ライフサイエンスコーパス: merlin

1 lecular conformation and binding activity of Merlin.

2 at encodes a tumor-suppressor protein called merlin.

3 exon 7 and did not express the NF2 protein, merlin.

4 K1 phosphorylation and that of its substrate Merlin.

5 rge to be handled by the imputation software Merlin.

6 membrane-cytoskeleton adapter protein called merlin.

7 fibromatosis type 2 tumor-suppressor protein merlin.

8 ed tumour disease, is also caused by loss of merlin.

9 1, and both were restored by mutation of NF2/merlin.

10 MET signaling; the latter via inhibition of merlin.

11 itical for the growth-regulatory function of merlin.

12 out the role of phosphoinositide binding for merlin.

13 the cytosol without altering the folding of merlin.

14 growth-suppressive properties to the mutant merlin.

15 hat encodes for the tumor suppressor protein merlin.

16 d in a manner dependent on Rab5, Dynamin and Merlin.

17 LK3 and residues in the C-terminal region of merlin.

18 CAF1 counteracts the antimitogenic effect of Merlin.

19 52 proteins in close proximity to wild-type Merlin.

20 loss of function of the NF2-encoded protein, Merlin.

21 dependent complex comprised of Amot, YAP and Merlin.

22 he vulnerability of tumor cells with loss of Merlin.

23 Our results show that (1) GIGI outperforms Merlin; (2) family-based imputation outperforms populati

24 In contrast, neurofibromin 2 (or Merlin), a molecule upstream of the Hippo pathway and th

25 w that the closed, growth-inhibitory form of Merlin accumulates in the nucleus, binds to the E3 ubiqu

26 We also demonstrate that Cdc42 and Merlin act together with Pak1 to control lumen size.

27 des the tumor suppressor merlin, and loss of merlin activity promotes tumorigenesis and causes NF2.

28 ar trafficking might be a mechanism by which merlin acts.

29 20 SOTR plasma samples, viral stocks (Towne, Merlin, AD169) and the first World Health Organization (

30 ositol 4,5-bisphosphate lipid, the wild-type Merlin adopts a more open conformation than in solution,

31 entiate an apical domain that recruits CRB3, Merlin (also known as NF2), KIBRA (also known as WWC1) a

32 molecular structure and binding activity of Merlin and a Merlin(S518D) mutant that mimics the inacti

33 oplasm further demonstrated that both mutant merlin and active Rac specifically reduce anterograde mi

34 Thus, NF2/merlin and cAMP function downstream of Rac1 signaling in

35 strate a novel role for the tumor suppressor Merlin and closely related ERM proteins (Ezrin, Radixin,

36 ed proteins such as the FERM domain proteins Merlin and Expanded (Ex), and the WW- and C2-domain prot

37 s the effects of the upstream HSW components Merlin and Expanded, consistent with the idea that Tao-1

38 We show that Merlin and Ezrin are essential components of a mechanism

39 duoHMM in SHAPEIT (Impute2_duoHMM) for PBI, MERLIN and GIGI for FBI and PedBLIMP for a hybrid approa

40 In general, FBI in both MERLIN and GIGI outperformed other approaches with imput

41 elucidate an important molecular function of Merlin and highlight the plasma membrane as a critical s

42 on of Merlin-Hippo signaling by showing that Merlin and Hippo can be physically linked by the Salvado

43 Here we provide evidence that Merlin and Kibra activate Hippo signaling in parallel to

44 Merlin and Kibra together recruit the adapter protein Sa

45 the mechanism of Hippo pathway activation by Merlin and Kibra, identify a subcellular domain for Hipp

46 indicate that upstream regulators, Expanded, Merlin and Kibra, play a critical role in promoting Hpo

47 Furthermore, Merlin and Lgl are continuously required to maintain R8

48 ron scattering shows that, in solution, both Merlin and Merlin(S518D) adopt a closed conformation, bu

49 have developed a discriminatory model using Merlin and OPN expression in breast tumor tissues.

50 As Axl is negatively regulated by merlin and positively regulated by E3 ubiquitin ligase C

51 Re-expression of Merlin and silencing of DCAF1 implement a similar, tumor

52 onstruction output from Allegro, GeneHunter, Merlin and Simwalk.

53 Drosophila revealed a potential link between Merlin and the Hippo pathway by placing Merlin genetical

54 e have identified completely novel roles for Merlin and the Hippo pathway effector Yes-associated pro

55 ivating the intracellular NF2 (also known as merlin) and Hippo signalling pathway.

