL-4) in which patients with HCV-related decompensat
5 virological response rates were sourced from ASTRAL-4, SOLAR-1, and SOLAR-2.
6 l ones by querying a flexible protein in the Astral-40 database (11 154 protein domains).
7                                   We present ASTRAL, a fast method for estimating species trees from
8 n both retrieval and statistical accuracy on ASTRAL, a SCOP-based test set.
9 e capture via loss of cortical dynein causes astral and cortical microtubules to be greatly reduced i
10  tracking revealed that mEg5 punctae on both astral and midzone microtubules rapidly bind and unbind.
11  OCLN loss impaired spindle pole morphology, astral and mitotic microtubule integrity.
12  by Aurora B-INCENP, led to assembly of mono-astral and monopolar structures instead of bipolar spind
13 EB1, which localized to polymerizing ends of astral and spindle microtubules, was used to track their
14  of the homotetrameric kinesin-5, KLP61F, in astral, centrosome-controlled Drosophila embryo spindles
15 ure prediction program, is used to build the astral compendium for sequence and structure analysis, a
16 than 40% sequence identity as defined by the ASTRAL compendium of protein structures are included.
17                                          The ASTRAL compendium provides several databases and tools t
18                                          The ASTRAL Compendium provides several databases and tools t
19                                          The ASTRAL compendium provides several databases and tools t
20 ral major improvements have been made to the ASTRAL compendium since its initial release 2 years ago.
21      SCOPe also incorporates and updates the ASTRAL compendium, which provides multiple databases and
22      SCOPe also incorporates and updates the ASTRAL compendium, which provides several databases and
23      These new features are reflected in the ASTRAL compendium.
24                       The current release of ASTRAL contains 54,745 domains, more than three times as
25 egative regulation of myosin distribution by astral cues.
26 ery that a plasmid-partitioning ATPase forms astral cytoskeletal structures both unveils a new family
27      SCOPe also incorporates and updates the ASTRAL database.
28 e database, as well as integrated into other ASTRAL databases such as representative subsets.
29            Hexylene glycol resulted in rapid astral elongation due to decreased MT catastrophe and pr
30 , certain rituals were scheduled by solar or astral events and restricted to initiates/social achieve
31 ld be partially suppressed by disrupting the astral forces that pull spindle poles apart in the 1 cel
32                                              ASTRAL has undergone major transformations in the past 2
33 tion and multispecies coalescent approaches (ASTRAL-II and SVDquartets).
34                                 We show that ASTRAL-II has substantial advantages over ASTRAL: it is
35 L's running time is [Formula: see text], and ASTRAL-II's running time is [Formula: see text], where n
36 esent a new version of ASTRAL, which we call ASTRAL-II.
37 cally reduces running time, and enables both ASTRAL-III and RAxML to complete on datasets (that they
38 es tree estimation with two leading methods, ASTRAL-III and RAxML.
39 CL, can have up to 158x speedups compared to ASTRAL-III.
40 ing the number of gene trees required by the ASTRAL inference method, and the approach has potential
41                                              ASTRAL is a widely used summary method and has been able
42 he current single-threaded implementation of ASTRAL is falling behind the data growth trends is not a
43 ition to several complete updates each year, ASTRAL is now updated on a weekly basis with preliminary
44                                              ASTRAL is often more accurate than concatenation using m
45                                              ASTRAL is statistically consistent, can run on datasets
46 pite the limitation to allowed bipartitions, ASTRAL is statistically consistent.
47 at ASTRAL-II has substantial advantages over ASTRAL: it is faster, can analyze much larger datasets (
48                                              Astral-like microtubules are not usually prominent in pl
49           The elongated spindle has numerous astral-like microtubules, and aPKCzeta, normally associa
50 position in concert with the position of the astral microtubule anchoring complex LGN-NuMA to yield t
51 it as astrin because of its association with astral microtubule arrays assembled in vitro.
52 ntained bipolar spindles with dense and long astral microtubule arrays but with poorly organized kine
53 orylates MISP, thus stabilizing cortical and astral microtubule attachments required for proper mitot
54 e orientation via regulation of actin cortex-astral microtubule attachments.
