ライフサイエンスコーパス: NGF

1 NGF also has central actions in the brain, where it regu

2 NGF and serotonin are positively correlated in the sera

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

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

5 NGF treatment displaced PI3K C2A from the Golgi and opto

6 NGF triggers prenylation of proteins including the Rac1

7 NGF was not expressed by MM cells, yet bone stromal cell

8 NGF(R100W) interferes with peripheral and central NGF bi

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

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

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

12 de of NGF (Nsp) previously shown to activate NGF signaling in rat PC12 cells was used as an NGF signa

13 In AD, NGF metabolism is altered, but it is not known whether t

14 osin receptor kinase A (TrkA) (high-affinity NGF receptor) pathway plays a role in the calcification

15 ice carrying the human R100W-mutated allele (NGF(R100W/wt)).

16 F signaling in rat PC12 cells was used as an NGF signaling agonist, and recombinant NGF and the pan-T

17 to bind to internalized TrkA receptors in an NGF-dependent manner, where it was essential for maintai

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

19 permissive factors including FGF2, BDNF, and NGF.

20 ng downstream of the EGF receptor (EGFR) and NGF receptor (TrkA).

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

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

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

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

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

26 the conformational properties of proNGF and NGF.

27 sophageal cancer cells was inhibited by anti-NGF blocking antibodies.

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

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

30 While anti-NGF antibodies have demonstrated analgesia both preclini

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

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

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

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

35 Collectively, we demonstrate beta-NGF's ability to promote endochondral repair in a murine

36 Gene expression data from beta-NGF stimulated cartilage callus explants show a promotio

37 injection regimens and found that local beta-NGF injections during the endochondral/cartilaginous pha

38 vements to bone healing following local beta-NGF injections which resulted in a decrease in cartilage

39 onfirmed Wnt activation following local beta-NGF injections.

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

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

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

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

44 The median limit of detection achieved by NGF was 2.9 x 10(-6).

45 roles in its dimerization and activation by NGF.

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

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

48 Activation of TrkA by NGF enhances the expansion of human MK progenitors (MKPs

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

50 100W) interferes with peripheral and central NGF bioavailability, but this does not impact on CNS fun

51 (NGF)- TrkA signaling in axons communicates NGF-mediated trophic responses in signaling endosomes.

52 In comparison, NGF was used to evaluate its neurotrophic and neuritogen

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

54 actor (proNGF) to NGF and those that degrade NGF.

55 x metalloproteinase 9 (MMP9), which degrades NGF, was overactive in MCI and AD.

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

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

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

59 mes transcriptionally upregulated to enhance NGF signaling.

60 Moreover, miR-204/-211 ablation enhances NGF expression in a Runx2-dependent manner, and thus hyp

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

62 mRNA that regulates axon growth by enhancing NGF-TrkA signaling in a translation-independent manner.

63 activation in vitro independent of exogenous NGF administration.

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

65 rototypic target-derived neurotrophic factor NGF leads to aberrant subtype-restricted patterns of tra

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

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

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

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

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

71 In this study, we test nerve growth factor (NGF) as an understudied therapeutic for fracture repair.

72 ), bradykinin (BK), and nerve growth factor (NGF) as well as multiple kinases, including protein kina

73 lation and secretion of nerve growth factor (NGF) by PDAC cells to promote tumor innervation.

74 ignificant induction of nerve growth factor (NGF) by the tumour-bearing bone microenvironment, alongs

75 T The R100W mutation in nerve growth factor (NGF) causes Hereditary Sensory and Autonomic Neuropathy

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

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

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

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

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

81 Nerve growth factor (NGF) is a key mediator of nociception, acting during the

82 Nerve growth factor (NGF) is a key regulator of chronic osteoarthritic pain,

83 Nerve growth factor (NGF) is a neurotrophin that activates nociceptive neuron

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

85 ctivation by its ligand nerve growth factor (NGF) is still unsolved.