56 the Hippo pathway, the tumor suppressor Nf2 (Merlin) and the transcriptional coactivator Yap (Yap1),

57 ect repression of two Hippo activators, Nf2 (Merlin) and WWC1 (Kibra), leading to exaggerated YAP fun

58 Three membrane-associated proteins, Kibra, Merlin, and Expanded, regulate pathway activity, but the

59 The NF2 gene encodes the tumor suppressor merlin, and loss of merlin activity promotes tumorigenes

60 PAKs and the tumor suppressive functions of Merlin are mediated, at least in part, through inhibitio

61 the other Hippo pathway components, Fat and Merlin, are unaffected.

62 rofibromatosis type 2 (NF2) tumor suppressor Merlin as a critical mediator of contact-dependent inhib

63 Collectively, these results establish merlin as a potent inhibitor of MLK3, ERK and JNK activa

64 mouse Schwann (SC4) cells, re-expression of merlin as well as inhibition of Rac or its effector kina

65 ng the genomes of strains TR, TB40, FIX, and Merlin, as well as from Merlin-BAC recombinants containi

66 inally, we identify several point mutants of Merlin associated with neurofibromatosis type 2 that dis

67 Merlin associates with several transmembrane receptors a

68 erved that high expression of phosphorylated Merlin at serine 518 (S518-Merlin), NOTCH1 and epidermal

69 The Merlin BAC clone had mutations in the RL13 gene and UL12

70 Viruses derived from a Merlin-BAC derivative in which RL13 and UL128L were eith

71 Viruses derived from Merlin-BAC in fibroblasts had mutations in UL128L, but m

72 s TR, TB40, FIX, and Merlin, as well as from Merlin-BAC recombinants containing variant nucleotides i

73 This was not observed for Merlin-BAC, from which the vector is excised in derived

74 same samples at the MERIXS endstation of the MERLIN beamline at the Advanced Light Source storage rin

75 ual mitotic phosphorylation not only reduces Merlin binding to microtubules but also timely modulates

76 teins, we identified a previously unreported Merlin-binding protein, apoptosis-stimulated p53 protein

77 Here, we report that merlin binds phosphoinositides, including PIP(2), via a

78 inactivation of the tumor suppressor role of Merlin but also an independent process implicating a Mer

79 graded by the minimally passaged HCMV strain Merlin but not the extensively passaged strain AD169.

80 Our studies reveal that Merlin can associate directly with alpha-catenin and lin

81 Here we report that merlin can be sumoylated on Lysine residue (K76) in vitr

82 dies indicating that the Nf2-encoded protein Merlin can control the abundance and signaling of membra

83 Here we demonstrate that merlin can directly interact with both Ras and p120RasGA

84 Regulatory modules inferred by MERLIN capture co-regulatory relationships between signa

85 s in the gene coding for a tumour suppressor merlin cause development of multiple tumours of the nerv

86 (NF2) gene, coding for a tumour suppressor, Merlin, cause multiple tumours of the nervous system suc

87 Compared to strain Merlin containing wild-type UL128L, all three strains pr

88 nine (R) abolishes its sumoylation, disrupts merlin cortical cytoskeleton residency and attenuates it

89 ht to determine whether, in mammalian cells, merlin could positively regulate Mst2.

90 e identification and discriminatory power of Merlin, cumulatively presenting a powerful substantiatio

91 To study the relationship between Merlin deficiency and tumourigenesis, we have developed

92 le complementary methods, we also found that merlin deficiency leads to a reprogramming of energy met

93 g targets for NF2 and tumors associated with merlin deficiency.

94 lar schwannomas from NF2 patients and human, merlin-deficient (MD) Schwann cells have high levels of

95 vity compromised the aggressive phenotype of Merlin-deficient cells indicating a clear dependence of

96 nd is involved in increased proliferation of merlin-deficient meningioma and mesothelioma.

97 ient mesothelioma cell line TRA and in human Merlin-deficient meningiomas.

98 verexpression of PrP(C) is observed in human Merlin-deficient mesothelioma cell line TRA and in human

99 drug target driving NF-kappaB signaling and Merlin-deficient schwannoma genesis.

100 ling connection sustains the oncogenicity of Merlin-deficient tumor cells.

101 Using a primary human in vitro model for Merlin-deficient tumors, we report that the Ras/Raf/mito

102 serves as a potential therapeutic target for Merlin-deficient tumors.

