ライフサイエンスコーパス: NuMA

1 NuMA also binds to 18S and 28S rRNAs and localizes to rD

2 NuMA and dynein/dynactin are specifically enriched at ne

3 NuMA can interact directly with MTs, and the MT binding

4 NuMA coimmunoprecipitates with RNA polymerase I, with ri

5 NuMA coimmunoprecipitates with SNF2h, regulates its diff

6 NuMA expression decreased in late disease stage 4 endome

7 NuMA is a cell cycle-related protein essential for norma

8 NuMA is a spindle protein whose disruption results in nu

9 NuMA is an abundant long coiled-coil protein that plays

10 NuMA is recruited to new minus-ends independently of dyn

11 NuMA keeps the decondensing chromosome mass compact at m

12 NuMA localization to minus-ends involves a C-terminal re

13 NuMA's anaphase localization is independent of LGN and 4

14 NuMA's C terminus binds DNA in vitro and chromosomes in

15 NuMA's cortical recruitment requires LGN; however, LGN i

16 NuMA, an upstream targeting factor, localized asymmetric

17 NuMA-retinoic acid receptor alpha fusion proteins have b

18 tion (p = 0.007), and aneuploidy (p = 0.008).NuMA is highly expressed in EOC tumours and high NuMA le

19 es with nuclear mitotic apparatus protein 1 (NuMA) and that NuMA binding and the ability to induce dy

20 is is functionally important, as loss of 4.1/NuMA interaction results in spindle orientation defects,

21 erminal domain of NuMA binds MTs, allowing a NuMA dimer to function as a "divalent" crosslinker that

22 g site for Rae1 on NuMA that would convert a NuMA dimer to a "tetravalent" crosslinker of MTs.

23 le pole formation requires the addition of a NuMA-like minus-end cross-linker and directed transport

24 In cancer cells, ACRBP restricted a NuMA-dependent abrogation of a mitotic spindle assembly

25 f their distal ends toward centrosomes via a NuMA-dependent mechanism.

26 ition of such traits as defined by the ACRBP-NuMA complex may represent conceptually ideal interventi

27 hich confer polarity, and Galpha(i)-LGN/AGS3-NuMA-dynein/dynactin, which govern spindle positioning.

28 aratus protein-retinoic acid receptor alpha (NuMA-RARalpha) is the fourth of five fusion proteins ide

29 m covalent modification sites on PARP-5a and NuMA and binding noncovalently to NuMA and that this fun

30 at the codependent relationship of ACRBP and NuMA in cancer cells reflects their passage through a se

31 Without centrosomes and NuMA, initial establishment of spindle microtubule focus

32 apparatus protein NuMA, and both CEP170 and NuMA are TBK1 substrates.

33 nase C, the Par3-LGN-Inscuteable complex and NuMA-dynactin to align the spindle.

34 tubule minus-end-directed motor complex, and NuMA, a microtubule cross-linker, regulate spindle lengt

35 tion of Xenopus oocytes, and that dynein and NuMA are required for organization of the MTOC-TMA.

36 clustering of microtubule ends by dynein and NuMA is essential for mammalian spindles to hold a stead

37 Thus, end-clustering by dynein and NuMA is required for mammalian spindles to reach a stead

38 Although we know that dynein and NuMA mediate pole formation, our understanding of the fo

39 E7 and the interaction between HPV16 E7 and NuMA correlate with the induction of defects in chromoso

40 on-regulatory proteins Insc, LGN (Gpsm2) and NuMA, and the cell fate determinant Numb are asymmetrica

41 addition, these data show that both Kid and NuMA contribute to chromosome alignment in mammalian cel

42 r after simultaneous perturbation of Kid and NuMA despite appropriate kinetochore-microtubule interac

43 indle organization in the absence of Kid and NuMA function.

