ライフサイエンスコーパス: NGF

1 NGF binding to its protein kinase receptor TrkA is known

2 NGF binding to TrkA affects TLR signaling, favoring path

3 NGF binds the tropomysin receptor kinase A (TrkA) and p7

4 NGF caused progressive neurite elongation; a significant

5 NGF did not alter bradykinin-induced M-current inhibitio

6 NGF exists in both a mature form and a pro-form (proNGF)

7 NGF induces neuronal differentiation by modulating [Ca(2

8 NGF is the best-studied NT in the bladder and its role i

9 NGF signals through the ERK/MAPK pathway to promote expr

10 NGF treatment displaced PI3K C2A from the Golgi and opto

11 NGF treatment evoked sustained increases in peripheral a

12 On laminin-1, NGF induced greater vinculin-dependent adhesion-cytoskel

13 rising number of questions that remain about NGF expression patterns and NGF's various functions and

14 This feedforward ACh-NGF axis activates the gastric cancer niche and offers a

15 r that induces priming-PKCepsilon activator, NGF, and TNF-alpha-when injected into the ganglion produ

16 le Sprague Dawley rats with or without added NGF and compared their responsiveness to bradykinin, a p

17 the formation of the so-called high-affinity NGF binding sites.

18 work suggests that periods before and after NGF-TrkA-induced Coronin-1 expression (and likely other

19 Preinjection of an NGF-neutralizing antibody or Trk inhibitor GNF-5837 prev

20 Thus, an NGF/TrkA-MAPK-CBFbeta pathway converges with Islet1-Runx

21 we demonstrate that early treatment with an NGF antibody reduced tumor-induced bone destruction, del

22 Cyclic AMP and NGF also protect NS-1 cells from serum withdrawal-induce

23 to neuronal differentiation by androgens and NGF is also novel.

24 permissive factors including FGF2, BDNF, and NGF.

25 CNA1B, CACNA1C, CACNA1D, CACNG2, CAMK2A, and NGF.

26 Hence, cAMP- and NGF-dependent signaling for differentiation are also com

27 ts with bovine serum albumin (BSA), GDNF and NGF increased the motor and sensory axon content, respec

28 naling that involves mobilization of NGF and NGF-dependent sensitization of TRPV1.

29 hat remain about NGF expression patterns and NGF's various functions and interaction partners in rela

30 the conformational properties of proNGF and NGF and help provide a rationale for the diverse biologi

31 onformational differences between proNGF and NGF are central to a better understanding of the opposin

32 the conformational properties of proNGF and NGF.

33 feedback regulation between Lhx8, TrkA, and NGF is an important regulatory mechanism for cholinergic

34 Because of the recent development of anti-NGF blocking antibodies as a possible new pain treatment

35 Given the clinical efficacy of anti-NGF monoclonal antibody (mAb) therapies, there is signif

36 pain and the potential side effects of anti-NGF therapy.

37 In vivo, we demonstrated that anti-NGF blocking antibodies prevent and reverse PH in rats t

38 While anti-NGF antibodies have demonstrated analgesia both preclini

39 inhibition were evaluated in vivo with anti-NGF blocking antibodies administered both in rat chronic

40 protein 2 (IGFBP-2), nerve growth factor (b-NGF), platelet-derived growth factor receptor beta polyp

41 ion of synaptic growth factors such as BDNF, NGF, and IGF.

42 y unanswered question is what other benefits NGF blockade might confer in patients with bone cancer.

43 Nerve growth factor-beta (NGF) is essential for the correct development of the ner

44 IgG1-antibody and nerve growth factor-beta (NGF).

45 Functionally relevant interactions between NGF and these receptors have been proposed, on the basis

46 Inhibition of MII blocked NGF stimulation, indicating the central role of restrain

47 stingly, inhibition of Trk signaling blocked NGF-stimulated BTIC proliferation and p75NTR cleavage, i

48 uantitatively summarize the peripheral blood NGF data in SCZ patients compared with healthy control (

49 ccompanied by the decreased peripheral blood NGF levels, strengthening the clinical evidence of an ab

50 -(15)N correlation spectra confirm that both NGF and a competing small molecule interact at the known

51 nisotropy experiments demonstrated that both NGF and proNGF induce conformational changes in p75(NTR)

52 sicles to the outgrowth responses induced by NGF and L1CAM.

53 Sprouting induced by NGF persists for 10 years after gene transfer.

54 cades, analogous to the responses induced by NGF.