103 an primary schwannoma cells, the most common Merlin-deficient tumour and the hallmark for NF2.

104 Axl/FAK/Src/NFkappaB pathway is relevant in merlin-deficient tumours and is a potential therapeutic

105 The benign character of merlin-deficient tumours makes them less responsive to c

106 therapeutic target for schwannoma and other merlin-deficient tumours.

107 esized that Axl is a good target to study in merlin-deficient tumours.

108 rtant therapeutic target in the treatment of merlin-deficient tumours.

109 herapeutic targets for schwannomas and other Merlin-deficient tumours.

110 ked kinase to adhesion sites, which leads to Merlin degradation, downregulation of the Hippo pathway,

111 lmitate is reduced by cell density in an Nf2/Merlin-dependent manner.

112 provides new insight into the mechanisms of merlin-dependent Ras regulation and may have additional

113 ion and may have additional implications for merlin-dependent regulation of other small GTPases.

114 y for LFV, although imputation accuracy from MERLIN depends on pedigree splitting for larger families

115 tion site and we show that KIBRA, Willin and Merlin differentially regulate genes controlled by YAP.

116 Instead, Merlin directly binds and recruits the effector kinase W

117 domain-mediated phosphoinositide binding of merlin displaces merlin from the membrane and releases i

118 While merlin does not increase the catalytic activity of RasGA

119 emonstrates that KSR1 interacts with several Merlin downstream effectors, including E3 ubiquitin liga

120 Introduction of these substitutions into Merlin dramatically increased yields of cell-free virus

121 ut also an independent process implicating a Merlin-driven regulation of NOTCH1 and EGFR.

122 phospho-inactivates the tumor suppressor NF2/Merlin, driving Rac1(P29S) cell proliferation in growth

123 In the absence of Merlin, ectopic cortical Ezrin yields mispositioned cent

124 Merlin encoded by the Nf2 gene is a bona fide tumor supp

125 Merlin, encoded by the Neurofibromatosis 2 (NF2) gene, i

126 These data uncover fundamental roles for Merlin/ERM proteins in spatiotemporally organizing the c

127 However, the mechanism through which merlin exerts its tumor-suppressive function remains obs

128 The Merlin-Expanded-Kibra complex is required at the apical

129 We assessed Merlin expression in breast cancer tissues by immunohist

130 RasGAP in Schwann cells, unlike the loss of merlin, failed to promote tumorigenic growth in an ortho

131 In PI4KIIIalpha mutant follicle cells, Merlin fails to localize to the apical domain.

132 We found that Drosophila Merlin formed cytoplasmic particles that move bidirectio

133 phosphoinositide binding of merlin displaces merlin from the membrane and releases it into the cytoso

134 firmed a critical role for PIP(2) binding in Merlin function and identified a large cohort of protein

135 sight into the mechanisms underlying loss of merlin function in NF2, we investigated mutated merlin h

136 ort that mouse Schwann cells (MSCs) in which merlin function is lost as a result of Nf2 exon2 deletio

137 sequences of the NF2 gene can cause loss of merlin function, the mechanism of this functional loss i

138 mational states is often employed to explain Merlin function.

139 dies suggest alternative molecular models of Merlin function.

140 ement of microtubule-dependent transport for Merlin function.

141 ast to the commonly depicted linear model of Merlin functioning through Hpo/Mst, here we show that in

142 Little is known about how Merlin functions endogenously as a tumor suppressor and

143 Our data reveal that Merlin functions to restrict the cortical distribution o

144 ween Merlin and the Hippo pathway by placing Merlin genetically upstream of the kinase Hpo/Mst.

145 These data suggest that Merlin gO is less efficient than other gO isoforms at co

146 Merlin has broad tumor-suppressor functions as its mutat

147 Because Merlin has high level of sequence similarity to the Ezri

148 or suppressor gene NF2 The NF2 gene product, Merlin, has no intrinsic catalytic activity; its tumor s

149 As such, the role of the tumor suppressor, Merlin, has not been investigated in breast cancer.

150 69 tagged, stably-expressed canonical strain Merlin HCMV proteins, and two non-canonical HCMV protein

151 We extend functional characterization of Merlin-Hippo signaling by showing that Merlin and Hippo

152 e activity in glial cells is controlled by a Merlin-Hippo signaling pathway, whereas the upstream Hip

153 lin function in NF2, we investigated mutated merlin homeostasis and function in NF2-associated tumors

154 BRA associates with neurofibromatosis type 2/Merlin in a Ser(539) phosphorylation-dependent manner.

155 Using a K76R mutant merlin in a subcutaneous U87MG xenograft model, we demon

156 es Merlin-Wts interactions, which implicates Merlin in actin-mediated regulation of Hippo signaling.