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

87 proliferation, whereas nerve growth factor (NGF) promotes sustained ERK activation and cell differen

88 ript interacts with the nerve growth factor (NGF) receptor TrkA, regulating TrkA endocytosis and sign

89 ably, we identified the nerve growth factor (NGF) receptor tyrosine kinase (NTRK1), a molecule not pr

90 Nerve growth factor (NGF) regulates many aspects of neuronal biology by retro

91 mediates high levels of nerve growth factor (NGF) secretion from astrocytes, causing neurite outgrowt

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

93 ssential for retrograde nerve growth factor (NGF) signaling and neuron target tissue innervation and

94 he primary receptor for Nerve Growth Factor (NGF) signaling.

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

96 h membrane regions upon nerve growth factor (NGF) stimulation: We argue that this is the origin of th

97 intravenously injected nerve growth factor (NGF) to enter the CNS in healthy mice and nonhuman prima

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

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

100 imulating expression of nerve growth factor (NGF), a neurotrophin associated with airway remodeling a

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

102 he neurotrophin family: nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotro

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

104 d neurotrophic factors; nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotro

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

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

107 During this process, nerve growth factor (NGF)- TrkA signaling in axons communicates NGF-mediated

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

109 fission is required for nerve growth factor (NGF)-induced collateral branching in vitro and expressio

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

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

112 versed by inhibition of nerve growth factor (NGF)-mediated tropomyosin receptor kinase A (TrkA) signa

113 ention is mediated by a nerve growth factor (NGF)-regulated checkpoint that delays the export of DOR

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

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

116 se to the neurotrophin, nerve growth factor (NGF).

117 following receptors for nerve growth factor (NGF): neurotrophic receptor tyrosine kinase 1 and nerve

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

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

120 larly when assessed by next-generation flow (NGF) cytometry.

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

122 s, here, we seek to test this hypothesis for NGF and NT-3.

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

124 hat the cysteine residue is not required for NGF binding, but is essential for inhibition of the NGF/

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

126 -arginine (RXR) motifs that are required for NGF- and phosphoinositide-regulated DOR export from intr

127 Fission is also required for NGF-induced mitochondria-dependent intra-axonal translat

128 -terminal tail of DOR that is sufficient for NGF-mediated regulation.

129 ted Wnt signaling and stimulation of further NGF release.

130 Furthermore, NGF treatment augments glucose-induced insulin secretion

131 ditional number of 14 modular genes (GABRG1, NGF, APOBEC2, STAT5B, STAT3, SMAD4, MED1, CACNB1, SLAIN2

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

133 We demonstrate that heterozygous NGF(R100W/wt) mice display impaired nociception.

134 ng and memory, in contrast with heterozygous NGF knock-out mice.

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

136 Surprisingly, however, NGF(R100W/wt) mice, unlike heterozygous mNGF(+/-) mice,

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

138 ic formalin injection induced an increase in NGF expression in the bladder urothelium, which depended

139 monstrate that nicotine-induced increases in NGF and other markers of airway remodeling are negativel

140 also abrogated nicotine-induced increases in NGF, FN1, and ET-1 in LFs.

141 was sufficient to recapitulate increases in NGF, FN1, and ET-1, whereas treatment with a miR-98 mimi

142 8 and reversed nicotine-induced increases in NGF, FN1, and ET-1.

143 rve fibers within the reactive periosteum in NGF-enriched cellular domains were evident at time point

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

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

146 with unexposed controls, nicotine increased NGF, FN1, ET-1, COL1A1, and COL3A1 expression in human a

147 2 activation or IL-1beta treatment increased NGF protein secretion.

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

149 ngiocytes that was associated with increased NGF expression.

150 lored the hypothesis that nicotine increases NGF by reducing lung fibroblast (LF) microRNA-98 (miR-98

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

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

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

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

155 rons and signals in response to two ligands, NGF and neurotrophin-3 (NT-3), with very different funct

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

157 uce higher basal levels of proNGF and mature NGF compared to SCs.