44 es formed after perturbation of both Kid and NuMA in stark contrast to splayed spindle poles observed

45 LASP1, which does not restore proper LGN and NuMA localization but stabilizes astral MT interactions

46 Complexes of the LGN and NuMA proteins, fundamental components of force generator

47 cs, as well as in mislocalization of LGN and NuMA, leading to misoriented spindles.

48 Interestingly, spindle misorientation and NuMA mislocalization were reversed by treatment with a l

49 /LGN/NuMA-dependent pathway and a 4.1G/R and NuMA-dependent, anaphase-specific pathway.

50 itotic-specific interaction between Rae1 and NuMA and have explored the relationship between Rae1 and

51 e explored the relationship between Rae1 and NuMA in spindle formation.

52 unced oscillation of metaphase spindles, and NuMA binding to LGN is required for these spindle moveme

53 to the known colocalization of tankyrase and NuMA at mitotic spindle poles.

54 o its other partners TRF1 (at telomeres) and NuMA (at spindle poles).

55 s to form a complex in vivo with tubulin and NuMA in highly synchronized mitotic HeLa extracts.

56 XMAP215, XKCM1, and NuMA were all localized to the base of the MTOC-TMA and

57 nally, microinjection of anti-dynein or anti-NuMA disrupted the organization of the MTOC-TMA and subs

58 rm alteration of NuMA distribution with anti-NuMA C-terminus antibodies in live acinar cells indicate

59 rt of Galphai/LGN/nuclear mitotic apparatus (NuMA) complex from cell cortex to spindle poles and show

60 ion allele of the nuclear mitotic apparatus (NuMA) protein in mice and cultured primary cells, we dem

61 The large nuclear mitotic apparatus (NuMA) protein is an essential player in mitotic spindle

62 protein (LGN) and nuclear mitotic apparatus (NuMA) protein, two essential factors for spindle orienta

63 er of Inscuteable/nuclear mitotic apparatus (NuMA) ternary complex.

64 x, including LGN, nuclear mitotic apparatus (NuMA), and dynein/dynactin, plays a key role in establis

65 e non-motile MT-associated proteins, such as NuMA, TPX2, and HURP [7, 10-12], Ran also controls motor

66 In gel-shift assays, NuMA-RARalpha bound to retinoic acid response elements (

67 ogy, and we propose that this occurs because NuMA forms functional linkages between kinetochore and n

68 This interaction between NuMA and LANA is critical for segregation and maintenanc

69 Yet, the precise link between NuMA and nucleolar function remains undetermined.

70 cortical localization of the dynein-binding NuMA orthologue LIN-5.

71 Both NuMA's minus-end-binding and dynein-dynactin-binding mod

72 dynein and more quickly than dynactin; both NuMA and dynactin display specific, steady-state binding

73 sed state, the N and C termini interact, but NuMA or Galphai can disrupt this association, allowing L

74 nism involving the sequestration of 53BP1 by NuMA in the absence of DNA damage.

75 contribution of microtubule cross-linking by NuMA compensated for the loss of Eg5 motor activity.

76 ration to nuclear sites normally occupied by NuMA and is distinct from RARalpha.

77 oliferative fitness that could be rescued by NuMA codepletion.

78 In cell lines and breast carcinoma NuMA prevents 53BP1 accumulation at DNA breaks, and high

79 e, we show that in mammary epithelial cells, NuMA is present in both the nuclear matrix and chromatin

80 sient transfection assays using HepG2 cells, NuMA-RARalpha inhibited wild-type RARalpha transcription

81 In synchronized cells, NuMA and LANA are colocalized in interphase cells and se

82 In contrast, CFP-NuMA-RARalpha(deltaCC) exhibited a diffuse granular patt

83 Furthermore, CFP-NuMA-RARalpha colocalized with yellow fluorescent protei

84 Within the nucleus, CFP-NuMA-RARalpha exhibited a speckled pattern identical to

85 that observed in cells transfected with CFP-NuMA.