55                                Comparison of astral microtubule behavior in mitosis with microtubule
56 nd positioning around chromosomes depends on astral microtubule connections to a moving cell cortex.
57  yeast, Schizosaccharomyces pombe, depend on astral microtubule dynamics that drag the nucleus throug
58 ctility both preceded and was independent of astral microtubule elongation, suggesting that the initi
59 Delta and gfh1Delta cells exhibit defects in astral microtubule formation and anchoring, suggesting t
60 or EB1 in processes that promote equality of astral microtubule function at both poles in a spindle.
61 g that these proteins have specific roles in astral microtubule function.
62 bly, although it is required for cytoplasmic astral microtubule growth during mitosis.
63 n surrounding the nucleus, which we term the astral microtubule interaction zone (AMIZ).
64 s to regulate cell cycle-specific changes in astral microtubule length to ensure proper spindle align
65 on we found that cenexin depletion decreased astral microtubule length, disrupted astral microtubule
66 equired for proper chromosome separation and astral microtubule length.
67 iated role for the Astrin/SKAP complex as an astral microtubule mediator of mitotic spindle positioni
68 creased astral microtubule length, disrupted astral microtubule minus-end organization, and increased
69 turb spindle orientation solely by affecting astral microtubule nucleation or whether centrosome prot
70                                    Moreover, astral microtubule number and length correlated with the
71  of SPB maturation, control the asymmetry of astral microtubule organization between the preexisting
72                                   Asymmetric astral microtubule organization drives the polarized ori
73 ove the differential activity of the SPBs in astral microtubule organization rather than intrinsic di
74 icrotubules (aMTs) while the new pole delays astral microtubule organization.
75 NA is involved in negative regulation of the astral microtubule organizing capacity of the spindle po
76 ), Polo, and Fascetto (Prc1) localize to the astral microtubule overlap region.
77 gly, most of the suppressors that rescue the astral microtubule phenotype also reduce Cdk1-CycB activ
78 by gating the recruitment of dynactin to the astral microtubule plus end, a prerequisite for offloadi
79                          Khc-73 localizes to astral microtubule plus ends, and Dlg/Khc-73 and Dlg/Pin
80 ng abnormally stretched or fragmented due to astral microtubule pulling forces.
81 contain mitotic actin bundles, which prevent astral microtubule-actin cortex attachments.
82 ryogenesis is characterized by shifting from astral microtubule-based to central spindle-based positi
83  interactions with mutations that deactivate astral microtubule-dependent nuclear migration.
84  Caenorhabditis elegans one-cell embryo, the astral microtubule-dependent pathway requires anillin, N
85                           Reestablishment of astral microtubule-mediated forces align the spindle pol
86          We provide evidence for dynein- and astral microtubule-mediated transport of Galphai/LGN/nuc
87 hem as kinetochore (KMTs), spindle (SMTs) or astral microtubules (AMTs) according to their positions,
88 n, is a dynamic complex whose recruitment to astral microtubules (aMTs) increases dramatically during
89 ll cycle) contacting the bud by its existing astral microtubules (aMTs) while the new pole delays ast
90 -300 nuclear ring and a polarized network of astral microtubules (aMTs).
91 in to the cell cortex followed by capture of astral microtubules (aMTs).
92  they grow, their minus ends are captured by astral microtubules (MTs) and transported poleward throu
93                                              Astral microtubules (MTs) are known to be important for
94      Contacts between cytoplasmic dynein and astral microtubules (MTs) at the cell cortex generate pu
95 cess begins with the capture of pole-derived astral microtubules (MTs) by the polarity determinant Bu
96                                              Astral microtubules (MTs) emanating from the mitotic app
97 e positioning in budding yeast by pulling on astral microtubules (MTs) from the cell cortex.
98 A), proteins that generate pulling forces on astral microtubules (MTs) through cytoplasmic dynein.
99 ynactin was sufficient to generate forces on astral microtubules (MTs) to orient the spindle, with Nu
100 of the spindle apparatus by associating with astral microtubules (MTs), and this association is essen
101 ates MF-dependent cortical forces applied to astral microtubules (MTs).
