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1 emoval and retention of the scaffold protein Anillin.
2 eopontin, PRX1, LMCD1, GPR91, leiomodin, and anillin.
3 a gene involved in cellularization, encodes Anillin.
4 on of APC/C(Cdh1) increased the half-life of anillin.
5 reconstituted by adding an adaptor protein, anillin.
6 phanous and in furrow-progression mutants of Anillin.
7 uler for the recruitment and localization of anillin, a contractile protein and a crucial regulator o
9 n-independent interaction between Sticky and Anillin, a key scaffold also required for midbody ring f
11 recombinant fragments, we determine that the anillin ActBD harbors three distinct actin-binding sites
13 d cell biological data suggest that multiple anillin-actin interaction modes promote the faithful pro
19 to the overall F-actin bundling activity of anillin and enables anillin to switch between two actin-
24 ity and limit localization of both canonical anillin and non-muscle myosin II (NMM-II) to intercellul
25 his is evidenced by increased RhoA activity, anillin and nonmuscle myosin II in the cytokinetic ring,
27 for Diaphanous in recruitment of myosin II, anillin and Peanut to the cortical region between actin
31 R proteins are required for the retention of anillin and septin in the anterior pole, which are cytok
35 is maintained at the intercellular bridge by anillin, and CYK-4 is localized independently of ZEN-4 b
36 t early and late furrow proteins (Pavarotti, Anillin, and Myosin) are localized to the neuroblast bas
38 ocodazole-induced upregulation of cyclin B1, anillin, and securin was decreased in DNA-PKcs-deficient
41 In the absence of both PIG-1/MELK and the anillin ANI-1, myosin accumulates at the anterior cortex
43 rs promote accumulation of the noncannonical anillin ANI-2 at the stable cytoplasmic bridge, which in
44 ate that the cytoskeletal organizing protein anillin (ANI-1) promotes the formation of an aster-direc
46 hat loss of the cytoskeletal adaptor protein anillin (ANLN) from oligodendrocytes disrupts myelin sep
47 , we identified a missense mutation R431C in anillin (ANLN), an F-actin binding cell cycle gene, as a
48 7A, its substrate Sqh/MRLC, and the effector Anillin/ANLN regulate mitosis and cytokinesis in gliomas
51 an in vitro expression screen, we identified anillin as a substrate of the anaphase-promoting complex
52 to recruit actin regulators and the scaffold anillin as well as to regulate RhoA and Rac via its intr
58 al spindle is also disrupted, revealing that anillin can also act at an early stage of cytokinesis.
59 acid changes in the C-terminal PH domain of Anillin cause defects in septin recruitment to the furro
60 video microscopy, we show that three genes: anillin, citron-kinase (CG10522), and soluble N-ethylmal
62 Like other metazoan homologs, Drosophila anillin contains a conserved domain that can bind and bu
68 estigate how the actomyosin scaffold protein anillin contributes to epithelial mechanics in Xenopus l
70 LKB1 impinges on myosin via two pathways, an anillin-dependent pathway that also responds to the cull
71 at midcell is achieved through positive Mid1/anillin-dependent signaling emanating from the central n
72 e absence of anillin, furrows cannot form in anillin-depleted cells in which the central spindle is a
73 regulate late steps of maturation including anillin dispersal, ESCRT-III recruitment, and the format
75 nut, actin, and the actin-associated protein Anillin, do not become correctly localized in pav mutant
77 d1 and show that duplication of an ancestral anillin early in the Schizosaccharomyces lineage may hav
79 esults highlight specialization of divergent anillin family proteins in the C. elegans life cycle and
82 SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adaptor anillin form previously unrecognized filaments that exte
84 f the division plane positioning factor Mid1/anillin from the nucleus and negatively by the Pom1/DYRK
88 rm and initiate ingression in the absence of anillin, furrows cannot form in anillin-depleted cells i
92 tify and characterize a second fission yeast anillin homologue, Mid2p, which is not orthologous with
97 ely, our data point to an important role for Anillin in scaffolding cleavage furrow components, direc
102 hat also responds to the cullin CUL-5 and an anillin-independent pathway involving the kinase PIG-1/M
103 ole of anillin in this process and show that anillin inhibits not only the accumulation of myosin II
104 -dependent but may also be mediated by known anillin interactions with F-actin and myosin II, which a
106 emonstrate that the contractile ring protein anillin interacts directly with nonmuscle myosin II and
116 dly showed that junctions recoil faster when anillin is depleted and slower when anillin is overexpre
118 Collectively, these findings suggest that anillin is important in maintaining the integrity of the
