ライフサイエンスコーパス: neurofibromin

1 ctly interacts with and negatively regulates neurofibromin.

2 r suppressor gene, which encodes the protein neurofibromin.

3 unction are seen with the loss of myocardial neurofibromin.

4 ) portion of the GAP-related domain (GRD) of neurofibromin.

5 s in the NF1 gene, which encodes the protein neurofibromin.

6 AP (RAS-GTPase activating protein) domain of neurofibromin.

7 e biogenesis was increased in the absence of neurofibromin.

8 hat the mTOR pathway is tightly regulated by neurofibromin.

9 to those in mice lacking the Ras-GAP protein neurofibromin.

10 acent to the catalytic GAP-related domain of neurofibromin.

11 rve injury by response to cytokines, through neurofibromin.

12 hways closely related to those influenced by neurofibromin.

13 caused by mutations in the NF1 gene encoding neurofibromin.

14 ch encodes the RAS GTPase-activating protein neurofibromin.

15 mor suppressor gene that encodes the protein neurofibromin.

16 ymphoma (c-CBL), ikaros zinc fingers (IKZF), neurofibromin 1 (NF1) and runt-related transcription fac

17 Here, we identify neurofibromin 1 (Nf1) as a key mediator of epicardial EM

18 these studies, we identify the gene encoding neurofibromin 1 (Nf1) as an ICSBP target gene, by chroma

19 neurofibromas because they harbor biallelic neurofibromin 1 (NF1) gene mutations.

20 , particularly deletion of the RAS inhibitor Neurofibromin 1 (Nf1) in nearly all cases.

21 ed potential roles for the RasGAPs RASA1 and neurofibromin 1 (NF1) in T cells through the generation

22 Using mice lacking neurofibromin 1 (Nf1) in type II collagen-expressing cel

23 onsensus sequence binding protein (ICSBP) or neurofibromin 1 (Nf1) increases the proliferative respon

24 Loss of neurofibromin 1 (NF1) leads to hyperactivation of RAS, w

25 Inactivation of the tumor suppressor neurofibromin 1 (NF1) presents a newly characterized mel

26 In mouse, we found that inactivation of neurofibromin 1 (Nf1), a gene mutated in neurofibromatos

27 Here, we identify a major Ras regulator, neurofibromin 1 (NF1), as a direct effector of GPCR sign

28 as with Ras GTPase activating protein (GAP), neurofibromin 1 (NF1), Raf-1, and ral guanine nucleotide

29 on Hippel-Lindau (VHL; n = 2); RET (n = 12); neurofibromin 1 (NF1; n = 2); and MYC-associated factor

30 Nf1 (neurofibromin 1) is a Ras-GAP protein that regulates cyt

31 Neurofibromin 1-mutant (NF1-mutant) cancers are driven b

32 expanded the VCP interactome by identifying neurofibromin-1 (NF1) as a novel VCP interactor in the C

33 rease CRMP2 coprecipitation with its partner neurofibromin-1 but decreased CRMP2 coprecipitation with

34 Neurofibromin 2 (Nf2) is strongly expressed in slowly ex

35 genesis resulting from YAP overexpression or Neurofibromin 2 (NF2)/Merlin inactivation.

36 In contrast, neurofibromin 2 (or Merlin), a molecule upstream of the

37 d for the first time, the presence of merlin/neurofibromin 2 in ICC.

38 NF2 (neurofibromin 2) is an established tumor suppressor that

39 se activity of LATS1/2 through inducing NF2 (neurofibromin 2).

40 r report that the regulatory protein merlin (neurofibromin 2, NF2) interacts with both YAP1 and LATS1

41 the Ras-GTPase activating protein (Ras-GAP) neurofibromin, a 5-HT6 receptor partner.

42 s in the NF1 tumor suppressor, which encodes neurofibromin, a GTPase activating protein for Ras.

43 The NF1 tumor suppressor gene encodes neurofibromin, a GTPase-activating protein (GAP) for p21

44 Nf1 encodes neurofibromin, a GTPase-activating protein that terminat

45 disorders of humans and is caused by loss of neurofibromin, a large and highly conserved protein whos

46 by mutations in the NF1 gene, which encodes neurofibromin, a large protein that modulates the activi

47 the NF1 tumor-suppressor gene, which encodes neurofibromin, a negative regulator of diverse Ras signa

48 e NF1 gene result in decreased expression of neurofibromin, a negative regulator of p21(Ras), and inc

49 by mutations in the NF1 locus, which encodes neurofibromin, a negative regulator of Ras.

