ライフサイエンスコーパス: GDNF

1 GDNF also enhanced mitochondrial fatty acid beta-oxidati

2 GDNF appeared to be well tolerated and safe, and no drug

3 GDNF application to cultured explants of human aganglion

4 GDNF attenuates inflammation-induced impairment of IEB f

5 GDNF binds to GDNF family receptor alpha1 (GFRa1), and t

6 GDNF blocked all inflammation-induced changes in the IEB

7 GDNF content in myotubes and GDNF in conditioned culture

8 GDNF expression and EGC apoptosis were determined by imm

9 GDNF is synthesized and secreted by neuronal target tiss

10 GDNF might be developed for treatment of HSCR.

11 GDNF not only prevented the reductions in the liver leve

12 GDNF prolonged survival, induced enteric neurogenesis, a

13 GDNF seems to be normally synthesized in neurons, but nu

14 GDNF significantly prolonged mean survival times of Hol(

15 GDNF, acting through the receptor tyrosine kinase Ret, r

16 GDNF-transfected macrophages administered through intrat

17 creased levels of neurotrophic factors NT-3, GDNF and BDNF.

18 survival in patients with cancer(5-8), and a GDNF family receptor alpha like (GFRAL)-Ret proto-oncoge

19 We also identify Ar as a GDNF-repressed gene and Gdnf and Gfralpha1 as androgen-r

20 We now show that a GDNF-dependent ligand-receptor-based Turing mechanism qu

21 vation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma.

22 ed significant levels of NGF, BDNF, NT-3 and GDNF.

23 ciprocal regulatory crosstalk between AR and GDNF signaling in prostate development.

24 growth and branching in response to BDNF and GDNF compared with control neurons, indicating that PTPR

25 cific inhibitor (666-15) diminished BDNF and GDNF production induced by n-3 PUFA, suggesting CREB dep

26 BDNF and GDNF production were increased in the astrocytes derived

27 f mRNA for the neurotrophic factors BDNF and GDNF, but not their receptors.

28 of intestinal microbiota had ENS defects and GDNF deficiency, similar to Tlr2(-/-) mice; these defect

29 ression of several neurotrophic factors, and GDNF and Artemin, both of which encode ligands for the R

30 S-BBB opening, while both the luciferase and GDNF protein expression were successfully measured via W

31 GDNF content in myotubes and GDNF in conditioned culture medium were quantified by en

32 nt fetal testes, including Nodal, Notch, and GDNF.

33 ively controls the activity of BDNF/TrkB and GDNF/Ret signaling.

34 specific positive feedback between WNT11 and GDNF permits the dense packing of ureteric tips.

35 ated that in normal or injured adult animals GDNF is expressed by striatal neurons and is not synthes

36 d upon addition of GDNF or neutralizing anti-GDNF antibody.

37 nd patch-clamp experiments with bath-applied GDNF (100 nM) confirm the presynaptic inhibition of SDH

38 naling might be a means to augment astrocyte GDNF secretion in the context of innate immune activatio

39 innate immune activation increases astrocyte GDNF production and that this is regulated by specific e

40 ulation of innate immunity-induced astrocyte GDNF expression and suggest that selective inhibition of

41 okines due to inflammatory process attracted GDNF-expressing macrophages and ensured targeted drug de

42 e treated intravenously with (a) saline, (b) GDNF alone, (c) the cTfRMAb-GDNF fusion protein alone, o

43 Our study suggests that balanced GDNF signaling plays a role in normal development and ma

44 ed by PTN (12.7:1) when compared to a BDNF + GDNF choice.

45 NTF expression-neurotrophin-3 (NT-3), BDNF, GDNF, neurturin, artemin, and CNTF-in the OC and cochlea

46 exercise increased levels of mRNA for BDNF, GDNF and NT-4.

47 nes encoding key components in the TGF-beta, GDNF, AKT, and JAK-STAT signaling pathways.

48 r addressing the potential interplay between GDNF neurotrophic signaling and transcriptional regulati

49 lated with decreased levels of retinal bFGF, GDNF, and BDNF.

50 ine-derived neurotrophic factor (GDNF) binds GDNF family receptor alpha1 (GFRalpha1) and signals thro

51 GFRalpha1-TM still binds GDNF and promotes Ret activation but does not translocat

52 , a small-molecule inhibitor of RET, blocked GDNF-mediated activation of ERK and AKT.

