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 4.1R partially colocalize in the interphase nuc

3 NuMA and dynein/dynactin are specifically enriched at ne

4 NuMA and other APA components are discharged from import

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

6 NuMA coimmunoprecipitates with RNA polymerase I, with ri

7 NuMA coimmunoprecipitates with SNF2h, regulates its diff

8 NuMA expression decreased in late disease stage 4 endome

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

10 NuMA is a large nuclear protein whose relocation to the

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

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

13 NuMA transport is required for spindle pole assembly and

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

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

16 NuMA, an upstream targeting factor, localized asymmetric

17 NuMA, gamma-tubulin, and centrin localize to each pole,

18 NuMA-retinoic acid receptor alpha fusion proteins have b

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

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

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

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

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

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

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

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

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

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

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

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

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

32 vant heterogeneity in the spectrin-actin and NuMA binding domains.

33 es the interaction between importin-beta and NuMA.

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

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

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

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

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

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

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

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

42 , simultaneous perturbation of both HSET and NuMA severely suppresses directed chromosome movement in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ted by overlapping mechanisms involving both NuMA and HSET is essential for chromosome movement durin

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

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

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

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

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

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

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

84 that observed in cells transfected with CFP-NuMA.

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

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

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

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

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

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

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

92 ian cells by limiting the levels of cortical NuMA.

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

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

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

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

97 w here that this process depends on directed NuMA transport toward microtubule minus ends powered by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 High NuMA levels decreased with increased tumour invasion in

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

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

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

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

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

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

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

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

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

124 unction (with an antibody) strongly inhibits NuMA translocation and accumulation and disrupts spindle

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

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

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

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

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

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

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

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

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

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

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

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

137 Importin-beta therefore links NuMA to regulation by Ran.

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

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

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

141 When mitotic NuMA function is disrupted, centrosomes provide initial

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

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

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

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

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

147 cases, and in a few cases to the PLZF, NPM, NuMA and STAT5b genes respectively.

148 cases, and in a few cases to the PLZF, NPM, NuMA and Stat5b genes, respectively, leading to the gene

149 cases, and in a few cases to the PLZF, NPM, NuMA and STAT5b genes.

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

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

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

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

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

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

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

157 also promotes the decrease in the amount of NuMA.

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

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

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

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

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

163 of a reversible, mitosis-specific complex of NuMA with dynein and dynactin.

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

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

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

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

168 rm of 4.1R alters the normal distribution of NuMA in the interphase nucleus.

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

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

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

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

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

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

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

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

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

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

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

180 associated protein, as a novel interactor of NuMA.

181 Knockdown of NuMA by RNA interference dramatically impaired Astrin re

182 of Galphai caused concomitant liberation of NuMA from LGN.

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

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

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

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

187 Overexpression of NuMA enhances cohesin accumulation at spindle poles.

188 Perturbation of NuMA alone disrupts spindle pole organization and delays

189 spindle poles observed after perturbation of NuMA alone.

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

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

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

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

194 e actions of NGF by antagonizing the role of NuMA in mitosis.

195 Silencing of NuMA expression by small interfering RNA and expression

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

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

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

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

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

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

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

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

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

205 -8A-stimulated release of Galphai-GTP and/or NuMA regulates the microtubule pulling forces on centros

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

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

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

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

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

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

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

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

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

215 of APA is the microtubule-associated protein NuMA.

216 domain with the microtubule binding protein NuMA.

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

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

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

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

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

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

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

224 ys and mislocalized the spindle pole protein NuMA.

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

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

227 d and contain the nuclear structural protein NuMA.

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

229 bation of nuclear mitotic apparatus protein (NuMA) and the human homologue of the KIN C motor family

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

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

232 on of the nuclear-mitotic apparatus protein (NuMA), a nuclear protein required for organizing mitotic

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

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

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

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

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

238 erpart of nuclear mitotic apparatus protein (NuMA).

239 tion with nuclear mitotic apparatus protein (NuMA).

240 oding the nuclear mitotic apparatus protein (NuMA).

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

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

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

244 mplex with spindle pole organizing proteins, NuMA, dynein, and dynactin during cell division.

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

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

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

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

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

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

251 es of green fluorescent protein (GFP)-tagged NuMA stream poleward along spindle fibers in association

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 This NuMA fragment also specifically interacted with the nucl

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

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

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

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

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

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

278 Similar to NuMA, a significant amount of cohesin was found to assoc

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

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

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

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

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

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

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

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

287 Protein 4.1R associates with NuMA in the interphase nucleus and forms a complex with

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

289 he nucleus and promotes its association with NuMA.

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

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

292 4.1R, including motifs for interaction with NuMA and FKBP13.

293 The interaction with NuMA persists during interphase.

294 ndle poles during mitosis and interacts with NuMA, a spindle pole-associated factor required for mito

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.