157 the global metabolomics profile impacted by Merlin in breast cancer cells.

158 We further demonstrate that the loss of Merlin in breast cancer is brought about, in part, due t

159 , there have been no mutations identified in Merlin in breast cancer.

160 nt loss of immunohistochemical expression of Merlin in breast tumor tissues.

161 bulin and ezrin suggest a potential role for Merlin in cell cycle progression.

162 our findings uncover a critical role for Nf2/Merlin in controlling homeostasis of the liver stem cell

163 ead cell to cell more rapidly than wild-type Merlin in fibroblasts but more slowly in epithelial cell

164 emonstrates that the phosphorylation of S518-Merlin in glioblastoma promotes oncogenic properties tha

165 d with wild-type and various mutant forms of Merlin in immortalized Schwann cells.

166 e metabolites that uncovered novel facets of Merlin in impacting the cancer cell metabolome.

167 we demonstrate for the first time a role for Merlin in impeding breast malignancy, identify a novel m

168 This study supports a rheostat model of Merlin in NHERF1 binding and contributes to resolving a

169 f proteins that specifically interacted with Merlin in the closed conformation.

170 We find that loss of Merlin in these cells causes a catastrophic failure of a

171 kage analyses were conducted with Morgan and Merlin in these families using a selected panel of singl

172 Interestingly NF2 mutations and merlin inactivation also occur in spontaneous schwannoma

173 NF2 mutations and/or Merlin inactivation are also seen in other cancers inclu

174 YAP overexpression or Neurofibromin 2 (NF2)/Merlin inactivation.

175 The tumor suppressor protein Merlin inhibits cell proliferation upon establishing cel

176 We have previously reported that merlin inhibits Ras and Rac activity during contact inhi

177 of proliferation and specifically found that Merlin inhibits the internalization of, and signaling fr

178 Conversely, enforced expression of a Merlin-insensitive mutant of DCAF1 counteracts the antim

179 Merlin integrates Rho GTPase family signaling with MAPK

180 ally intact source of HCMV, we cloned strain Merlin into a self-excising BAC.

181 Retargeting the mutant merlin into the membrane using a dual-acylated amino-ter

182 Our results demonstrate that Merlin is a component of cell junctional mechanosensing

183 We previously found that Merlin is a critical mediator of contact-dependent inhib

184 atosis type 2 (NF2) tumor-suppressor protein Merlin is a member of the ERM family of proteins that li

185 immunoprecipitation, we show that Ser-518 of Merlin is a substrate of the Aurora protein kinase A dur

186 Merlin is a tumour suppressor involved in the developmen

187 Merlin is closely related to the membrane-cytoskeleton l

188 ggested that the subcellular distribution of Merlin is critical to its function, and that several NF2

189 hat has been reported when the expression of Merlin is diminished in relation to EGFR and NOTCH1 expr

190 ivation of the NF2 gene encoding the protein Merlin is found in most sporadic and inherited schwannom

191 igenesis, our molecular studies suggest that Merlin is not a major regulator of YAP in liver progenit

192 The tumor suppressor protein Merlin is proteasomally degraded in breast cancer.

193 Interestingly, sumoylation of merlin is regulated by its phosphorylation via Akt and P

194 Taken together, our findings indicate that merlin is sumoylated and that this post-translational mo

195 f the NF2 tumor suppressor (encoding NF2, or Merlin) is associated with upregulation of the Rac1 smal

196 ibromatosis type 2 tumor suppressor protein, merlin, is related to the ERM (ezrin, radixin, and moesi

197 , we show that a subset of the Hippo pathway-Merlin, Kibra, and Lethal(2)giant larvae (Lgl), but not

198 These results reveal roles for Merlin, Kibra, and Lgl in neuronal specification and mai

199 PN-initiated Akt-mediated phosphorylation of Merlin leading to its proteasomal degradation.

200 tumor cell metabolomic portrait modulated by Merlin, leading to activation of Hedgehog signaling.

201 e tumor suppressor neurofibromatosis 2 (Nf2; merlin) limits the expansion of neural progenitor cells

202 regulator; however, the mechanisms by which merlin localizes to the membrane are less clear.