120 ns and adherens junctions are disrupted when Anillin is knocked down, leading to altered cell shape a
121 ment of vinculin to cell-cell junctions when anillin is overexpressed suggested that anillin promotes
126 suggest the interaction between Rho-GEFs and anillins is an important step in the signaling pathways
127 sed on the regulation of bridge stability by anillins, key regulators of cytokinetic rings and cytopl
128 have investigated embryonic morphogenesis in anillin knockdown (scra RNAi) embryos, where basal cell
131 ion-and-rescue assay in Drosophila S2 cells, anillin lacking the entire actin-binding domain (ActBD)
132 which prevents CR assembly in the absence of anillin-like Mid1 and causes CRs to collapse when cytoki
133 ration of the spindle pole bodies (SPB), the anillin-like protein (Mid1p) migrates from the nucleus a
134 otide-exchange factor (RhoGEF) Bud3, and the anillin-like protein Bud4 exclusively at the outer zones
135 e [5-8]; then, massive nuclear export of the anillin-like protein Mid1 at mitosis entry confirms or r
141 a mutation affecting the septin-interacting, anillin-like protein Mid2, suggesting that Scw1 function
142 n important factor in this process is mid1p (anillin-like protein), which is a peripheral-membrane pr
144 lay the groundwork for future studies on how anillin may contribute to mechanical events in developme
146 divide in the middle, only S. pombe uses the anillin Mid1 as a primary nucleus-derived cue to assembl
149 ombe, symmetric division is achieved through anillin/Mid1-dependent positive cues released from the c
150 s containing kinase Cdr1p, kinase Cdr2p, and anillin Mid1p form in the cortex around the nucleus earl
151 (cell cycle kinases Cdr1p, Cdr2p, Wee1p, and anillin Mid1p) are constant even when the nodes disassem
153 G2, mature into cytokinetic nodes by adding anillin Mid1p, myosin-II, formin Cdc12p, and other prote
155 complexes called nodes whereas cells without Anillin/Mid1p ( mid1) lack visible nodes yet assemble co
157 also defines the essential roles of a RhoGEF-anillin module in septin architectural remodeling during
159 itiate central spindle formation, accumulate anillin or actin at the cell equator, or undergo equator
160 pression of a septin-interacting fragment of anillin or by septin depletion via siRNA causes loss of
167 the apical surface of epithelial cells, and anillin promotes the tensile forces stored in this netwo
168 dev et al. reveal that the scaffold protein, anillin, promotes asymmetric ring closure by locally seq
169 suggests the conserved function of Mid1-like anillin proteins may be in scaffolding, not positioning,
170 otein nanobody suggests that supervillin and anillin regulate the myosin II and actin cortical cytosk
177 ows stable filamentous structures containing anillin, Rho1, and septins to form directly at the equat
181 anillin during interphase serves to restrict anillin's function at the cell membrane to mitosis and a
182 ugh importin beta2 binding does not regulate anillin's function in mitosis, it is required to prevent
184 ctive Ran to the equatorial membrane affects anillin's localization and causes cytokinesis phenotypes
188 laevis embryos as a model system to examine Anillin's role in the intact vertebrate epithelium, we f
189 aging-associated diminishment of the septin/anillin-scaffold causes myelin outfoldings that impair t
190 er, reduced nocodazole-induced expression of anillin, securin, and cyclin B1 and phosphorylation of P
193 ate epithelium, we find that a population of Anillin surprisingly localizes to epithelial cell-cell j
195 utant analysis between scraps, a mutation in anillin that eliminates microfilament rings, and bottlen
198 with an unusual distribution of F-actin and Anillin, these phenotypes are consistent with defective
200 n at the cell membrane to mitosis and allows anillin to be rapidly available when the nuclear envelop
201 eptin cytoskeleton acts on the C terminus of Anillin to locally trim away excess membrane from the la
204 tin bundling activity of anillin and enables anillin to switch between two actin-bundling morphologie
205 1 and CCM-3 are recruited by active RhoA and anillin to the cytokinetic ring, where they in turn limi
206 olleagues report how the scaffolding protein anillin uses cycles of transient binding interactions to
209 Overexpression of Cdh1 reduced the levels of anillin, whereas inactivation of APC/C(Cdh1) increased t
210 red to prevent the cytosolic accumulation of anillin, which disrupts cellular architecture during int
211 Similarly, the essential cytokinetic factor anillin, which functions at the cell membrane to promote
212 contain the COOH-terminal 197 amino acids of anillin, which includes a pleckstrin homology (PH) domai
214 wn of the essential regulator of cytokinesis anillin, which resulted in cytokinesis failure and forma
215 put promotes the simultaneous association of anillin with the plasma membrane, septins, and MTs, inde