86 Studies comparing NuMA-RARalpha with NuMA-RARalpha(deltaCC) demonstrated t

87 The spindle pole component NuMA and gamma-tubulin were present at the foci of perip

88 p37 controls cortical NuMA levels via the phosphatase PP1 and its regulatory s

89 thermore, we observe an increase in cortical NuMA localization as cells enter anaphase.

90 function of PP1, resulting in lower cortical NuMA levels and correct spindle orientation.

91 es anaphase-specific enhancement of cortical NuMA and dynein.

92 ric establishment and regulation of cortical NuMA-dynein complexes that position the mitotic spindle.

93 ian cells by limiting the levels of cortical NuMA.

94 uring anaphase and demonstrate that cortical NuMA and dynein contribute to efficient chromosome separ

95 this interpretation, we found that coupling NuMA overexpression to Rae1 overexpression or coupling R

96 The microtubule crosslinker NuMA is needed for the local load-bearing observed, wher

97 ogenous NuMA with membrane-binding-deficient NuMA, we can specifically reduce the cortical accumulati

98 d the consequences of loss of the Drosophila NuMA homolog Mud, which interacts with the dynein comple

99 ells by altering the localization of dynein, NuMA, and the p150(Glued) subunit of dynactin to the spi

100 urbation of the chromokinesin Kid and either NuMA, CENP-E, or HSET.

101 In early mitosis, the END (Emi1/NuMA/Dynein-dynactin) network anchors the anaphase-promo

102 e-associated mechanism, called the END (Emi1/NuMA/dynein-dynactin) network, that spatially restricts

103 By replacing endogenous NuMA with membrane-binding-deficient NuMA, we can specif

104 r disrupting its interaction with endogenous NuMA or Galpha proteins all lead to spindle misorientati

105 On mitotic entry, NuMA is released from the nucleus and competes LGN from

106 In GST-pull down experiments, NuMA-RARalpha formed a complex with the corepressor SMRT

107 the microtubule depolymerase Kif2b, and for NuMA binding to dynein.

108 binding of NuMA and competes with Astrin for NuMA binding, also led to similar results.

109 ling two distinct mechanisms responsible for NuMA cortical recruitment at different stages of mitosis

110 A potential role for NuMA in nuclear organization or gene regulation is sugge

111 Females without functional NuMA in oocytes are sterile, producing aneuploid eggs wi

112 poles, we determine that without functional NuMA, microtubules lose connection to MI spindle poles,

113 irect evidence that LGN (also called Gpsm2), NuMA and dynactin (Dctn1) are involved.

114 nt impaired the localization of LGN (GSPM2), NuMA (microtubule binding nuclear mitotic apparatus prot

115 High NuMA levels decreased with increased tumour invasion in

116 s 53BP1 accumulation at DNA breaks, and high NuMA expression predicts better patient outcomes.

117 is highly expressed in EOC tumours and high NuMA levels correlate with increases in mitotic defects

118 IF of primary cultures revealed that high NuMA levels at mitotic spindle poles were significantly

119 scontinuous data analysis revealed that high NuMA levels in tumours decreased with grade (p = 0.02) b

120 d asymmetric division machinery by hijacking NuMA from LGN binding, thereby favoring TIC self-renewal

121 Proteomic investigation has identified NuMA among hundreds of nucleolar proteins.

122 A nonsynonymous SNP (A794G) in NuMA was identified that showed a stronger association w

123 live acinar cells indicates that changes in NuMA and chromatin organization precede loss of acinar d

124 n of Cdk1 or mutation of a single residue in NuMA mimics this effect.

125 In mitosis, reducing Rae1 or increasing NuMA concentration would be expected to alter the valenc

126 Lowering Rae1 or increasing NuMA levels in cells results in spindle abnormalities.

127 In interphase, NuMA is localized to the nucleus and hypothesized to con

128 Spindles were disorganized if Kid, NuMA, and HSET were perturbed, indicating that HSET is s

129 the astral microtubule anchoring complex LGN-NuMA to yield the distinct epithelial division phenotype

130 on is regulated by the conserved Galphai-LGN-NuMA complex, which targets the force generator dynein-d

131 DCK cells correlated with a single or no LGN-NuMA crescent, tilted spindles, and the development of l

132 critical for the correct localization of LGN-NuMA force generator complexes and hence for proper spin

133 hoA activity that correlated with robust LGN-NuMA recruitment to the metaphase cortex, spindle alignm

134 mediated by the evolutionarily conserved LGN/NuMA complex, which regulates cortical attachments of as

135 ct such transport by maintaining Galphai/LGN/NuMA and dynein at the cell cortex.