50 s due to a reduction of the tumor suppressor neurofibromin, a negative regulator of the small GTPase

51 der caused by mutations in the gene encoding Neurofibromin, a p21Ras GTPase Activating Protein (GAP).

52 The disease gene, NF1, encodes neurofibromin, a protein of over 2,800 amino acids that

53 e for neurofibromatosis type 1 (NF1) encodes neurofibromin, a protein that negatively regulates signa

54 The NF1 gene encodes for neurofibromin, a RAS GTPase-activating protein, and thus

55 ous mutations in the NF1 gene, which encodes neurofibromin, a RAS GTPase-activating protein.

56 We report here that neurofibromin, a Ras-GAP encoded by Nf1, has an overlapp

57 The NF1 gene encodes neurofibromin, a Ras-GAP, highly expressed in developing

58 The NF1 gene encodes neurofibromin, a tumor suppressor postulated to function

59 The disease gene, NF1, encodes neurofibromin, a ubiquitously expressed protein that act

60 pression of the Ras regulatory GAP domain of neurofibromin also did not rescue the body weight or Igf

61 studies from our laboratory have shown that neurofibromin also regulates the mammalian target of rap

62 are located in a highly conserved region of neurofibromin and are expected, therefore, to have a fun

63 these results underscore the requirement of neurofibromin and ERK1/2 for normal endochondral bone fo

64 Deficits in signaling pathways involving neurofibromin and extracellular-regulated kinase (ERK) h

65 The gene products neurofibromin and merlin (schwannomin), respectively, ar

66 ine (MK) were found to be induced by loss of neurofibromin and MK was further characterized.

67 Neurofibromin and p120GAP differ markedly outside of the

68 ress this question, we expressed the GRDs of neurofibromin and p120GAP in primary cells from Nf1 muta

69 Thus, the GRDs of neurofibromin and p120GAP specify nonoverlapping functio

70 The data reveal a key role for neurofibromin and Ras signaling in the maintenance of CN

71 ither of the two tumor suppressor genes NF1 (neurofibromin) and NF2 (merlin) result in Neurofibromato

72 r suppressor genes NF1 (encoding the protein neurofibromin) and SPRED1 (encoding sprouty-related, EVH

73 he intracellular signal transduction protein neurofibromin, and Pax3, a transcription factor gene mut

74 n the Nf1 GTPase activating protein for Ras, neurofibromin, and Ras-GTP.

75 similar to the GAP domains from p120 RasGAP, neurofibromin, and SynGAP.

76 rvations suggest that MetAP2 is regulated by neurofibromin, and that MetAP2 inhibitors could be poten

77 een beta-amyloid precursor protein (APP) and neurofibromin, and their localization to the melanosome,

78 abeling immunofluorescence experiments using neurofibromin antibodies and in vitro microtubule assemb

79 in multiple mast cell functions and identify neurofibromin as a GAP for K-ras in mast cells.

80 t cell functions and to identify the role of neurofibromin as a GAP for K-ras in this lineage.

81 Collectively, these results identify neurofibromin as a GAP for Ras in T cells for maintainin

82 Thus, these studies identify neurofibromin as a novel regulator of Ras activity in VS

83 neural cells; the mechanism of regulation of neurofibromin as a Ras-GAP, remains however unknown.

84 These results establish neurofibromin as an essential regulator of bone minerali

85 sed proteomics approach to identify Ira2 and neurofibromin binding partners.

86 Since neurofibromin both negatively regulates Ras activity and

87 and gene expression analyses suggested that neurofibromin, by inhibiting Rankl expression, attenuate

88 l bone formation and support the notion that neurofibromin, by restraining RAS-ERK1/2 signaling, is a

89 ions in Nf1, which encodes the Ras inhibitor neurofibromin, cause the human genetic disorder neurofib

90 Loss of neurofibromin causes sustained Ras activation in spines,

91 Last, the reintroduction of a fragment of neurofibromin containing residues sufficient for restori

92 oform of the neurofibromatosis 1 (NF1) gene (neurofibromin) containing the alternatively spliced exon

93 The absence of neurofibromin could therefore lead to higher Ras activit

94 Neurofibromin deficiency in explant cultures is reproduc

95 tion, known to be induced in the presence of neurofibromin deficiency, was increased in the dentate g

96 We used astrocytes from neurofibromin-deficient (Nf1(-/-)) mice expressing a dom

97 es 5-HT6 receptor-operated cAMP signaling in neurofibromin-deficient cells.