158 ing in the R100W missense mutation in mature NGF.

159 in preclinical and clinical AD while mature NGF degradation is enhanced.

160 higher in AD, MCI, and HA-NCI, while mature NGF was lower.

161 Mechanistically, NGF transactivates Wnt/beta-catenin signalling.

162 factor, and we show that TNF-alpha-mediated NGF induction is suppressed by adiponectin-directed ther

163 s, in particular the M2 subtype, to modulate NGF production and maturation from the precursor (proNGF

164 particular M2 subtype stimulation, modulates NGF production and maturation in both SCs and dASCs.

165 cells, above the levels observed with mouse NGF.

166 of generating specificity in multifunctional NGF signaling.

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

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

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

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

171 12.5 muM alone, or in combination with 50 nM NGF, showed a marked stimulation of neuritogenesis, but

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

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

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

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

176 affect the central and peripheral actions of NGF.

177 er-dimer equilibrium and that the binding of NGF induces an increase of the dimeric and oligomeric fo

178 This Review recaps the biology of NGF and the studies that have been performed to evaluate

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

180 tactin, a previously determined component of NGF-induced branching.

181 The functional consequences of NGF-TrkA signaling were examined in human healthy articu

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

183 der pathological conditions, the delivery of NGF enables neural regeneration, tissue remodeling, and

184 However, the higher tested doses of NGF inhibitors also increased the risk of rapidly progre

185 the TGN-induced deltaR export downstream of NGF.

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

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

188 clinical studies to evaluate the efficacy of NGF inhibition as a form of analgesia in chronic pain st

189 e been performed to evaluate the efficacy of NGF inhibition for chronic musculoskeletal pain states.

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

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

192 Antibodies that inhibit the function of NGF and small molecule inhibitors of NGF receptors have

193 The physiological function of NGF as a pain mediator is altered in patients with Hered

194 neurotrophic and pronociceptive functions of NGF to be split, with interesting implications for the t

195 The results exclude haploinsufficiency of NGF as a mechanistic cause for heterozygous HSAN V mice

196 calcification of hACs and the importance of NGF signaling in articular cartilage homeostasis.

197 tion of NGF and small molecule inhibitors of NGF receptors have been developed and tested in clinical

198 e findings suggest functional involvement of NGF signaling in calcification of hACs and the importanc

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

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

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

202 DPSC-CM contained significant levels of NGF, BDNF, NT-3 and GDNF.

203 Levels of NGF, miR-98, PPARgamma, fibronectin 1 (FN1), endothelin-

204 a reduction in secretion and brain levels of NGF.

205 tributes to the modulation and maturation of NGF, improving the regenerative properties of dASCs.

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

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

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

209 DRG neurons of NGF(R100W/wt) mice are morphologically normal, with no a

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

211 A 14-aa small peptide of NGF (Nsp) previously shown to activate NGF signaling in

212 Perturbation of NGF signaling with NGF, Nsp, and GNF-5837 resulted in a

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

214 ion was suggested between high production of NGF by cancer cells and the presence of nerves (P = 0.02

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

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

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

218 a unique role for Elp1 in the regulation of NGF-dependent TrkA activity.

219 Role of NGF-TrkA signaling in calcification of articular chondro

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

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

222 steoarthritic pain, but the exact targets of NGF action on human articular cartilage is unknown.

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

224 acture demonstrated a marked upregulation of NGF expression in periosteal stromal progenitors and fra

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

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

227 timulating TGNC survival than co-cultures or NGF treated culture.

228 nonaromatizable synthetic androgen R1881 or NGF.

229 -3 and SREBP2 cleavage following NGF and pro-NGF stimulations.

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

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

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

233 ility of rat dASCs and native SCs to produce NGF in vitro.

