ライフサイエンスコーパス: neurofibromin

1 mor suppressor gene that encodes the protein neurofibromin.

2 ctly interacts with and negatively regulates neurofibromin.

3 r suppressor gene, which encodes the protein neurofibromin.

4 unction are seen with the loss of myocardial 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 ) portion of the GAP-related domain (GRD) of neurofibromin.

14 caused by mutations in the NF1 gene encoding neurofibromin.

15 ch encodes the RAS GTPase-activating protein neurofibromin.

16 often associated with genomic aberrations in neurofibromin 1 (NF1) and phosphoinositide 3-kinases/mam

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

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

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

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

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

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

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

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

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

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

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

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

29 The ITD prevented interaction with neurofibromin 1 (NF1)-GTPase-activating protein (GAP), p

30 s B and D, von Hippel-Lindau (VHL), RET, and neurofibromin 1 (NF1).

31 neated by the multifaceted signaling protein neurofibromin 1 (NF1).

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

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

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

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

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

37 The tumor suppressor and FERM domain protein Neurofibromin 2 (NF2) controls diverse processes in canc

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

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

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

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

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

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

44 By regulating ARIH1, neurofibromin 2, a tumor suppressor, enhances cisplatin

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

46 ll cycle length, and associated reduction in neurofibromin 2/Merlin protein, an upstream regulator of

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

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

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

50 NF1 encodes neurofibromin, a GTPase-activating protein for RAS proto

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 We report that neurofibromin, a tumor suppressor and Ras-GAP (GTPase-ac

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

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

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

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

70 in the NF1 gene, which encodes the protein, neurofibromin, an inhibitor of Ras activity.

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

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

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

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

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

76 Neurofibromin and p120GAP differ markedly outside of the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 Since neurofibromin both negatively regulates Ras activity and

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

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

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

98 Loss of neurofibromin causes sustained Ras activation in spines,

99 KRAS G13-mutated colorectal cancers that are neurofibromin-competent may respond to EGFR therapies.

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

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

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

103 Neurofibromin deficiency in explant cultures is reproduc

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

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

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

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

108 Neurofibromin-deficient ER(+) breast cancer cells initia

109 and ER signaling, and co-targeting may treat neurofibromin-deficient ER(+) breast tumors.

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

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

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

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

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

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

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

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

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

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

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

121 ed cells can respond to EGFR inhibitors in a neurofibromin-dependent manner.

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

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

124 Consequently, neurofibromin depletion causes estradiol hypersensitivit

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

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

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

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

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

130 Neurofibromin exhibits Ras GTPase activating protein (Ra

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

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

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

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

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

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

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

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

139 ene mutation resulted in different levels of neurofibromin expression.

140 germline mutations have dramatic effects on neurofibromin expression.

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

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

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

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

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

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

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

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

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

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

151 Neurofibromin gene (NF1) mutation causes neurofibromatos

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

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

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

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

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

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

158 Although neurofibromin has several known properties and functions

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

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

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

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

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

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

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

166 Overexpression of ETEA downregulates neurofibromin in human cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 Neurofibromin inhibits cell proliferation, at least in p

183 report that the leucine-rich domain (LRD) of neurofibromin inhibits invasion of human glioblastoma ce

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

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

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

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

188 Thus, neurofibromin is a dual repressor for both Ras and ER si

189 Neurofibromin is a multidomain protein encoded by the NF

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

191 Neurofibromin is a tumor suppressor protein that has Ras

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

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

194 Neurofibromin is encoded by NF1 and functions as a negat

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

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

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

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

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

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

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

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

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

204 Neurofibromin is widely expressed in the developing and

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

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

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

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

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

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

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

212 xplaining the poor prognosis associated with neurofibromin loss in endocrine therapy-treated ER(+) br

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

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

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

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

217 GAP domain) provide the structural basis for neurofibromin-mediated GTP hydrolysis.

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

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

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

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

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

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

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

225 Because neurofibromin negatively regulates mammalian target of r

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

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

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

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

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

231 Neurofibromin (NF1) gene mutations lead to increased ris

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

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

234 rength between KRAS and the tumor suppressor neurofibromin (NF1).

235 This gene encodes the RasGAP Neurofibromin (NF1).

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

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

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

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

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

241 These results demonstrate that neurofibromin positively influences cAMP generation and

242 Neurofibromin protein (encoded by the NF1 gene) hydrolyz

243 The neurofibromin protein contains at least four major domai

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

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

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

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

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

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

250 bitor SL327, revealing a mechanism whereby a neurofibromin/Ras/MEK pathway regulates a critical CIN d

251 type and G13D mutant of KRAS in complex with neurofibromin (RasGAP domain) provide the structural bas

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

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

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

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

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

257 Thus, neurofibromin regulates longevity and stress resistance

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

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

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

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

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

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

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

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

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

267 sults reveal that KRAS G13D is responsive to neurofibromin-stimulated hydrolysis and suggest that a s

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

269 h encodes a GTPase-activating protein called neurofibromin that negatively regulates Ras proteins.

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

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

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

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

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

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

276 Neurofibromin, the protein encoded by NF1, negatively re

277 Neurofibromin, the protein encoded by NF1, possesses an

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

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

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

281 Neurofibromin, the protein encoded by the tumor suppress

282 Neurofibromin, the protein product of NF1, functions as

283 Neurofibromin, the protein product of NF1, functions as

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

285 Neurofibromin, the protein product of the NF1 tumor supp

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

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

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

289 -1426) present evidence that Spred1 recruits neurofibromin to the membrane, where it dampens growth f

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

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

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

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

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

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

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

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

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

299 ds directly to both c-KIT and to the RasGAP, neurofibromin, whose function is completely dependent on

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