136 rtex by two distinct pathways: a Galphai/LGN/NuMA-dependent pathway and a 4.1G/R and NuMA-dependent,

137 mammalian Ric-8A dissociates Galphai-GDP/LGN/NuMA complexes catalytically, releasing activated Galpha

138 E-cadherin instructs the assembly of the LGN/NuMA complex at cell-cell contacts, and define a mechani

139 LGN from E-cadherin to locally form the LGN/NuMA complex.

140 Mud is a functional orthologue of mammalian NuMA and Caenorhabditis elegans Lin-5, and that Mud coor

141 Manipulating NuMA expression alters PARP inhibitor sensitivity of BRC

142 otubule interaction for three nonmotor MAPs (NuMA, PRC1, and EB1) required for cell division.

143 ypes of defective spindles have mislocalized NuMA (nuclear mitotic apparatus protein), a 4.1R binding

144 When mitotic NuMA function is disrupted, centrosomes provide initial

145 motor (dynein, HSET, and Eg5) and non-motor (NuMA) proteins involved in microtubule aster organizatio

146 ment of the microtubule binding protein Mud (NuMA) occurs over a very narrow Galphai concentration ra

147 s, LGN) and coiled-coil protein (LIN-5, Mud, NuMA).

148 conserved Galpha-GPR-1/2(Pins/LGN)-LIN-5(Mud/NuMA) cortical complex interacts with dynein and is requ

149 tes) [3-6], which recruits the conserved Mud/NuMA protein and the dynein/dynactin complex to the cort

150 ation machinery, including Discs Large1, Mud/NuMA, and Canoe/Afadin, mislocalize in dividing Eph muta

151 orientation across systems, most notably Mud/NuMA and cortical dynein, the precise mechanism by which

152 e nuclear shape defects observed upon mutant NuMA expression are due to its potential to polymerize i

153 fuses to variable partners (PML, PLZF, NPM, NuMA and STAT5B: X genes) leading to the expression of A

154 ifically reduce the cortical accumulation of NuMA and dynein during anaphase and demonstrate that cor

155 s, PP1/Repo-Man promotes the accumulation of NuMA at the cortex.

156 pindles when the pole focusing activities of NuMA and HSET are perturbed.

157 or each of the known oncogenic activities of NuMA fusion proteins as well as its sequestration to nuc

158 observed that antibody-induced alteration of NuMA distribution in growth-arrested and differentiated

159 Short-term alteration of NuMA distribution with anti-NuMA C-terminus antibodies i

160 also promotes the decrease in the amount of NuMA.

161 cell cycle-regulated membrane association of NuMA underlies anaphase-specific enhancement of cortical

162 P150-CC1), which disrupts the association of NuMA with microtubules, resulted in the loss of KSHV ter

163 GN), which blocks the microtubule binding of NuMA and competes with Astrin for NuMA binding, also led

164 We show that the membrane binding of NuMA is cell cycle regulated-it is inhibited during prop

165 A complex of NuMA and dynein/dynactin is required for robust spindle

166 This work highlights the complexity of NuMA localization and reveals the importance of NuMA cor

167 To date, the precise contribution of NuMA to nuclear function remains unclear.

168 hanges in the distribution of the density of NuMA bright features when nonneoplastic cells underwent

169 valency of NuMA toward MTs; the "density" of NuMA-MT crosslinks in these conditions would be diminish

170 The carboxy terminal domain of NuMA binds MTs, allowing a NuMA dimer to function as a "

171 ssion of the specific Rae1-binding domain of NuMA in HeLa cells led to aberrant spindle formation.