234 as an NGF signaling agonist, and recombinant NGF and the pan-Trk inhibitor GNF-5837 were employed as

235 2 blockade together with gemcitabine reduced NGF expression and nerve density, and increased survival

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

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

238 s that may be driven by cancer cell-released NGF.

239 Basal forebrain cholinergic neurons require NGF for maintenance of cholinergic phenotype, are critic

240 tase activity in the absence of Elp1 rescued NGF-dependent retrograde signaling, and in an animal mod

241 nnervated by nerve growth factor-responsive (NGF-responsive) tropomyosin receptor kinase A-expressing

242 esults suggest that regulation of retrograde NGF signaling in sympathetic neurons by Elp1 may explain

243 t (recombinant human nerve growth factor, rh-NGF) predominantly targeting secondary degeneration in a

244 Topical application of rh-NGF twice daily for 3 weeks significantly improves RGC s

245 Topical rh-NGF also promotes greater axonal survival and inhibits a

246 ively, these results suggest that topical rh-NGF exhibits neuroprotective effects on retinal neurons

247 As topical rh-NGF is already involved in early clinical trials, this h

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

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

250 lp1 as a protein that is required to sustain NGF signaling by blocking the activity of its phosphatas

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

252 t humanized monoclonal antibody that targets NGF.

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

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

255 ee and hip osteoarthritis have revealed that NGF inhibitors substantially reduce joint pain and impro

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

257 The NGF metabolic pathway entails the proteins that mature p

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

259 The NGF(R100W) protein has reduced capability to activate pa

260 The NGF-mimetic bioactivity of Nsp was first confirmed on th

261 ompelling evidence of crosstalks between the NGF-NTRK1 and Hippo cancer pathways.

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

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

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

265 linked to the putative seed sequence in the NGF 3'UTR and also abrogated nicotine-induced increases

266 whether peptides might similarly inhibit the NGF/TrkA interaction and so serve as future therapeutic

267 Starting from two peptides that inhibit the NGF/TrkA interaction, we sought to eliminate a cysteine

268 Moreover, the NGF antibody tanezumab has provided clinical proof of co

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

270 tiation through anterograde transport of the NGF receptor TRKA.

271 r show differences in the stabilities of the NGF- and NT-3-bound Trk-A dimers in the plasma membrane

272 ding, but is essential for inhibition of the NGF/TrkA interaction at pharmacologically relevant pepti

273 Inhibition of the NGF/TrkA interaction presents an interesting alternative

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

275 study aimed to test the hypothesis that the NGF-tropomyosin receptor kinase A (TrkA) (high-affinity

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

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

278 Thus, NGF and NT-3 are "biased" ligands for Trk-A.

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

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

281 for reactivation after treatment with Ab to NGF.

282 t mature pro-nerve growth factor (proNGF) to NGF and those that degrade NGF.

283 No adverse pathological effects related to NGF were observed.

284 erating neurons in the AD brain responded to NGF.

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

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

287 y neuronal innervation using LOXO-101, a Trk-NGF inhibitor, further decreased PDAC tumor growth.

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

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

290 that a rotation of the TMD dimers underlies NGF-induced TRKA activation.

291 heir axonal recruitment and translation upon NGF withdrawal.

292 uch as osteoblasts expressed and upregulated NGF when cultured with MM cells, or MM-related factors s

293 induces bladder overactivity and urothelial NGF overexpression in the bladder, both dependent on act

294 In vitro, NGF production in esophageal cancer cells was shown by W

295 th plasminogen, neuroserpin, and VAChT while NGF correlated with MMP9 activity.

296 The adverse events associated with NGF inhibition and the current state of knowledge about

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

298 Perturbation of NGF signaling with NGF, Nsp, and GNF-5837 resulted in a strong induction of

299 nase A (TrkA) signalling, and treatment with NGF recapitulates the intestinal phenotype of NMS mice i

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