98 ch alters the proliferation and migration of neurofibromin-deficient ECs in response to neurofibroma-

99 was to examine the tumorigenic properties of neurofibromin-deficient human Schwann cells (SCs) that w

100 hese studies identify the Ras-Erk pathway in neurofibromin-deficient macrophages as the aberrant path

101 ry cell migration and standard cell culture, neurofibromin-deficient macrophages demonstrate enhanced

102 These studies identify neurofibromin-deficient myeloid cells as critical cellul

103 essary for the survival of the wild-type and neurofibromin-deficient neurons.

104 Lastly, engraftment of neurofibromin-deficient SC cultures into the peripheral

105 f TC21/R-Ras2 activation in the migration of neurofibromin-deficient Schwann cells.

106 pathways involved in mast cell migration to neurofibromin-deficient Schwann cells.

107 These findings indicate that neurofibromin-deficient SCs are involved in neurofibroma

108 he neurofibroma SC cultures, indicating that neurofibromin-deficient SCs had a substantial growth adv

109 harvested from Nf1+/- mice and primary human neurofibromin-deficient VSMCs, we identify a discrete Ra

110 olecular mechanisms linking dysregulation of neurofibromin-dependent pathways to spatial learning def

111 to rescue receptor constitutive activity in neurofibromin-depleted cells.

112 enetic inhibition approaches, we report that neurofibromin differentially controls neural stem cell (

113 d reduced cyclic AMP generation, there was a neurofibromin dose-dependent reduction in dopamine (DA)

114 Deficiency in neurofibromin (encoded by Nf1) in mice results in mid-em

115 Here we investigated the neurofibromin-ERK cascade in the hippocampus of wild-typ

116 The NF1 tumor suppressor gene product neurofibromin exhibits GTPase-activating activity (GAP)

117 Neurofibromin exhibits Ras GTPase activating protein (Ra

118 This increased neurofibromin expression correlated with elevated levels

119 y Asn-17 dominant-negative mutant, levels of neurofibromin expression decreased.

120 xperiments showed a marked downregulation of neurofibromin expression in the dentate gyrus of both na

121 s support the hypothesis that alterations in neurofibromin expression in the developing brain have si

122 all anterior pituitary size reflects loss of neurofibromin expression in the hypothalamus, leading to

123 These results suggested that neurofibromin expression is increased in human astrocyti

124 activity (GAP) toward RAS, such that loss of neurofibromin expression leads to high levels of activat

125 We found dose-dependent effects of neurofibromin expression on NSC proliferation and surviv

126 bility was observed in six of six tumors and neurofibromin expression was lost in all tumors analysed

127 Although neurofibromin expression was maintained, P(0)-GGFbeta3 M

128 ene mutation resulted in different levels of neurofibromin expression.

129 d Schwann cells correlate with a decrease in neurofibromin expression.

130 germline mutations have dramatic effects on neurofibromin expression.

131 ate the hypothesis that reduced NF1 protein (neurofibromin) expression may confer a growth advantage

132 ne NF1 gene mutations differentially dictate neurofibromin function in the brain.

133 e intriguing possibility that, while loss of neurofibromin function is necessary for NF1-associated l

134 t of the germline NF1 gene mutation on brain neurofibromin function relevant to learning.

135 gative regulators of Ras/MAPK signaling with neurofibromin functioning as a Ras-specific GTPase activ

136 The NF1 gene product, neurofibromin, functions as a negative regulator of RAS,

137 The NF1 tumor suppressor gene product, neurofibromin, functions as a Ras GTPase-activating prot

138 The NF1-encoded protein, neurofibromin, functions as a Ras-GTPase activating prot

139 Although its encoded protein, neurofibromin, functions as a Ras-GTPase activating prot

140 that lacks the UBX domain, ubiquitinates the neurofibromin GAP-related domain in vitro.

141 d the Ras GTPase-stimulating activity of the neurofibromin GAP-related domain.

142 osophila melanogaster that lack a functional neurofibromin gene (nf1).