53 onal guidance related gene expression (Bmp2, GDNF, and Shh) in Acomys compared to Mus (p < .05).

54 ompartments with bovine serum albumin (BSA), GDNF and NGF increased the motor and sensory axon conten

55 Upon activation by GDNF, Ret is rapidly polyubiquitinated and degraded.

56 Interestingly, the tumors induced by GDNF stimulation contain enteric neuronal progenitors ca

57 ected migration of caErbB2-expressing SCs by GDNF might be useful to enable axon regrowth in a non-pe

58 f spermatogenesis in mammals is supported by GDNF, an essential growth factor required for spermatogo

59 cholinergic neurons and engage the canonical GDNF receptor Ret inhibit Shh expression in dopaminergic

60 Combining GDNF treatment with digestion of inhibitory CSPGs did no

61 both present, a scenario that may constrain GDNF breadth of action.

62 Mice were given rectal enemas containing GDNF or saline (control) from postnatal days 4 through 8

63 -human primates received a pellet containing GDNF, releasing 2 ug/day for 90 days, on one medial rect

64 on that requires the nonsignaling coreceptor GDNF family receptor (GFRalpha3).

65 n protein alone, or (d) the combined cTfRMAb-GDNF and cTfRMAb-TNFR fusion proteins, following a 1-h r

66 these fusion proteins are designated cTfRMAb-GDNF and cTfRMAb-TNFR, respectively.

67 Combined treatment with the cTfRMAb-GDNF and cTfRMAb-TNFR fusion proteins caused a significa

68 The cTfRMAb-GDNF fusion protein alone caused a significant 25% and 3

69 (a) saline, (b) GDNF alone, (c) the cTfRMAb-GDNF fusion protein alone, or (d) the combined cTfRMAb-G

70 o-dimensional and three-dimensional culture, GDNF-mediated RET signaling is enhanced in a model of ar

71 In primary rat EGC cultures, GDNF receptors were assessed by western blot and indirec

72 e expressing single mutations in the Cx3cr1, GDNF and CCR2 genes.

73 ncapsulated GDNF-secreting cells can deliver GDNF in a sustained, targeted, and efficacious manner, p

74 ce of gamma-MNs on a muscle spindle-derived, GDNF-independent signal during the first postnatal week.

75 rbors a mix of glomeruli that either display GDNF/somatostatin (GIb)-IR or GFRalpha1/IB4 labeling (GI

76 Embryonic GDNF deletion in the CNS did not affect striatal dopamin

77 oncept that the implantation of encapsulated GDNF-secreting cells can deliver GDNF in a sustained, ta

78 Functionally, endogenous GDNF released from peptidergic CGRP/somatostatin+ nocice

79 /Tg) mice, inducing production of endogenous GDNF, and new enteric neurons and glia appeared to arise

80 dnf knock-out mice, we found that endogenous GDNF affects striatal dopamine homeostasis and regulates

81 ively, these results suggest that endogenous GDNF plays an important role in regulating the function

82 or long-term electrical stimulation enhances GDNF production by skeletal muscle.

83 Together, our results establish GDNF-RET signaling as a rational therapeutic target to c

84 eive a strong DA innervation, do not express GDNF.

85 tidergic CGRP/somatostatin+ cells expressing GDNF and the nonpeptidergic IB4+ neurons expressing the

86 reases in glial-derived neurotrophic factor (GDNF) and ephrin receptor B2 (EPHB2) mRNA.

87 Glial cell line-derived neurotrophic factor (GDNF) and its receptor GFRalpha1 are prominently express

88 glial cell line-derived neurotrophic factor (GDNF) and its receptor tyrosine kinase, Ret, in the regu

89 glial cell line-derived neurotrophic factor (GDNF) as a potential stimulus for salivary stem cell gro

90 Glial cell line-derived neurotrophic factor (GDNF) binds GDNF family receptor alpha1 (GFRalpha1) and

91 Glial cell line-derived neurotrophic factor (GDNF) binds the GFRalpha1 receptor, and the GDNF-GFRalph

92 glial cell line-derived neurotrophic factor (GDNF) directly to the hippocampus of epileptic rats.

93 glial cell line-derived neurotrophic factor (GDNF) expression in intestinal smooth muscle cells.