203 Concordantly, Merlin loss increased oxidative stress causing aberrant

204 jority of meningiomas and 1/3 of ependymomas Merlin loss is causative.

205 This review discusses the influence of merlin loss of function in NF2-related tumors and common

206 eficient meningioma cell lines revealed that merlin loss of function is due to a reduction in mutant

207 ed in many pathological phenotypes caused by Merlin loss, namely multipolar morphology, enhanced cell

208 Merlin loss-of-function is associated with increased act

209 d ERM proteins (Ezrin, Radixin, and Moesin), Merlin may organize the plasma membrane by assembling me

210 bacterial artificial chromosome (BAC) clone Merlin (ME) expresses abundant UL128-131, is RL13 impair

211 nalyzed in the backgrounds of strains TR and Merlin (ME).

212 , loosening cell-cell contacts, and YAP-TRIO-Merlin mediated regulation of Rho GTPase family proteins

213 Previous studies have established that merlin mediates contact inhibition of proliferation; how

214 The FERM domain proteins Merlin (Mer) and Expanded (Ex) are upstream components t

215 The FERM domain proteins Merlin (Mer) and Expanded (Ex) represent one mode of ups

216 Here, we show that Merlin (Mer), a homolog of the human tumor suppressor ne

217 Merlin (Moesin-ezrin-radixin-like protein, also known as

218 We found that schwannoma cells, containing merlin mutations and constitutive activation of the Rho/

219 e Neurofibromatosis-2 (NF2) tumor suppressor merlin negatively regulates cell proliferation in numero

220 Deidentified data from the remote monitoring Merlin.net (St. Jude Medical) database were used to exam

221 e further report that the regulatory protein merlin (neurofibromin 2, NF2) interacts with both YAP1 a

222 observed for the first time, the presence of merlin/neurofibromin 2 in ICC.

223 he tumor suppressors neurofibromin (NF1) and Merlin (NF2) has been gained.

224 Merlin/NF2 (moesin-ezrin-radixin-like protein/neurofibro

225 Multiple Merlin/NF2 effector pathways including the Hippo-YAP/TAZ

226 Merlin/NF2 is a bona fide tumor suppressor whose mutatio

227 It is currently unclear whether Merlin/NF2 suppresses tumorigenesis by activating upstre

228 ional knockout mice, we demonstrate that the Merlin/NF2 tumor suppressor and the YAP oncoprotein func

229 Although Merlin/NF2 was discovered two decades ago as a tumor sup

230 43, vimentin, desmin, PDGFbeta receptor and merlin/NF2.

231 of phosphorylated Merlin at serine 518 (S518-Merlin), NOTCH1 and epidermal growth factor receptor (EG

232 ondingly, reintroduction of SOX10 into human Merlin-null cells restores the ability of these cells to

233 lin gene expression and cell cycle arrest in Merlin-null cells.

234 development, is also key to the pathology of Merlin-null schwannoma tumours.

235 mediated by activation of YAP expression in Merlin-null SCs, and loss of YAP restores axonal regrowt

236 dicate that a significant fraction of either Merlin or Merlin(S518D) is capable of binding to the tar

237 on in the FERM domain dramatically inhibited Merlin particle movement.

238 herited tumor disease because of the loss of Merlin, patients suffer from multiple nervous system tum

239 e in cell-contact inhibition with changes in Merlin phosphorylation directly affecting NOTCH1 and EGF

240 PAK1-mediated merlin phosphorylation on Ser-518 reduced merlin's inter

241 ector p21-activated kinase and decreased NF2/merlin phosphorylation.

242 osophila, we find no evidence that mammalian merlin positively regulates mammalian Mst2.

243 Tp53bp2), that bound to closed-conformation Merlin predominately through the FERM domain.

244 we show that in both Drosophila and mammals, Merlin promotes downstream Hippo signaling without activ

245 The expression of Merlin protein (assessed immunohistochemically) was sign

246 in and RT-PCR analysis revealed that whereas merlin protein expression was significantly reduced in N

247 , identify a novel mechanism for the loss of Merlin protein in breast cancer, and have developed a di

248 Importantly, a merlin protein whose FERM domain cannot bind phosphoinos

249 and associated reduction in neurofibromin 2/Merlin protein, an upstream regulator of the Hippo signa

250 Most of the Merlin-proximal proteins were components of cell junctio

251 ated networks of known ground truth, we find MERLIN reconstructs regulatory programs of individual ge

252 Merlin regulates contact inhibition of growth and contro

253 activity during contact inhibition, but how merlin regulates Ras activity has remained elusive.