55 urite outgrowth of PC-12 cells stimulated by NGF.

56 Lis1 synthesis is also triggered by NGF withdrawal and required for the transport of a death

57 Ca(2+)-permeable TRPV channel upregulated by NGF via the mitogen-activated protein kinase (MAPK) sign

58 gnaling in pain processing and identify C5a, NGF, and TRPV1 as key players in this cross-cellular com

59 he hippocampus, whereas reductions in CD200, NGF, and MBP were evident.

60 ent virus and incubated in medium containing NGF and EGF.

61 or delayed reactivation in medium containing NGF and epidermal growth factor (EGF).

62 ntracellular signaling molecule coordinating NGF signaling to regulate collateral sprouting and struc

63 -CTF impact the endocytic pathway to disrupt NGF trafficking and signaling, resulting in trophic defi

64 induced endosomal enlargement and disrupted NGF signaling and axonal trafficking.

65 uired trajectories of retrograde quantum-dot-NGF-endosomes with <20-nm accuracy at 32 Hz in microflui

66 but not ERK1/2 activity, blocked TLR2-driven NGF up-regulation at both the transcript and protein lev

67 Interestingly, during NGF-induced differentiation, the NCX1 protein level incr

68 High glucose rapidly enhances NGF secretion and increases TrkA phosphorylation in mous

69 Conversely, exogenouous NGF stimulated BTIC proliferation through alpha- and gam

70 Finally, the administration of exogenous NGF to wild-type mice was found to significantly increas

71 Effects of exogenous NGF were evaluated ex vivo on pulmonary arterial inflamm

72 pathology and neurons free of tau expressed NGF, indicating that degenerating cells can be infected

73 a mechanism whereby the neurotrophic factor NGF and the transcription factor Runx1 coordinate postmi

74 ompounds that mimic the nerve growth factor (NGF) activity for the protection against neurodegenerati

75 with gene expression of nerve growth factor (NGF) and calneuron 1 (CALN1) genes.

76 d by luminar release of nerve growth factor (NGF) and neurotrophin-3 (NT-3), respectively.

77 SorCS3 binds the nerve growth factor (NGF) and platelet-derived growth factor (PDGF-BB), but t

78 Nerve growth factor (NGF) antagonism is on the verge of becoming a powerful a

79 ophic factor (BDNF) and nerve growth factor (NGF) are crucial modulators in the neurodevelopment and

80 Levels of nerve growth factor (NGF) are elevated in inflamed tissues.

81 this paper, we identify nerve growth factor (NGF) as a binding partner for MOG and demonstrate that t

82 s show that blockade of nerve growth factor (NGF) attenuates both malignant and nonmalignant skeletal

83 TrkA activation by nerve growth factor (NGF) binding the second extracellular immunoglobulin (Tr

84 Nerve growth factor (NGF) contributes to the development of chronic pain asso

85 analysis of retrograde nerve growth factor (NGF) endosomes in axons to show that mechanical tugs-of-

86 tric epithelium induced nerve growth factor (NGF) expression, and in turn NGF overexpression within g

87 ted a clinical trial of nerve growth factor (NGF) gene therapy in AD, the first effort at gene delive

88 The neurotrophin nerve growth factor (NGF) has been implicated as a key mediator of chronic pa

89 , member 8 (TRPM8); and nerve growth factor (NGF) in nasal biopsy specimens.

90 Nerve growth factor (NGF) influences the survival and differentiation of a sp

91 Nerve growth factor (NGF) is elevated in certain chronic pain conditions and

92 aling by target-derived nerve growth factor (NGF) is necessary for soma-to-axon transcytosis of TrkA

93 Nerve growth factor (NGF) levels are highly increased in inflamed tissues, bu

94 containing antibody to nerve growth factor (NGF) or delayed reactivation in medium containing NGF an

95 Nerve growth factor (NGF) promotes growth, differentiation, and survival of s

96 on of the high-affinity nerve growth factor (NGF) receptor Trk occurs through multiple processes cons

97 ting endocytosis of the nerve growth factor (NGF) receptor, TrkA.

98 neuregulin 1 (NRG1) and nerve growth factor (NGF) recombinant proteins.

99 ndent PDAC development, nerve growth factor (NGF) secretion, and pancreatic nerve density.