143 pendence on mTOR suggests that PTEN and NF1 (neurofibromin) glial growth regulation requires TSC/Rheb

144 Here we show that expression of neurofibromin GRD, but not the p120GAP GRD, restores nor

145 ts show that K-RAS is the primary target for neurofibromin GTPase-activating protein activity in vitr

146 Importantly, neurofibromin has been identified as a key protein in th

147 eficiency, and argue against the notion that neurofibromin has separable Ras- and cAMP-related functi

148 Although neurofibromin has several known properties and functions

149 define these targets of Gpb1/2 as the yeast neurofibromin homologs Ira1 and Ira2, which function as

150 The yeast Saccharomyces cerevisiae has two neurofibromin homologs, Ira1 and Ira2.

151 kinase domain reversed tumor suppression by neurofibromin, implicating Raf-1 as the primary downstre

152 Further supporting a role of neurofibromin in agonist-independent Gs signaling elicit

153 n blot analysis failed to detect full-length neurofibromin in any of the neurofibroma SC cultures, in

154 Previous studies have suggested a role for neurofibromin in brain function.

155 se findings establish a distinctive role for neurofibromin in CNS neurons with respect to vulnerabili

156 diovascular defects due to a requirement for neurofibromin in embryonic endothelium.

157 Overexpression of ETEA downregulates neurofibromin in human cells.

158 However, the function of neurofibromin in human endothelial cells (ECs) and the b

159 , these data demonstrate a critical role for neurofibromin in hypothalamic-pituitary axis function an

160 These data define a specific role for neurofibromin in negatively regulating GM-CSF signaling

161 Lack of expression of neurofibromin in neurofibromatosis 1 and its lethal deri

162 -/-) mutant mice), we then show that lack of neurofibromin in post-mitotic chondrocytes triggers a nu

163 We also provide evidence suggesting that neurofibromin in prehypertrophic chondrocytes, downstrea

164 ls of Ral activation, implicating a role for neurofibromin in regulating RalA activation.

165 Despite these observations, the function of neurofibromin in regulating VSMC function and how Ras si

166 To explore roles for neurofibromin in the development of the CNS, we took adv

167 We show that mice that lack neurofibromin in the majority of cortical neurons and as

168 helial cells and confirm the requirement for neurofibromin in the neural crest.

169 onal expression suggests novel functions for neurofibromin in the postmitotic brain that are perhaps

170 entify a novel interaction between c-kit and neurofibromin in vivo, and offer experimental evidence t

171 s from wild-type mice and mice deficient for neurofibromin in which the survival and differentiation

172 ting the RasGAP proteins Ira2 (in yeast) and neurofibromin (in humans).

173 th 2-photon glutamate uncaging, we show that neurofibromin, in which loss-of-function mutations cause

174 Neurofibromin inhibits cell proliferation, at least in p

175 Based on previous evidence that neurofibromin inhibits Ras-ERK signaling in chondrocytes

176 dings suggest that disrupting 5-HT6 receptor-neurofibromin interaction prevents agonist-independent 5

177 have demonstrated that the NF1 gene product, neurofibromin, interacts with cytoplasmic microtubules.

178 lnerability to injury, define a CNS-specific neurofibromin intracellular signaling pathway responsibl

179 a complex intracellular machinery, of which neurofibromin is a critical component.

180 Neurofibromin is a multidomain protein encoded by the NF

181 The NF1-encoded protein neurofibromin is a Ras GTPase-activating protein (GAP) a

182 Neurofibromin is a tumor suppressor protein that has Ras

183 Expression of exon 9a neurofibromin is developmentally regulated, with express

184 We show here that neurofibromin is dynamically regulated by the ubiquitin-

185 Neurofibromin is encoded by NF1 and functions as a negat

186 Neurofibromin is encoded by NF1 and functions as a negat

187 We show first that neurofibromin is expressed in FGFR-positive prehypertrop

188 We now show that, in response to EGF, neurofibromin is in vivo phosphorylated on serine residu

189 Exon 9a neurofibromin is localized in the cytoplasm, sediments i

190 neurofibroma Schwann cells and suggest that neurofibromin is not an essential regulator of Ras activ

191 llectively, our results suggest that loss of neurofibromin is not sufficient for astrocytoma formatio

192 r progenitors or neonatal GNPs, we show that neurofibromin is required for appropriate development of