94 e for the glial derived neurotrophic factor (GDNF) family ligands (GFLs), during development and in t

95 glial cell line-derived neurotrophic factor (GDNF) family of neuronal growth factors.

96 Glial cell line-derived neurotrophic factor (GDNF) family of neurotrophic factors.

97 glial cell line-derived neurotrophic factor (GDNF) family receptor GFRalpha3 is expressed in a subpop

98 glial cell line-derived neurotrophic factor (GDNF) family that has been strongly implicated in develo

99 glial cell line-derived neurotrophic factor (GDNF) family that includes GDNF, artemin (ARTN) and neur

100 glial cell line-derived neurotrophic factor (GDNF) has been studied extensively in various disorders

101 glial cell line-derived neurotrophic factor (GDNF) in injured muscle and increased expression of GDNF

102 glial cell line-derived neurotrophic factor (GDNF) in nociceptive pathways is still controversial, as

103 glial cell line-derived neurotrophic factor (GDNF) in Parkinson's disease, using intermittent intrapu

104 glial cell line-derived neurotrophic factor (GDNF) in skin keratinocytes or topical application of XI

105 glial cell line-derived neurotrophic factor (GDNF) in the development and subsequent diversification

106 e role of Glial-derived neurotrophic factor (GDNF) in the regulation of EGC apoptosis.

107 n of glial cell derived neurotrophic factor (GDNF) induces enteric nervous system regeneration in mou

108 Glial cell line-derived neurotrophic factor (GDNF) is a growth factor that regulates the health and f

109 Glial cell line-derived neurotrophic factor (GDNF) is a neurotrophic factor required for survival of

110 Glial cell line-derived neurotrophic factor (GDNF) is a protein that is required for the development

111 Glial cell line-derived neurotrophic factor (GDNF) is absolutely required for survival of dopaminergi

112 Glial cell line-derived neurotrophic factor (GDNF) is essential for this process.

113 ound that glial derived neurotrophic factor (GDNF) is reduced in SMA astrocytes.

114 T ligand, glial-derived neurotrophic factor (GDNF) is upregulated by inflammatory cytokines.

115 level of glial-derived neurotrophic factor (GDNF) markedly decreased in the nigra of male mice.

116 glial cell line-derived neurotrophic factor (GDNF) may be key mediators of the therapeutic response t

117 ther glial cell-derived neurotrophic factor (GDNF) nor serotonin are additive with CDNF.

118 techol or glial-derived neurotrophic factor (GDNF) promotes hematopoietic recovery.

119 glial cell line-derived neurotrophic factor (GDNF) promotes IEB function, the mechanisms are poorly u

120 Glial cell line-derived neurotrophic factor (GDNF) promotes PNS development and kidney morphogenesis

121 glial cell line-derived neurotrophic factor (GDNF) promotes the function, plasticity, and survival of

122 glial cell line-derived neurotrophic factor (GDNF) readily migrate to the mouse brain with acute toxi

123 tify glial cell-derived neurotrophic factor (GDNF) receptor alpha-like (GFRAL) as a brainstem-restric

124 glial cell line-derived neurotrophic factor (GDNF) receptor RET have both been independently linked t

125 increased glial-derived neurotrophic factor (GDNF) to dopaminergic neurons.

126 glial-cell-line-derived neurotrophic factor (GDNF) to increase cocaine intake was potentiated by a de

127 glial cell line-derived neurotrophic factor (GDNF) to produce a strabismus in infant non-human primat

128 glial cell line-derived neurotrophic factor (GDNF) were analysed by specific enzyme-linked immunosorb

129 glial cell line-derived neurotrophic factor (GDNF) were determined using quantitative reverse transcr

130 ine, glial cell-derived neurotrophic factor (GDNF), and dibutyryl cAMP.

131 glial cell line-derived neurotrophic factor (GDNF), and produce potent effects in Parkinson's disease

132 glial cell line-derived neurotrophic factor (GDNF), and the model anti-inflammatory agent is the type

133 glial cell line-derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), pleiotr

134 glial cell line-derived neurotrophic factor (GDNF), but not the removal of chondroitin sulfate proteo

135 d medium, glial-derived neurotrophic factor (GDNF), hepatocyte growth factor (HGF), or fibronectin.