100 ated with alteration in nerve growth factor (NGF) signaling and its relation to Abeta plaque and neur

101 e axonal trafficking of nerve growth factor (NGF) signals.

102 ies of PC12 cells under nerve growth factor (NGF) stimulation for up to 7 days using both conventiona

103 s to local secretion of nerve growth factor (NGF) upon carious injury.

104 Nerve growth factor (NGF), a classical trophic factor for nerve cells, is exp

105 in, neuromedin-B (NMB), nerve growth factor (NGF), and leukotriene-synthesis enzymes (ALOX5, ALOX5AP,

106 ction were regulated by nerve growth factor (NGF), and the effect of NGF was potentiated by Lhx8-indu

107 -associated protein 43, nerve growth factor (NGF), and tyrosine kinase receptor A (NTRK1) by immunohi

108 h factors, comprised of nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotro

109 al antibodies targeting nerve growth factor (NGF), for which we compare the predicted and measured so

110 eurotrophins, including nerve growth factor (NGF), increase neurite outgrowth in part by altering the

111 matory factors, such as nerve growth factor (NGF), interleukin-6 (IL-6), and carrageenan, produce dec

112 ds of gp130 but also to nerve growth factor (NGF), which does not bind to gp130-containing receptors.

113 F1Bbeta is required for nerve growth factor (NGF)-dependent neuronal differentiation through anterogr

114 ects the development of nerve growth factor (NGF)-dependent neurons including sympathetic cholinergic

115 in PC-12 cells inhibit nerve growth factor (NGF)-induced neurite outgrowth.

116 Nerve growth factor (NGF)-induced transport of large vesicles requires local

117 d signaling to suppress nerve growth factor (NGF)-mediated neurite growth, survival, excitability, an

118 itions and also enhance nerve growth factor (NGF)-mediated trkA promoter activation.

119 ons, the target-derived nerve growth factor (NGF)-tropomyosin-related kinase type 1 (TrkA, also calle

120 milar to treatment with nerve growth factor (NGF).

121 rowth-promoting factor, nerve growth factor (NGF).

122 owth and brain derived neurotrophic factors (NGF, BDNF).

123 On fibronectin, NGF caused inactivation of myosin IIA, which negatively

124 Following NGF stimulation, Neurotropin significantly facilitated t

125 n of caspase-3 and SREBP2 cleavage following NGF and pro-NGF stimulations.

126 f a Runx1/CBFbeta holocomplex is crucial for NGF-dependent nonpeptidergic nociceptor maturation.

127 A-dependent for cAMP and PKA-independent for NGF.

128 this association may offer new insights for NGF/TrkA-related Alzheimer's disease mechanisms.

129 es transactivation of TrkA, the receptor for NGF.

130 e found that myosin II (MII) is required for NGF to stimulate faster axon outgrowth.

131 ted Wnt signaling and stimulation of further NGF release.

132 Furthermore, NGF treatment augments glucose-induced insulin secretion

133 wo previously discovered painlessness genes, NGF and SCN9A, are currently in late-stage clinical tria

134 d-type neurons) suppresses but does not halt NGF-TrkA-dependent growth and branching.

135 The homodimer NGF (nerve growth factor) exerts its neuronal activity u

136 Little is known about how NGF elicits faster axon outgrowth or how growth cones in

137 gle x-ray scattering solution study of human NGF, we propose that it is the oligomerization state of

138 vels in Down syndrome mice markedly improves NGF-dependent receptor trafficking, neuronal survival an

139 not only in androgen signaling, but also in NGF signaling.

140 in the regulation of TrkA expression and in NGF-mediated functions through modulation of the trkA pr

141 using shRNA increases neuronal apoptosis in NGF-dependent sensory neurons deprived of NGF and compro

142 In conclusion, culture in NGF reduces the activity of L-type calcium channels, and

143 old monosynaptic glutamatergic excitation in NGF interneurons and a disynaptic, nicotinic excitation

144 In sensory neurons, increases in NGF augment neuronal sensitivity (sensitization) to noxi

145 tugs-of-war and multiple-motor mechanics in NGF-endosome transport.

146 system, the Na(+)/Ca(2+) exchanger (NCX), in NGF-induced differentiation remains unexplored.

147 urotrophin receptor plays a critical role in NGF-mediated functions, such as neuronal survival and se

148 nsmitter molecules released from vesicles in NGF-differentiated PC12 cells using carbon-fiber amperom

149 ased production of growth factors, including NGF and pro-NGF.