102 nuclear complex (PNC) and its two associated astral microtubules (MTs).
103 ell axis, so that cortical motors pulling on astral microtubules align bipolar spindles with the inte
104                                              Astral microtubules also inhibit RhoA accumulation at th
105 rk in mitotic cells with an extension of the astral microtubules and a reduction of kinetochore micro
106 rnover of LGN relies, at least partially, on astral microtubules and DYNC1H1.
107 nted spindles were associated with disrupted astral microtubules and near complete loss of a unique s
108 (TCJs) localize force generators, pulling on astral microtubules and orienting cell division via the
109 e involved in generating forces that pull on astral microtubules and position the spindle asymmetrica
110 CLASPs act partially redundantly to regulate astral microtubules and position the spindle during asym
111  microtubules with a significant increase in astral microtubules and reduction in K-fiber fluorescenc
112 l deposition of new furrow membrane requires astral microtubules and release of internal stores of Ca
113 centrin-gamma TuRC interaction and perturbed astral microtubules and spindle bipolarity.
114 cordingly, Hook2-depleted cells have reduced astral microtubules and spindle positioning defects.
115 ed to be governed by the interaction between astral microtubules and the cell cortex and involve cort
116 itioning depends on interactions between the astral microtubules and the cell cortex.
117 enter to the cortex, a process that requires astral microtubules and the microtubule-based motor dyne
118             Cytokinesis is regulated by both astral microtubules and the midzone microtubules of the
119  molecular mechanism for the organization of astral microtubules and the mitotic spindle through Rab1
120                              The majority of astral microtubules are dynamically unstable.
121                                     Although astral microtubules are known to play roles in these pro
122  demonstrate that dynein-dependent forces on astral microtubules are propagated through the spindle d
123                    Our results indicate that astral microtubules are required for establishing bipola
124 physical centrosome removal demonstrate that astral microtubules are required for such spindle elonga
125 racted to form spindles joined in series via astral microtubules as revealed by live cell imaging.
126 he stabilization of cortical associations of astral microtubules at cell-cell adhesions to orient the
127  to examine the residence time of individual astral microtubules at the cell cortex of developing emb
128 raction at SPBs compromises the anchorage of astral microtubules at the SPB and surprisingly also inf
129 f, while making contact with the cortex, the astral microtubules buckle as they exert compressive, pu
130 h MUG and normal mitosis, chromatin attracts astral microtubules but cannot induce spindle assembly.
131 absence of a functional exclusion mechanism, astral microtubules can associate with Pins over the ent
132                Remarkably, cells depleted of astral microtubules conduct accurate, complete cytokines
133                      These forces act before astral microtubules contact the cortex; thus, dynein mus
134   During mitosis, spindle poles align so the astral microtubules contact the lateral cortex.
135  cortical dynein-generated pulling forces on astral microtubules contribute to anaphase spindle elong
136  same cytokinetic signaling ensemble-opposed astral microtubules decorated with Ect2 and Cyk4.
137                        We show that reducing astral microtubules decreases the frequency of spindle m
138 in movement to orient the mitotic spindle as astral microtubules depolymerize.
139                      Before cellularization, astral microtubules determine metaphase furrow position
140 ow the cortex causes the depolymerization of astral microtubules during asymmetric spindle positionin
141 held assumptions that the centrosome and the astral microtubules emanating from it are essential for
142 pindles prevented recapture of the cortex by astral microtubules emanating from the pole pivoting awa
143                         The distance between astral microtubules ends and the anterior cortex was sig
144 contact geometry from "end-on" to "side-on." Astral microtubules engage cortically anchored motors al
145                      Simultaneous contact of astral microtubules from both poles with the AMIZ direct
146                                              Astral microtubules from one pole only then contact the
147                                              Astral microtubules grow out from the two spindle poles,
148  In this study, we investigate how forces on astral microtubules impact the genome during cell divisi
149 g that Ect2 migrates from spindle midzone to astral microtubules in anaphase and that Ect2 shapes the
150 port a role for both the central spindle and astral microtubules in cytokinesis in animal cells.