193 l2a1-positive chondrocytes, we asked whether neurofibromin is required to control FGFR1-Ras-ERK signa

194 Taken together, these data suggest that neurofibromin is required to downregulate Ras activation

195 ght to determine whether the GAP activity of neurofibromin is sufficient to rescue complete loss of f

196 Neurofibromin is widely expressed in the developing and

197 fibromatosis type 1 tumor suppressor protein neurofibromin, is a GTPase activating protein for H-, N-

198 The NF1 protein, neurofibromin, is a Ras-GAP that acts downstream of a fe

199 The product of the NF1 gene, neurofibromin, is a tumor suppressor which most likely a

200 The NF1 gene product, neurofibromin, is hypothesized to function as a tumor su

201 the Nf1 tumor suppressor gene, which encodes neurofibromin, is necessary but not sufficient to initia

202 Silencing of ETEA expression increases neurofibromin levels and downregulates Ras activity.

203 However, whereas degradation is rapid, neurofibromin levels are re-elevated shortly after growt

204 lin and dibutyryl-cAMP on Nf1-/- astrocytes, neurofibromin likely functions at the level of adenylyl

205 l, biological, and tumorigenic properties of neurofibromin loss.

206 xpressed these NF1 constructs suggested that neurofibromin may interfere with the interaction between

207 These results suggest that neurofibromin may possess activities outside of the GRD

208 ractivation, but rather result from impaired neurofibromin-mediated cAMP generation.

209 ells resulted in only partial restoration of neurofibromin-mediated cAMP regulation.

210 ether other as yet unidentified functions of neurofibromin might also exist.

211 on Nf1 mutant Drosophila have suggested that neurofibromin might also regulate cAMP signaling.

212 Our results demonstrate that neurofibromin modulates ERK/synapsin I-dependent GABA re

213 In the absence of neurofibromin, mouse embryo hearts develop overabundant

214 genetics approach to reveal STAT3 as a novel neurofibromin/mTOR pathway signaling molecule, define it

215 ve SCs, whereas the remainder contained both neurofibromin-negative and neurofibromin-positive SCs.

216 d the majority were comprised principally of neurofibromin-negative SCs, whereas the remainder contai

217 Because neurofibromin negatively regulates mammalian target of r

218 The NF1 gene product neurofibromin negatively regulates Ras and mammalian tar

219 The tumor suppressor proteins neurofibromin (NF1) and adenomatous polyposis coli (APC)

220 biological function of the tumor suppressors neurofibromin (NF1) and Merlin (NF2) has been gained.

221 ers encode tumor suppressor proteins, termed neurofibromin (NF1) and merlin (NF2), which function in

222 the epidermal growth factor receptor (EGFR), neurofibromin (NF1) and Ras, but not Galpha(s).

223 Neurofibromin (NF1) gene mutations lead to increased ris

224 g mice that carry a targeted mutation at the Neurofibromin (Nf1) locus and consequently lack RAS-GAP

225 Here we report that genetic deletion of neurofibromin (Nf1), a tumor suppressor with RAS-GAP act

226 This gene encodes the RasGAP Neurofibromin (NF1).

227 These results indicate that neurofibromin normally acts to modulate epithelial-mesen

228 ic regulation of GRD by CSRD, which requires neurofibromin phosphorylation by PKC and association wit

229 Neurofibromin plays a critical role in the downregulatio

230 Taken together, our results suggest that neurofibromin plays a crucial role in modulating MSPC di

231 isrupting association of 5-HT6 receptor with neurofibromin Pleckstrin Homology (PH) domain also inhib

232 er contained both neurofibromin-negative and neurofibromin-positive SCs.

233 These results demonstrate that neurofibromin positively influences cAMP generation and

234 well studied, regulation of the NF1-encoded neurofibromin protein is less clear.

235 Our analysis suggests that the Drosophila neurofibromin protein NF1 is required to constrain synap

236 g domain on Ira1/2 is conserved in the human neurofibromin protein, an analogous signaling network ma

237 This novel mechanism for the regulation of neurofibromin provides a molecular bridge for understand

238 disorder caused by impaired function of the neurofibromin RAS regulator.