150 ce TrkA expression that results in increased NGF-mediated TrkA activation and signaling that augments

151 2 activation or IL-1beta treatment increased NGF protein secretion.

152 s, or IL-1beta (control) treatment increased NGF, brain-derived neurotrophic factor (BDNF), and IL-1b

153 ngiocytes that was associated with increased NGF expression.

154 While existing tools have greatly informed NGF-mediated signaling, ongoing and future pathway resea

155 In contrast, THINs do not innervate NGF or fast spiking interneurons, showing significant sp

156 rk demonstrating the Coronin-1 expression is NGF dependent, this work suggests that periods before an

157 We used quantum dots to fluorescently label NGF and acquired trajectories of retrograde quantum-dot-

158 , IL-13, IL-17F, leptin, G-CSF, GM-CSF, LIF, NGF, SCF, and TGF-alpha.

159 that block TrkA interaction with its ligand, NGF, are in clinical trials for pain relief.

160 TR, TrkA, TrkB, and TrkC) and their ligands (NGF, brain-derived neurotrophic factor, and neurotrophin

161 rvival and target innervation under limiting NGF (NGF(+/-)) conditions.

162 sociated viral vectors (serotype 2)-mediated NGF gene transfer.

163 l component of a feedback loop that mediates NGF-TrkA endosome stability, recycling and signaling as

164 lline, blockers of Maxi-K channels, mimicked NGF treatment and sensitized neurons to bradykinin appli

165 In TLR-activated monocytes, NGF reduces inflammatory cytokine production (IL-1beta,

166 ic neurons, compared with controls, and more NGF-dependent neuronal sprouting in SH-SY5Y cells.

167 cells, above the levels observed with mouse NGF.

168 of generating specificity in multifunctional NGF signaling.

169 hreshold spike (PLTS) and NPY-neurogliaform (NGF) cells.

170 experiments on dorsal root ganglion neurons, NGF- and IL-6-induced increases in excitability were att

171 two forms have opposing effects on neurons: NGF induces proliferation, whereas proNGF induces apopto

172 ot TrkA, and they also express neurotrophins NGF, BDNF, and neurotrophin 3 (NT3).

173 -like growth factor-1, or the neurotrophins (NGF and BDNF).

174 l and target innervation under limiting NGF (NGF(+/-)) conditions.

175 12.5 muM alone, or in combination with 50 nM NGF, showed a marked stimulation of neuritogenesis, but

176 Notably, NGF-induced thermal hyperalgesia was unaffected by macro

177 stal structures of the TrkA/NGF and p75(NTR)/NGF complexes.

178 cing isoform, NCX1.4, even in the absence of NGF, induced an increase in Akt phosphorylation and GAP-

179 beta-strand-swapped dimer in the absence of NGF, occluding the binding surface.

180 ding of the opposing mechanisms of action of NGF and proNGF on neurons.

181 ng factor for the growth promoting action of NGF in adult sensory neurons.

182 Expression and/or activation of NGF and its receptors were evaluated in rat experimental

183 neuronal responses to NGF, and activation of NGF-related cell signaling.

184 In ex vivo experiments, the addition of NGF to LPS-activated juvenile idiopathic arthritis to bo

185 Binding of NGF to MOG may offer widespread implications into mechan

186 Ablation of Dclk1(+) cells or blockade of NGF/Trk signaling inhibited epithelial proliferation and

187 owth observed at suboptimal concentration of NGF (2ng/mL) in a manner depending on Trk kinase activit

188 significantly facilitated the time course of NGF-induced Trk autophosphorylation.

189 workflow increased the sequence coverage of NGF from 46% with chemical reduction to 99%, when electr

190 Tissue-specific deletion of NGF or TrkA, or acute disruption of TrkA signaling, impa

191 ers (56.1% increase) and staining density of NGF (89.3% increase) (P < .05 for all).

192 in NGF-dependent sensory neurons deprived of NGF and compromises PC12 cell differentiation in respons

193 the TGN-induced deltaR export downstream of NGF.

194 This confirms the differential effect of NGF signaling for sympathetic neural and chromaffin cell

195 nerve growth factor (NGF), and the effect of NGF was potentiated by Lhx8-induced TrkA expression.

196 ionale for the diverse biological effects of NGF and proNGF at the molecular level.