136 levels of glial-derived neurotrophic factor (GDNF), inducing phosphorylation of RET and downstream ac

137 glial cell line-derived neurotrophic factor (GDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), and

138 APPalpha, glial-derived neurotrophic factor (GDNF), P-T181-tau, and P-S396-tau were significantly (3-

139 t express glial derived neurotrophic factor (GDNF), which is essential for fusimotor neuron survival.

140 protein, glial-derived neurotrophic factor (GDNF), which is known to influence neuronal survival, di

141 glial cell line-derived neurotrophic factor (GDNF)-expression in the striatum.

142 glial cell line-derived neurotrophic factor (GDNF).

143 Whereas other members of this family (GDNF and neurturin) primarily target parasympathetic and

144 d primary murine astrocytes were assayed for GDNF expression and secretion.

145 sharply increased both mRNA and protein for GDNF, while the neurotrophic effects of TNFalpha or IL-1

146 ith increased expression of the receptor for GDNF (glial cell line-derived neurotrophic factor) famil

147 The receptor for GDNF comprises the lipid raft-resident, glycerophosphati

148 Conclusion: We demonstrate a role for GDNF in enhancing hepatic autophagy and in potentiating

149 es in mice have revealed essential roles for GDNF signaling in development; however, its role in pros

150 Furthermore, GDNF expression was upregulated upon radiation therapy i

151 Furthermore, GDNF-RET signaling promoted the survival of aromatase in

152 FAT4 perturbs the assembly of the RET-GFRA1-GDNF complex, reducing RET signaling.

153 Mice given GDNF developed neurons and glia in distal bowel tissues

154 d-type mice; fecal microbiomes of mice given GDNF were similar to those of wild-type mice except for

155 not more severe if Tlr2(-/-) mice were given GDNF before dextran sulfate sodium or 2,4 dinitrobenzens

156 secrete GDNF that produced high hippocampal GDNF tissue levels in a long-term manner.

157 mbination treatment with BBB penetrating IgG-GDNF and IgG-TNFR fusion proteins enhances the therapeut

158 utic effect of single treatment with the IgG-GDNF fusion protein following delayed intravenous admini

159 f patients with IBD, there was a decrease in GDNF concentrations accompanied by a loss of DSG2, chang

160 al pathologies via iNOS-mediated decrease in GDNF.

161 xpression restored mitochondrial function in GDNF/RET-deficient cells, while GDNF stimulation rescued

162 rn blotting showed a substantial increase in GDNF protein.

163 e existence and importance of lipid rafts in GDNF-Ret signaling under physiologic conditions is unres

164 Although reduction in GDNF dosage improved CAKUT it did not affect delayed mes

165 rotrophic factor (GDNF) family that includes GDNF, artemin (ARTN) and neurturin (NRTN).

166 Increased GDNF expression and Caspase 3/7 activities were detected

167 evels of beta-catenin also express increased GDNF.

168 rder for up to 10-fold selectively increased GDNF expression was activators of TLR3 > TLR2 or TLR4 >

169 Here, we report that increased GDNF/GFRalpha1 signaling to sensory neurons from ischemi

170 cancers defined a proliferation-independent GDNF response signature that prognosed poor patient outc

171 d opposing effects on TLR3 activator-induced GDNF expression: approximately 60% enhancement by blocki

172 We found that testosterone (T) induces GDNF expression in mouse PM cells in vitro and neonatal

173 Furthermore, 7a inhibited GDNF-induced RET phosphorylation of ERK1/2 in MCF-7 brea

174 Knockdown of TFAP2C or RET inhibited GDNF (glial cell line-derived neurotrophic factor)-media

175 Conversely, intravenous GDNF had no therapeutic effect.

176 erived macrophages expressing the RET ligand GDNF are highly abundant around nerves invaded by cancer

177 ssed with TRPM8 and their respective ligands GDNF and neurturin did not induce cold pain, whereas the

178 We found that, like GDNF, signaling through the parental compound Q121 is GF

179 Exogenous luminal GDNF penetrated aganglionic colon epithelium of Hol(Tg/T

180 utant mice, we demonstrate that RET-mediated GDNF signaling in UGS increases proliferation of mesench

181 ajor role in SMA pathology as viral-mediated GDNF re-expression did not improve astrocyte function or

182 sed ERK activity due to abnormal mesenchymal GDNF expression.