254 sociated protein, which is known to be under merlin regulation in schwannoma and is involved in incre

255 beta1/Src/FAK pathway has a crucial role in merlin-related tumourigenesis and therefore represents a

256 Suppression of UL128-131 expression during Merlin replication dramatically shifted the ratio toward

257 Mutation of NF2/merlin rescued the myelin deficit in Rac1-CKO mice in vi

258 Restoring expression of Merlin resulted in reduced malignant attributes of breas

259 Taken together, our data suggest loss of merlin results in the Rac-dependent decrease of anterogr

260 Tumor-derived mutations invariably disrupt Merlin's ability to interact with or inhibit CRL4(DCAF1)

261 Although Merlin's function as a tumor suppressor and regulator of

262 ed merlin phosphorylation on Ser-518 reduced merlin's interactions with both LATS1/2 and YAP1, result

263 Sumoylation mediates merlin's intramolecular and intermolecular binding activ

264 organizing the cell cortex and suggest that Merlin's role in restricting cortical Ezrin may contribu

265 es to, but is not sufficient to account for, merlin's tumor suppressor activity.

266 Molecular mechanisms regulating merlin's tumor-suppressive activity have not been clearl

267 ing shows that, in solution, both Merlin and Merlin(S518D) adopt a closed conformation, but binding e

268 t a significant fraction of either Merlin or Merlin(S518D) is capable of binding to the target protei

269 ructure and binding activity of Merlin and a Merlin(S518D) mutant that mimics the inactivating phosph

270 more open conformation than in solution, but Merlin(S518D) remains in a closed conformation.

271 We also discuss the NF2 gene status and merlin signaling pathways affected in the different tumo

272 iant-component analysis were performed using Merlin software.

273 ts from 130 families were conducted by using Merlin software.

274 al growth, and establish glia as a model for Merlin-specific Hippo signaling.

275 ulators such as Crumbs, Kibra, Expanded, and Merlin, spectrin regulates Hippo signaling in a distinct

276 nsidered a neuronal protein, the presence of merlin suggests ICC in bladder may have a role in neurot

277 s U87MG xenograft model, we demonstrate that merlin sumoylation is required for tumor-suppressive act

278 With mutant forms of Merlin that cannot bind to phosphatidylinositol 4,5-bisp

279 network learning with per gene information (MERLIN), that infers regulatory programs for individual

280 Merlin, the protein product of the NF2 gene, has been sh

281 treatment with ranolazine or placebo in the MERLIN-TIMI 36 (Metabolic Efficiency With Ranolazine for

282 S randomized to ranolazine or placebo in the MERLIN-TIMI 36 (Metabolic Efficiency With Ranolazine for

283 S randomized to ranolazine or placebo in the MERLIN-TIMI 36 (Metabolic Efficiency With Ranolazine for

284 me-Thrombolysis in Myocardial Infarction 36 (MERLIN-TIMI 36) trial randomized 6560 patients hospitali

285 We use MERLIN to dissect global transcriptional behavior in two

286 sociation with the membrane is important for merlin to function as a growth regulator; however, the m

287 The ability of merlin to regulate MLK3 activity requires a direct assoc

288 in, Radixin, and Moesin, and localization of Merlin to the cortical cytoskeleton is required for cont

289 Loss of the Merlin tumor suppressor and activation of the Hippo sign

290 Loss of the Merlin tumour suppressor causes abnormal de-differentiat

291 Inactivation of the tumor suppressor NF2/merlin underlies neurofibromatosis type 2 (NF2) and some

292 found that the expression in HeLa cells of a Merlin variant that is phosphorylation-defective on both

293 The strain Merlin viral inhibitor of apoptosis pUL36 was necessary

294 more gH/gL/gO than gH/gL/UL128-131, whereas Merlin virions contained mostly gH/gL/UL128-131, despite

295 crotubule association of the Hippo regulator Merlin was disrupted.

296 model using the relationship between OPN and Merlin was tested with a logistic regression model appli

297 Of note, we identified a function for S518-Merlin, which is distinct from what has been reported wh

298 eals that KSR1 is a novel binding partner of Merlin, which suppresses KSR1's function by inhibiting t

299 dings of an Aurora A-mediated interaction of Merlin with alpha-tubulin and ezrin suggest a potential

300 isruption of the actin cytoskeleton promotes Merlin-Wts interactions, which implicates Merlin in acti