197 In fact, the differentiating effects of NGF do not require activation of any of the cAMP sensors

198 Effects of NGF inhibition were evaluated in vivo with anti-NGF bloc

199 hanisms underlying the persistent effects of NGF remain incompletely understood.

200 tive mechanisms in the persistent effects of NGF.

201 a unique mechanism controlling efficiency of NGF signaling, and raise the therapeutic potential of Ne

202 us (Neurotropin((R))) enhanced efficiency of NGF signaling.

203 sity and sprouting, as well as expression of NGF and NTRK1, are significantly increased in mucosal ti

204 Our results show increased expression of NGF and/or increased expression/activation of its recept

205 ession of let-7a and increased expression of NGF compared to the control.

206 eta1R), let-7a, and downstream expression of NGF.

207 kA) is linked to pain and elevated levels of NGF (the ligand for TrkA) are associated with chronic pa

208 Levels of NGF protein were also increased in tissues from patients

209 icantly decreased peripheral blood levels of NGF when compared with the HC subjects (Hedges's g=-0.63

210 These results provide a novel mechanism of NGF regulation in the intervertebral disc and potentiall

211 dent signaling that involves mobilization of NGF and NGF-dependent sensitization of TRPV1.

212 We developed a rat model of NGF-induced persistent thermal hyperalgesia and mechanic

213 s critically implicated in the modulation of NGF secretion by LTA-stimulated pulp fibroblasts.

214 gen/deuterium exchange in the mature part of NGF and proNGF, we found that the presence of the pro-pa

215 ere, we evaluate the differential potency of NGF, glial cell line-derived neurotrophic factor (GDNF),

216 hown to induce the profound up-regulation of NGF in osteoblasts within 1 h of loading.

217 However, the regulation of NGF in SCZ remains unclear because of the inconsistent f

218 ngly little is known about the regulation of NGF in these conditions.

219 This study highlights the critical role of NGF in PH.

220 in treatment, such a therapeutic strategy of NGF inhibition may be of interest in PH.

221 However, whereas the structure of NGF has been determined by X-ray crystallography, the st

222 orts in this pathway beyond the targeting of NGF or its receptors.

223 al, that led to our current understanding of NGF biology.

224 a injection revealed a rapid upregulation of NGF, a mediator known to sensitize TRPV1.

225 e demonstrate that this signaling depends on NGF and is mediated by the heat-sensitive nociceptive ch

226 filamin A (FlnA) contributes to androgen or NGF neuritogenesis, likely through its interaction with

227 In addition, androgen or NGF triggers AR association with TrkA, TrkA interaction

228 nonaromatizable synthetic androgen R1881 or NGF.

229 In 2 patients, NGF protein levels were measured by enzyme-linked immuno

230 Precuneus NGF upstream and downstream signaling levels relative to

231 ed with GAP-43, and NCX1 silencing prevented NGF-induced effects on GAP-43 expression, Akt phosphoryl

232 -3 and SREBP2 cleavage following NGF and pro-NGF stimulations.

233 ion of growth factors, including NGF and pro-NGF.

234 observed here that NGF and its pro-form, pro-NGF, are elevated in fatty livers from leptin-deficient

235 of mouse primary hepatocytes with NGF or pro-NGF increased LDLR expression through the p75 neurotroph

236 xceptional tightly disulfide-bonded protein (NGF) as well as the largest protein attempted to date (I

237 2 blockade together with gemcitabine reduced NGF expression and nerve density, and increased survival

238 we investigated if TLR activation regulates NGF and which signaling mechanisms control this response

239 CD2AP also regulates NGF signaling through AKT, but not ERK, and regulates lo

240 f the extent and time course of pain relief, NGF blockade also reduced pain 40% to 70%, depending on

241 arginal evidence of replication: rs78701042 (NGF) with diastolic BP (P = 0.008 in the 1982 Pelotas Bi

242 On both substrates, the result was the same: NGF-induced weakening of MII-dependent restraint led to

243 phic factor, and neurotrophin 3) and secrete NGF.

244 is the oligomerization state of the secreted NGF that may drive the formation of the ternary heteroco

245 this interaction is capable of sequestering NGF from TrkA-expressing neurons to modulate axon growth

246 king, Coronin-1 is also required for several NGF-TrkA-dependent signaling events, including calcium r

247 rates TrkA degradation, attenuates sustained NGF-induced Akt activation, and reduces cell survival.