151 sh embryos, where cells are unusually large, astral microtubules in metaphase are too short to positi
152 dundantly to suppress the formation of basal astral microtubules in neuroblasts.
153 r RNAi leads to a reduction in the length of astral microtubules in syncytial embryos, larval neurobl
154  the actomyosin cytoskeleton to plus ends of astral microtubules in the equatorial region of the cell
155                Because the plus-ends of many astral microtubules in the spindle point to the cell cor
156 es delayed development and a failure to form astral microtubules in the zygote.
157 000, consistent with the several thousand of astral microtubules in these cells.
158 absence of Cdc28-Clb4 activity (G1/S phase), astral microtubules interact with the bud tip in a manne
159                         Dynamic plus ends of astral microtubules interact with the shmoo tip in matin
160 eavage plane geometry in which the length of astral microtubules is limited by interaction with these
161 ted at the cell cortex to generate forces on astral microtubules is not clear.
162     Rather, confinement increases numbers of astral microtubules laterally contacting the cortex, shi
163                                Disruption of astral microtubules leads to misalignment of the spindle
164 l release and transport of LGN complex along astral microtubules may contribute to spindle positionin
165                                 Transport on astral microtubules may provide a general mechanism for
166                 In contrast, mEg5 punctae on astral microtubules moved transiently toward microtubule
167 though these cells lack the radial arrays of astral microtubules normally associated with each spindl
168 process thought to include direct capture by astral microtubules of kinetochores and/or noncentrosoma
169 yeast spindle pole body [SPB]) nucleate more astral microtubules on one of the two spindle poles than
170                               Loss of either astral microtubules or Lis1/dynactin leads to spindle/co
171 primed to form furrows at either overlapping astral microtubules or the central spindle.
172     As nuclei divide, continued transport on astral microtubules partitions germ plasm to daughter nu
173                          Cortical pulling on astral microtubules positions the mitotic spindle in res
174 mal in these embryos, but reduced numbers of astral microtubules reach all regions of the cortex at t
175                                  A subset of astral microtubules stabilizes during anaphase, becoming
176 o2(S338N) and mto1Delta cells nucleate fewer astral microtubules than normal and have higher levels o
177 the most dramatic effect on the lifetimes of astral microtubules that extend toward the cell cortex.
178 le treatment revealed a population of stable astral microtubules that formed during anaphase; among t
179                                     The long astral microtubules that occur in the absence of Kif18B
180  However, mitotic C377S tub1 cells displayed astral microtubules that often appeared excessive in num
181 phases due to a tethering force, mediated by astral microtubules that reach the anterior cell cortex.
182 brane, where dynein captures and walks along astral microtubules to help orient the mitotic spindle.
183 ocalized cortical motor complexes can act on astral microtubules to orient the spindle.
184      The dynein/dynactin motor complex pulls astral microtubules to orient the spindle.
185 ar mitotic apparatus protein (NuMA)-positive astral microtubules to orientate the mitotic spindle.
186 chromosomes during anaphase, cooperates with astral microtubules to position the cleavage furrow.
187  anchored dynein generates pulling forces on astral microtubules to position the mitotic spindle acro
188 s and activates Dynein motors, which pull on astral microtubules to position the mitotic spindle.
189 c delay and prevents appropriate assembly of astral microtubules to promote spindle misorientation.
190                However, the motors that pull astral microtubules toward these actin structures are no
191 eted embryos, but the polymerization rate of astral microtubules was not slower than in wild type.
192 eation rate in LLCPK cells and the number of astral microtubules was similar in stathmin +/+ and -/-
193 rosome and a subset of differentially stable astral microtubules were also observed.
194 e alignment by regulating the interaction of astral microtubules with subdomains of the bud cortex.
195 tioned and oriented by interactions of their astral microtubules with the cellular cortex, followed b
196  rotation is dependent on the interaction of astral microtubules with the cortical actin cytoskeleton
197 ators connect epithelial polarity sites with astral microtubules, allowing dynein movement to orient
198 elial cells resulted in the disappearance of astral microtubules, and dividing spindle fiber formatio
199 om the cell cortex through interactions with astral microtubules, but neither the mechanism governing
200   Surprisingly, this disruption destabilizes astral microtubules, but not kinetochore-microtubule att
201 bules nucleated along the length of existing astral microtubules, but this increase negatively affect
202 tic centrosomes and has few or no detectable astral microtubules, can develop into an adult fly.