172 hing, we find that the 4.1-binding domain of NuMA is important for stabilizing its interaction with t

173 ation or alpha-helical coiled-coil domain of NuMA was required for homodimer formation, transcription

174 The rod domain of NuMA, expressed in bacteria, bound directly to pADPr.

175 lts indicate that the dimerization domain of NuMA-RARalpha is critical for each of the known oncogeni

176 Downregulation of NuMA expression triggers nucleolar stress, as shown by d

177 reveal an additional and direct function of NuMA during mitotic spindle positioning, as well as a re

178 ablishes the spindle-independent function of NuMA in choreographing proper chromatin decompaction and

179 This previously uncharacterized function of NuMA in rDNA transcription and p53-independent nucleolar

180 A localization and reveals the importance of NuMA cortical stability for productive force generation

181 organization, possibly through inhibition of NuMA function, but the mechanism of this effect has not

182 associated protein, as a novel interactor of NuMA.

183 Knockdown of NuMA by RNA interference dramatically impaired Astrin re

184 of Galphai caused concomitant liberation of NuMA from LGN.

185 prevented by a change in the localization of NuMA, an effector of spindle orientation.

186 n and modulates the cortical localization of NuMA-dynein complexes to correct mispositioned spindles.

187 spindle poles, detected by localizations of NuMA and the p150 component of dynactin.

188 Loss of NuMA-MT interactions in skin caused defects in spindle o

189 ssion of the DNA-binding-deficient mutant of NuMA affects chromatin decondensation at the mitotic exi

190 Overexpression of NuMA enhances cohesin accumulation at spindle poles.

191 spindle poles observed after perturbation of NuMA alone.

192 The binding profile of NuMA-RARalpha to a panel of RAREs was very similar to PM

193 n the nucleolus and reveal redistribution of NuMA upon actinomycin D or doxorubicin-induced nucleolar

194 tiation and results in the redistribution of NuMA, chromatin markers acetyl-H4 and H4K20m, and region

195 ely, we did not detect any reorganization of NuMA during formation of tumor nodules by malignant cell

196 Silencing of NuMA expression by small interfering RNA and expression

197 Here we report the crystal structure of NuMA:LGN hetero-hexamers, and unveil their role in promo

198 We show that the C-terminal tail of NuMA can directly bind to the C terminus of Astrin and t

199 with high affinity to the C-terminal tail of NuMA, a large nuclear protein that is required for spind

200 that a small domain within the C terminus of NuMA stabilizes microtubules (MTs), and that LGN blocks

201 Expression of a portion of the C terminus of NuMA that shares sequence similarity with the chromatin

202 membrane-binding domain at the C-terminus of NuMA.

203 on would be expected to alter the valency of NuMA toward MTs; the "density" of NuMA-MT crosslinks in

204 ectly with MTs, and the MT binding domain on NuMA overlaps by ten amino acid residues with the LGN bi

205 can explain the inhibitory effect of LGN on NuMA-dependent mitotic spindle organization.

206 e mapped a specific binding site for Rae1 on NuMA that would convert a NuMA dimer to a "tetravalent"

207 -8A-stimulated release of Galphai-GTP and/or NuMA regulates the microtubule pulling forces on centros

208 The 4.1 spectrin-actin binding domain or NuMA binding C-terminal domain peptides caused morpholog

209 embled when spectrin-actin-binding domain or NuMA-binding C-terminal domain peptides were present.

210 speckle microscopy reveals that dynactin or NuMA inhibition suppresses microtubule disassembly at sp

211 After dynein or NuMA deletion, the mitotic microtubule network is "turbu

212 inhibitor Emi1 binds the spindle-organizing NuMA/dynein-dynactin complex to anchor and inhibit the A

213 he NuMA/dynein complex and potentially other NuMA-containing complexes, contributes to viral maintena

214 us-ends involves a C-terminal region outside NuMA's canonical microtubule-binding domain and is indep

215 s involved in the cortical polarity pathway (NuMA, p150(glued), aPKC).

