ライフサイエンスコーパス: merlin

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

2 rge to be handled by the imputation software Merlin.

3 membrane-cytoskeleton adapter protein called merlin.

4 fibromatosis type 2 tumor-suppressor protein merlin.

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

6 1, and both were restored by mutation of NF2/merlin.

7 MET signaling; the latter via inhibition of merlin.

8 itical for the growth-regulatory function of merlin.

9 out the role of phosphoinositide binding for merlin.

10 the cytosol without altering the folding of merlin.

11 growth-suppressive properties to the mutant merlin.

12 hat encodes for the tumor suppressor protein merlin.

13 he vulnerability of tumor cells with loss of Merlin.

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

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

16 CAF1 counteracts the antimitogenic effect of Merlin.

17 on mediated by dMer, the orthologue of human merlin.

18 s the promitogenic effect of inactivation of Merlin.

19 n and phosphatidylinositol lipids binding to merlin.

20 mTORC1 signaling through the inactivation of merlin.

21 lecular conformation and binding activity of Merlin.

22 at encodes a tumor-suppressor protein called merlin.

23 dependent complex comprised of Amot, YAP and Merlin.

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

25 mor-suppressive function of the NF2 protein, merlin, a membrane-cytoskeleton linker, remains unclear.

26 s type 2 (NF2) tumor suppressor gene encodes merlin, a membrane/cytoskeleton protein necessary for th

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

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

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

30 20 SOTR plasma samples, viral stocks (Towne, Merlin, AD169) and the first World Health Organization (

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

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

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

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

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

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

37 To examine the roles of Merlin and EGFR in kidney tumorigenesis, we generated mi

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

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

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

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 and mechanism of intracellular transport of Merlin and its mutants.

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

45 Merlin and Kibra together recruit the adapter protein Sa

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

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

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

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

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

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

52 Akt feeds back and phosphorylates merlin and provokes its polyubiquitination and degradati

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

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

55 However, the biochemical function of merlin and the effector pathways critical for the pathog

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

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

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

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

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

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

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

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

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

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

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

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 Moreover, Akt phosphorylation enhances merlin binding affinity to phosphatidylinositols and inh

76 orylation and phosphatidylinositols increase merlin binding to CD44.

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 ols the function of the NF2 tumor suppressor Merlin by determining the output of Merlin's physical in

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

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

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

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

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

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

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

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

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

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

93 Merlin-deficient human meningioma cells and merlin knock

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

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

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

97 ts and suppresses the oncogenic potential of Merlin-deficient tumor cell lines.

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

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

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

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

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

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

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

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

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

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

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

111 The extreme NH(2) terminus of merlin directly interacts with phosphatidylinositols, fo

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

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

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

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

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

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

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

119 nt models imply that the FERM domain protein Merlin, encoded by the tumor suppressor NF2, inhibits mi

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

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

122 Using these tools, we find that merlin exists predominately as a monomer in a stable, cl

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

124 We assessed Merlin expression in breast cancer tissues by immunohist

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

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

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

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

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

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

131 dies suggest alternative molecular models of Merlin function.

132 ement of microtubule-dependent transport for Merlin function.

133 mational states is often employed to explain Merlin function.

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

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

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

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

138 Merlin has broad tumor-suppressor functions as its mutat

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

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

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

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

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

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

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

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

147 Here, we delineate the molecular function of Merlin in AJ establishment in epidermal keratinocytes in

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

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

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

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

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

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

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

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

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

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

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

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

160 AJ establishment is an essential function of Merlin in vivo.

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

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

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

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

165 We have shown that the NF2 tumor suppressor Merlin inhibits EGFR internalization and signaling in a

166 In this study, we show that merlin inhibits MLK3 activity, as well as the activation

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

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

169 Merlin integrates Rho GTPase family signaling with MAPK

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

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

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

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

174 Merlin is a tumour suppressor involved in the developmen

175 Merlin is closely related to the membrane-cytoskeleton l

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

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

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

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

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

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

182 ggests that the tumor suppressor function of merlin is similarly regulated and that only the closed f

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

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

185 ofibromatosis type 2 (NF2) tumor suppressor, Merlin, is a FERM (Four point one, Ezrin, Radixin, Moesi

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

187 rsely, the exogenous expression of wild-type merlin isoforms, but not a patient-derived L64P mutant,

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

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

190 Merlin-deficient human meningioma cells and merlin knockdown arachnoidal cells, the nonneoplastic ce

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

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

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

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

195 Concordantly, Merlin loss increased oxidative stress causing aberrant

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

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

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

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

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

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

202 re, we demonstrate that MLK3 is required for merlin-mediated suppression of cell proliferation and in

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

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

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

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

207 Surprisingly, the presence of this immotile Merlin mutant also inhibited trafficking of the WT prote

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

209 n Non-ST Elevation Acute Coronary Syndromes [MERLIN]; NCT00099788).

210 Merlin-negative lines are sensitive to the growth-inhibi

211 Furthermore, they reveal that merlin-negative mesotheliomas display unregulated mTORC1

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

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

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

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

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

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

218 , suggesting that YAP is a major effector of Merlin/NF2 in growth regulation.

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

220 Our studies link Merlin/NF2 to mammalian Hippo signaling and implicate YA

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

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

223 43, vimentin, desmin, PDGFbeta receptor and merlin/NF2.

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

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

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

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

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

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

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

231 rotein using RNAi and pull-downs showed that Merlin particles are associated with and moved by microt

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

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

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

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

236 nding of motors and movement is regulated by Merlin phosphorylation.

237 of merlin restores rapamycin sensitivity in merlin-positive lines.

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

239 markers were performed with the Fastlink and Merlin programs in conjunction with data obtained from o

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

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

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

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

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

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

246 Merlin regulates contact inhibition of growth and contro

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

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

249 rapamycin, and the expression of recombinant merlin renders them partially resistant to rapamycin.

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

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

252 Conversely, depletion of merlin restores rapamycin sensitivity in merlin-positive

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

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

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

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

257 Sumoylation mediates merlin's intramolecular and intermolecular binding activ

258 ppressor Merlin by determining the output of Merlin's physical interactions with active PAK2.

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

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

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

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

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

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

265 have previously shown that the NF2 protein (merlin/schwannomin) associates with mixed lineage kinase

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

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

268 iant-component analysis were performed using Merlin software.

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

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

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

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

273 Merlin suppresses phosphatidylinositol 3-kinase (PI3K)/A

274 We propose that Merlin suppresses tumorigenesis by translocating to the

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

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

277 randomized, double-blind, placebo-controlled MERLIN-TIMI (Metabolic Efficiency With Ranolazine for Le

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

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

280 mly assigned to ranolazine or placebo in the MERLIN-TIMI 36 (Metabolic Efficiency With Ranolazine for

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

282 e randomized to ranolazine or placebo in the MERLIN-TIMI 36 trial.

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

284 es-Thrombolysis in Myocardial Infarction 36 (MERLIN-TIMI 36).

285 or treatment and Akt phosphorylation provoke merlin to aggregate in the ruffled plasma membrane and p

286 We use MERLIN to dissect global transcriptional behavior in two

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

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

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

290 Inhibition of Merlin transport by expression of the dominant-negative

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

292 Loss of function mutations in the merlin tumor suppressor underlie neurofibromatosis type

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

294 regulates the tumor-suppressive activity of merlin via both Akt phosphorylation and phosphatidylinos

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

296 crotubule association of the Hippo regulator Merlin was disrupted.

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

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

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

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