203 entrosomes lose gamma-tubulin, spindles lose astral microtubules, chromosomes fail to reach a metapha
204  dominant-negative Rab11 expression disrupts astral microtubules, delays mitosis, and redistributes s
205                                 We show that astral microtubules, kinesin Khc-73, and Discs large (Dl
206 otic cells, including a drastic reduction in astral microtubules, malformed mitotic spindles, defocus
207        We report that even in the absence of astral microtubules, metaphase spindles in MDCK and HeLa
208 l the plus-end dynamics and cargoes of their astral microtubules, remotely from the minus-end.
209 cally, constitutively active Rab11 increases astral microtubules, restores gamma-tubulin spindle pole
210                                      Second, astral microtubules, structures that undergo similar pat
211 e at approximately 11 microm/min, similar to astral microtubules, suggesting polymerization velocity
212 ely associated with both the cell cortex and astral microtubules, suggesting that it may directly int
213 ed through a cortical machinery by capturing astral microtubules, thereby generating pushing/pulling
214 er to move from this SPB to the plus ends of astral microtubules, where Cdc28-Clb4 regulates the inte
215 nhibition of dynein blocked mEg5 movement on astral microtubules, whereas depletion of the Eg5-bindin
216  gamma-tubulin complex organizes spindle and astral microtubules, which, in turn, separate replicated
217 rst, Peg1 was required to form a spindle and astral microtubules, yet destabilized interphase microtu
218 nisms of mitotic spindle orientation rely on astral microtubules.
219 g by affecting the stability and dynamics of astral microtubules.
220 rces that act between the cell periphery and astral microtubules.
221 ndle misorientation accompanied by shortened astral microtubules.
222 teractions of cortical molecular motors with astral microtubules.
223 rganize in vitro into asters, which resemble astral microtubules.
224 ion plane and a reduced number and length of astral microtubules.
225 ioles and are not anchored to the cortex via astral microtubules.
226 n and activate the motor activity pulling on astral microtubules.
227 tic polarization via the central spindle and astral microtubules.
228 parallel with a second pathway that involves astral microtubules.
229 nents of the signaling pathway downstream of astral microtubules.
230 recruited, and thus modulate the behavior of astral microtubules.
231  proteins and large sizes, rely primarily on astral microtubules.
232  latter delivered cytoplasmic aurora B along astral microtubules.
233 determined site of cytokinesis by pulling on astral microtubules.
234 cal machine that mediates a pulling force on astral microtubules.
235 endent pulling forces exerted on the tips of astral microtubules.
236 tor complex, which exerts a pulling force on astral microtubules.
237 plus-end tracking, including localization to astral microtubules.
238 bule organization and a dramatic increase in astral microtubules.
239 rients the spindle through interactions with astral microtubules.
240 are thought to be organized differently from astral mitotic spindles, but the field lacks the basic s
241                                 Importantly, ASTRAL-MP can take advantage of not just multiple CPU co
242                                          The ASTRAL-MP code scales very well with increasing CPU core
243               Using GPUs and multiple cores, ASTRAL-MP is able to analyze datasets with 10 000 specie
244                  In this paper, we introduce ASTRAL-MP, the first version of ASTRAL that can exploit
245          To investigate the effect of excess astral MT activity, we depleted the MT depolymerizer mit
246 ally assemble a connected pair of polarized, astral MT arrays--termed an amphiaster ("a star on both
247                   Our findings indicate that astral MT contact with the cortex is necessary for furro
248  importazole treatment results in defects in astral MT dynamics, as well as in mislocalization of LGN
249 etween EB1 and p150glued suppressed anaphase astral MT elongation and resulted in a delay of cytokine
250                                  Analysis of astral MT growth rates during anaphase shows that MTs co
251 per LGN and NuMA localization but stabilizes astral MT interactions with the cortex.
252 y protein that interacts with EB1 to control astral MT length.