216 pression was associated with this phenomenon.NuMA protein levels in normal and tumour tissues, ovaria

217 gulatory and structural element: it prevents NuMA from binding chromosomes at mitosis, regulates its

218 CEP170 and to the mitotic apparatus protein NuMA, and both CEP170 and NuMA are TBK1 substrates.

219 domain with the microtubule binding protein NuMA.

220 The coiled-coil protein NuMA is an important contributor to mitotic spindle form

221 ear envelope and DNA, nuclear matrix protein NuMA (Nuclear mitotic apparatus), and splicing factors S

222 e report that the structural nuclear protein NuMA accumulates at sites of DNA damage in a poly[ADP-ri

223 ion of fluorescently stained nuclear protein NuMA in different mammary phenotypes obtained using 3D c

224 Kid and the spindle pole organizing protein NuMA influences spindle morphology, and we propose that

225 and increased levels of the polarity protein NuMA at the cell cortex.

226 g proteins included the spindle pole protein NuMA previously shown to bind to PARP-5a directly.

227 ys and mislocalized the spindle pole protein NuMA.

228 We identified the mitotic spindle protein NuMA as an ACRBP-interacting protein that could account

229 cells overexpression of the spindle protein NuMA interfered with dynein localization, promoting mult

230 53BP1 interacts with the structural protein NuMA, which controls 53BP1 diffusion.

231 LGN, and nuclear mitotic apparatus protein (NuMA) [3, 7-18].

232 that the nuclear mitotic apparatus protein (NuMA) and LANA can associate in KSHV-infected cells.

233 bulin and Nuclear Mitotic Apparatus protein (NuMA) in intact HeLa cells in vivo as well as with the m

234 The Nuclear Mitotic Apparatus protein (NuMA) is recruited from interphase nuclei to spindle MTs

235 e-binding nuclear mitotic apparatus protein (NuMA), and Galphai regulate a similar process.

236 proteins Nuclear Mitotic Apparatus protein (NuMA), dynein, and dynactin.

237 f LGN and nuclear-mitotic apparatus protein (NuMA), proteins that generate pulling forces on astral m

238 g site of nuclear mitotic apparatus protein (NuMA), which is implicated in anchoring microtubules at

239 apture of nuclear mitotic apparatus protein (NuMA)-positive astral microtubules to orientate the mito

240 erpart of nuclear mitotic apparatus protein (NuMA).

241 tion with nuclear mitotic apparatus protein (NuMA).

242 oding the nuclear mitotic apparatus protein (NuMA).

243 uding the nuclear/mitotic apparatus protein (NuMA).

244 complex (nuclear mitotic apparatus protein [NuMA]-LGN-Galpha in human cells and LIN-5-GPR-1/2-Galpha

245 The nuclear mitotic apparatus protein, NuMA, is involved in major cellular events such as DNA d

246 These data point to the Rae1-NuMA interaction as a critical element for normal spindl

247 During mitosis, LGN recruits NuMA to the cell cortex, while cortical association of L

248 n of C-terminal domain peptides with reduced NuMA binding caused severe microtubule destabilization i

249 tant C-terminal domain peptides with reduced NuMA binding had no deleterious effects on nuclear recon

250 interacted with mitotic spindle regulators, NuMA and RAN, while full-length OCLN loss impaired spind

251 What role NuMA plays in nuclear integrity, and whether its perceiv

252 enabling SNF2h function, cells with silenced NuMA exhibit reduced chromatin decompaction after DNA cl

253 Prominent features of fluorescently stained NuMA were detected by using a previously undescribed loc

254 mitotic apparatus protein 1 (NuMA) and that NuMA binding and the ability to induce dynein delocaliza

255 tion establishment in keratinocytes and that NuMA's MT-binding domain, which targets MT tips, is also