248 We describe ligands targeting NGF, its receptors, and downstream/related targets.

249 on-cytoskeletal coupling, we determined that NGF causes decreased vinculin-dependent actomyosin restr

250 In the absence of Coronin-1 we find that NGF-TrkA-PI3K signaling drives robust axon growth and br

251 We observed here that NGF and its pro-form, pro-NGF, are elevated in fatty liv

252 Here, we hypothesized that NGF also sensitizes sympathetic neurons to proinflammato

253 Collectively, these data indicate that NGF evokes a persistent nociceptive state mediated by in

254 Ex vivo/in vitro, we found out that NGF promotes pulmonary vascular cell proliferation and m

255 We show that NGF is part of a regulatory loop in monocytes: inflammat

256 Here, we show that NGF-TrkA signaling in skeletal sensory nerves is an earl

257 Finally, we showed that NGF treatment increased concentrations of linoleic and a

258 Our results suggest that NGF blockade immediately upon detection of tumor metasta

259 The NGF effect, which requires trkA receptors, takes hours t

260 The NGF secretion by LTA-stimulated pulp fibroblasts, which

261 The NGF-cultured neurons exhibited significant depolarizatio

262 In the absence of Coronin-1, the NGF-TrkA signaling endosome fuses to lysosomes sixfold t

263 to mutations in the NTRK1 gene encoding the NGF receptor TrkA.

264 through a disulfide bond, essential for the NGF signaling.

265 ane dimer in a conformation required for the NGF signaling.

266 head molecular assembly configuration of the NGF dimer of dimers has been validated.

267 tiation through anterograde transport of the NGF receptor TRKA.

268 rough TLRs, upregulate the expression of the NGF receptor TrkA.

269 Here we examine the role of the NGF-TrkA effector protein, Coronin-1, on postganglionic

270 inergic neuronal hypertrophy occurred on the NGF-treated side (P < .05).

271 d small molecule approaches to targeting the NGF-TrkA pathway both extra- and intracellularly.

272 ecifically, the simulations suggest that the NGF-endosomes are driven on average by 5-6 active dynein

273 F in the form of axonal sprouting toward the NGF source.

274 forms a novel multiprotein complex with the NGF receptor TrkA and the PI3K regulatory subunit p85, w

275 Therefore, NGF-evoked thermal and mechanical allodynia are mediated

276 tween osteoblasts and sensory nerves through NGF-TrkA signaling is essential for load-induced bone fo

277 mechanism of inflammatory responses through NGF and its receptor TrkA, for which abnormality may hav

278 nduced by receptor-mediated (i.e., TNFalpha, NGF, or IL-6 receptor) or direct activation of protein k

279 of the latently infected neurons with Ab to NGF resulted in production of infectious virus in about

280 for reactivation after treatment with Ab to NGF.

281 No adverse pathological effects related to NGF were observed.

282 erating neurons in the AD brain responded to NGF.

283 All patients exhibited a trophic response to NGF in the form of axonal sprouting toward the NGF sourc

284 he TrkA neurotrophin receptor in response to NGF is critical in the regulation of TrkA activation and

285 equired for their translation in response to NGF stimulation but not for their axonal recruitment and

286 ses PC12 cell differentiation in response to NGF.

287 lling their local translation in response to NGF.

288 xpression, cholinergic neuronal responses to NGF, and activation of NGF-related cell signaling.

289 hresholds caused by increased sensitivity to NGF.

290 ransient ternary heterocomplex, i.e., a TrkA/NGF/p75(NTR) ligand/receptors molecular assembly with a

291 Namely, a ternary TrkA/NGF/p75(NTR) complex is assumed to be crucial for the fo

292 found in the crystal structures of the TrkA/NGF and p75(NTR)/NGF complexes.

293 growth factor (NGF) expression, and in turn NGF overexpression within gastric epithelium expanded en

294 Ten patients with early AD underwent NGF gene therapy using ex vivo or in vivo gene transfer.

295 heir axonal recruitment and translation upon NGF withdrawal.

296 he wild-type fold of TrkAIg2 in complex with NGF ( 1WWW .pdb), and the (1)H-(15)N correlation spectra

297 timulation of mouse primary hepatocytes with NGF or pro-NGF increased LDLR expression through the p75

298 armacological TrkA inhibitor interferes with NGF- or androgen-induced neuritogenesis.

299 pplication, whereas neurons cultured without NGF showed only slight changes in membrane potential and

300 s more effective at 12.5 muM with or without NGF.