239 To investigate the neurofibromin-Ras interaction in a systematic manner, we

240 ion of NF1 in PA tissue and suggest that the neurofibromin-Ras signal transduction pathway is involve

241 ganglion cell (RGC) death, and Nf1 protein (neurofibromin)-regulated signaling pathway function (Ras

242 While PI3K/AKT governs neurofibromin-regulated NSC proliferation, multilineage

243 d to Nf1+/- mouse brains, demonstrating that neurofibromin regulates AC activity in both mammals and

244 Together, these data show that neurofibromin regulates actin cytoskeleton dynamics and

245 nesis approaches in vivo to demonstrate that neurofibromin regulates astrocyte cell growth and glioma

246 Thus, neurofibromin regulates longevity and stress resistance

247 (ECs) and the biochemical mechanism by which neurofibromin regulates neoangiogenesis are not known.

248 l mutants; Nf1(+/-)) to demonstrate that (i) Neurofibromin regulates prefrontal and striatal inhibito

249 r and bone marrow-derived cells (BMDCs), and neurofibromin regulates the function of each cell type.

250 To determine how the NF1 gene product (neurofibromin) regulates astrocyte growth and motility r

251 mice to establish, for the first time, that neurofibromin regulation of cAMP requires RAS activation

252 These data reveal a key role for neurofibromin regulation of TC21/R-Ras2 in Schwann cells

253 fector pathways responsible for NF1 protein (neurofibromin) regulation of neuronal function, with bot

254 Thus, the dynamic proteasomal regulation of neurofibromin represents an important mechanism of contr

255 However, the region of neurofibromin required for the interaction with Spred1 h

256 targeting function of the GAPex subdomain of neurofibromin that is present in all known canonical Ras

257 e encodes a GTPase-activating protein called neurofibromin that negatively regulates Ras signaling.

258 F1 tumour-suppressor gene encodes a protein (neurofibromin) that accelerates GTP hydrolysis on Ras pr

259 ternative splicing modulates the function of neurofibromin, the NF1 gene product, by inserting the in

260 Here we show that neurofibromin, the NF1 gene product, is a Spred1-interac

261 It is well established that neurofibromin, the NF1 gene product, is an antioncogene

262 Neurofibromin, the product of NF1, acts as a RasGAP and

263 Studies of neurofibromin, the protein encoded by NF1, have focused

264 Neurofibromin, the protein encoded by NF1, negatively re

265 Neurofibromin, the protein encoded by NF1, possesses an

266 Recently neurofibromin, the protein encoded by NF1, was shown to

267 In this study we demonstrate that neurofibromin, the protein encoded by the NF1 tumor supp

268 Neurofibromin, the protein encoded by the NF1 tumor-supp

269 Neurofibromin, the protein encoded by the tumor suppress

270 Neurofibromin, the protein product of NF1, functions as

271 Neurofibromin, the protein product of NF1, functions as

272 Neurofibromin, the protein product of the Nf1 gene, is b

273 Neurofibromin, the protein product of the NF1 tumor supp

274 selected NF1GRD mutations on the ability of neurofibromin to associate with microtubules.

275 , we sought to determine the contribution of neurofibromin to astrocyte cAMP regulation.

276 Thus, the ability of neurofibromin to interact with Ras is crucial for its fu

277 ector pathway, which is tightly regulated by neurofibromin to limit VSMC proliferation and migration.

278 y skipped in neurons, reduces the ability of neurofibromin to regulate Ras by 10-fold.

279 -1426) present evidence that Spred1 recruits neurofibromin to the membrane, where it dampens growth f

280 ased on the ability of the NF1 gene product (neurofibromin) to function as a GTPase activating protei

281 ne the contribution of the NF1 gene product, neurofibromin, to astrocyte growth regulation and NF1-as

282 reviously been demonstrated to interact with neurofibromin via its N-terminal Ena/VASP Homology 1 (EV

283 We provide here evidence that neurofibromin, via its Ras guanosine triphosphatase -act

284 To discover other downstream targets of neurofibromin, we performed an unbiased cell-based high-

285 Neurofibromin, which is encoded by NF1, is a GTPase acti

286 in the cysteine/serine-rich domain (CSRD) of neurofibromin, which lies in the N-terminus and upstream

287 encodes the GTPase-activating protein (GAP) neurofibromin, which negatively regulates Ras activity.

288 The NF1 tumor suppressor gene encodes neurofibromin, which regulates the growth of immature my

289 n significantly increased the association of neurofibromin with actin in co-immunoprecipitations.