256 We confirm that NuMA is present in the nucleolus and reveal redistributi

257 cultured primary cells, we demonstrate that NuMA is an essential mitotic component with distinct con

258 ere, we use live imaging to demonstrate that NuMA plays a spindle-independent role in forming a singl

259 is.Affymetrix microarray data indicated that NuMA was overexpressed in tumour tissue, primary culture

260 Here, we report that NuMA is associated with chromatin in interphase and prop

261 In this work, we show that NuMA is required to recruit dynactin to the cell cortex

262 tive imaging and laser ablation to show that NuMA targets dynactin to minus-ends, localizing dynein a

263 In addition, we show that NuMA-MT interactions are also required in adult mice for

264 These findings suggest that NuMA has a role in mammary epithelial differentiation by

265 Together, the data and model suggest that NuMA-mediated crosslinks locally bear load, providing me

266 We uncover that NuMA directly interacts with DNA via evolutionarily cons

267 the corepressor SMRT, was released from the NuMA-RARalpha/SMRT complexes by all-trans retinoic acid

268 lidation, we conclude that variations in the NuMA gene are likely responsible for the observed increa

269 ion and demonstrate the critical role of the NuMA-Astrin interaction for accurate cell division.

270 al activation of STAT3, and stability of the NuMA-RARalpha/SMRT complex.

271 totic events by HPV E7, via targeting of the NuMA/dynein complex and potentially other NuMA-containin

272 ressors, respectively, the disruption of the NuMA/dynein network may result in mitotic errors that wo

273 Here, we show that the NuMA- and Galpha-binding protein LGN is required for dir

274 ly binds, and coimmunoprecipitates with, the NuMA-related Mushroom body defect (Mud) protein.

275 her hand, if Astrin levels are reduced, then NuMA could not efficiently concentrate at the spindle po

276 Thus, NuMA is a defining feature of the mammalian spindle pole

277 Thus, NuMA is required for persistence of the KSHV episomes in

278 Thus, NuMA may serve as a mitosis-specific minus-end cargo ada

279 Thus, NuMA plays a structural role over the cell cycle, buildi

280 overexpression or coupling Rae1 depletion to NuMA depletion prevented the formation of aberrant spind

281 le-binding coiled-coil protein homologous to NuMA and LIN-5, is an essential component of a Netrin-in

282 ARP-5a and NuMA and binding noncovalently to NuMA and that this function helps promote assembly of ex

283 entrosome/spindle poles, in a similar way to NuMA.

284 exes with three spindle-pole proteins, TPX2, NuMA, and XRHAMM--a known TPX2 partner--and specifically

285 ause of the prominent mitotic phenotype upon NuMA loss, its precise function in the interphase nucleu

286 We verified NuMA as an RXXPDG-mediated partner of tankyrase and sugg

287 APC/C, linking the APC/C to the spindle via NuMA.

288 IHC revealed low to weak NuMA expression in normal tissues.

289 We investigated whether NuMA expression was associated with this phenomenon.NuMA

290 risk HPV6b and HPV11 E7s also associate with NuMA and also induce a similar mitotic defect.

291 self-organization activities associated with NuMA (i.e., cytoplasmic dynein) and HSET are not necessa

292 n of 4.1R also enhances its association with NuMA and tubulin.

293 ticular, we found that MCAK colocalized with NuMA and XMAP215 at the center of Ran asters where its a

294 Consistent with NuMA enabling SNF2h function, cells with silenced NuMA e

295 ubules and depend on filament polarity, with NuMA's friction being lower when moving toward minus end

296 Studies comparing NuMA-RARalpha with NuMA-RARalpha(deltaCC) demonstrated that the dimerizatio

297 crotubules (MTs) to orient the spindle, with NuMA acting as a passive tether.

298 Importantly, we identified a region within NuMA that mediates association with dynein.

299 localization and function of XMAP215, XKCM1, NuMA, and cytoplasmic dynein during oocyte maturation.

300 with yellow fluorescent protein-tagged (YFP)-NuMA.