253                                      Because astral MT minus-ends are anchored by centrosomes at spin
254 At the onset of mitosis, the position of the astral MT network, specifically its center, determines t
255 8 Kif18B functions during mitosis to control astral MT organization.
256 the nucleus in interphase and is enriched at astral MT plus ends during early mitosis.
257                                              Astral MT shrinkage linked to Bud6p involves its direct
258 ression had no effect on ER association with astral MTs and concentration around spindle poles in ear
259 protein She1 regulates dynein activity along astral MTs and directs spindle movements toward the bud
260 ndle MTs are partially destabilized, whereas astral MTs are dramatically destabilized.
261    The mechanisms that associate the ER with astral MTs are unknown.
262 and their interaction promotes elongation of astral MTs at anaphase onset.
263 of HIs between the MTs, the cytoplasm-filled astral MTs behave like a porous medium, with its permeab
264 ating MTs that form interpolar bundles or by astral MTs connected to the cell cortex.
265 row initiation but that the dynamic state of astral MTs does not affect their competency to stimulate
266 MCAK) from HeLa cells to produce ultra-long, astral MTs during mitosis.
267 ng normal contractile activity and that long astral MTs enlarge the blebs.
268 duction and spindle positioning, and loss of astral MTs has been reported to increase cortical contra
269 re was a sudden onset of ER association with astral MTs in dynein RNAi cells, revealing activation of
270   To maintain SPOC-mediated anaphase arrest, astral MTs must maintain persistent interactions with an
271            The data demonstrate that dynamic astral Mts search the cytoplasm for other Mts, as well a
272 ve role by serving as an attachment site for astral MTs to pull centrosomes apart [3-6].
273 n but did not prevent elongation of anaphase astral MTs toward the cortex, suggesting that EB1 and dy
274 monstrated that both motors decorated single astral MTs with dynein persisting at the plus end in ass
275   Urethane resulted in short, highly dynamic astral MTs with increased catastrophe that also stimulat
276 e cooperative activity of MSP-300, Klar, and astral MTs, and demonstrate its physiological significan
277 by nocodazole treatment, which depolymerizes astral MTs, or by overexpression of CLASP1, which does n
278                 In addition to localizing to astral MTs, She1 also targets to the spindle, but its ro
279 etter accuracy than prior methods, including ASTRAL-multi (the only method to date that has been prov
280               These results demonstrate that astral overlap in equilaterally dividing cells not only
281          In particular, we conclude that the astral pathway for cleavage-furrow formation involves th
282 ged nonmuscle myosin, we have found that the astral pathway for furrow formation involves the negativ
283      We tested the classical hypothesis that astral, prometaphase bipolar mitotic spindles are mainta
284 affected the assembly of microtubules in the astral region and impaired microtubule nucleation at the
285                                              ASTRAL runs in polynomial time, by constraining the sear
286                                              ASTRAL's running time is [Formula: see text], and ASTRAL
287                    Notably, coalescent-based ASTRAL species phylogenies inferred from Run1 and Run2 s
288 lex, which regulates cortical attachments of astral spindle microtubules.
289 ssociate with centrosomes and play a role in astral spindle pole integrity in mitotic systems.
290 bryo, GFP-Pav-KLP cyclically associates with astral, spindle, and midzone microtubules and also to ac
291 c pronuclei drift centripetally and assemble astral spindles lacking cortical interactions, leading t
292 ndles, and perhaps also to interpolar MTs in astral spindles.
293                          Previously reported astral spreading during embryonic micromere formation su
294 we introduce ASTRAL-MP, the first version of ASTRAL that can exploit parallelism and also uses random
295      Several search tools have been added to ASTRAL to facilitate retrieval of data by individual use
296                    To enhance the utility of ASTRAL to structural biologists, all SCOP domains are no
297                      In this analysis of the ASTRAL trials (non-opioid substitution therapy [OST], n
298                                              ASTRAL uses dynamic programing and is not trivially para
299 ecently developed a coalescent-based method, ASTRAL, which is statistically consistent under the mult
300                  We present a new version of ASTRAL, which we call ASTRAL-II.

 
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