183 Muscle GDNF signaling to neurons may, therefore, play an import

184 Approximately 95% of identified neostriatal GDNF-expressing cells in normal and injured animals are

185 n be prevented by nerve growth factor (NGF), GDNF and ARTN, but not NRTN.

186 NGF, GDNF, BDNF and NT-3 increased stem cell migration when c

187 e to cause glial activation, decrease nigral GDNF, augment the death of nigral dopaminergic neurons,

188 n of several neurotrophic factors and normal GDNF signaling.

189 fects were associated with the activation of GDNF receptors.

190 F on apoptosis was measured upon addition of GDNF or neutralizing anti-GDNF antibody.

191 Administration of GDNF improved saliva production and enriched the number

192 re completely corrected by administration of GDNF to Tlr2(-/-) mice.

193 Systemic administration of GDNF-macrophages at a severe late stage of the disease l

194 f XIB4035, a reported nonpeptidyl agonist of GDNF receptor alpha1 (GFRalpha1), are effective treatmen

195 nd sAPPbeta were significantly higher and of GDNF significantly lower in ADEs of patients with AD tha

196 Application of GDNF to cultured explants of aganglionic bowel from chil

197 s revealed that the neurological benefits of GDNF were associated with the normalization of anatomica

198 Deletion of GDNF expression by perineurial macrophages, or inhibitio

199 intermittent convection-enhanced delivery of GDNF produced a putamen-wide tissue engagement effect, o

200 perative in Crohn's disease and dependent of GDNF.

201 Here we investigated the effects of GDNF on hepatic autophagy in response to increased fat l

202 tenary culture system to test the effects of GDNF-mediated RET activation, we demonstrate the concurr

203 n injured muscle and increased expression of GDNF family receptor alpha1 (GFRalpha1) in dorsal root g

204 O is responsible for decreased expression of GDNF in activated astrocytes.

205 d rafts, that the developmental functions of GDNF in the periphery require the translocation of the G

206 is required for the physiologic functions of GDNF in vertebrates.

207 Cellular identification of GDNF by unequivocal histochemical methods demonstrated t

208 Furthermore, immobilization of GDNF protein promoted cell survival and differentiation

209 sciplinary strategy to address the impact of GDNF-RET signaling in the response to aromatase inhibito

210 Moreover, inactivation of GDNF sensitized in EGC cell to IFN-gamma/TNF-alpha induc

211 ecal route provided significant increases of GDNF levels in different brain sub-regions, including mi

212 NF-alpha and IFN-gamma, and the influence of GDNF on apoptosis was measured upon addition of GDNF or

213 ceived bilateral intraputamenal infusions of GDNF (120 ug per putamen) or placebo every 4 weeks for 4

214 Furthermore, intravenous injections of GDNF-macrophages at an early stage of disease resulted i

215 bules that were surrounded by high levels of GDNF also exhibited increased levels of activated beta-c

216 that delivers high and consistent levels of GDNF directly to the brain.

217 bnormal mucosal secretion, reduced levels of GDNF in smooth muscle cells, and impaired signaling via

218 o reported that transgenic overexpression of GDNF in mice prevented the HFD-induced liver accumulatio

219 ein, we validated a therapeutic potential of GDNF-transfected macrophages in a transgenic Parkin Q311

220 we tested the hypothesis that production of GDNF by PM cells is essential for spermatogonial develop

221 me, to our knowledge, that the production of GDNF by PM cells is essential for undifferentiated sperm

222 gly suggested that T-regulated production of GDNF by PM cells is required for spermatogonial developm

223 Production of GDNF in the PV+ neurons might be advantageous to supply

224 However, how the deletion or reduction of GDNF in the CNS affects the function of dopaminergic neu

225 ly synchronous activity-dependent release of GDNF in broad areas of the striatum.

226 ese data regarding the physiological role of GDNF are relevant in the context of neurological and neu

227 r understanding of the physiological role of GDNF on striatal dopaminergic function.

228 Here, we establish novel roles of GDNF signaling in mouse prostate development.

229 erineurial microenvironment and secretion of GDNF are essential for pancreatic cancer neural spread.

230 at cholinergic neurons regulate secretion of GDNF by skeletal muscle.

231 ge tracing were used to identify a source of GDNF-targeted neural progenitors.

232 acid to Tlr2(-/-) mice after termination of GDNF administration.

233 omote neurite growth through upregulation of GDNF, a novel process that may facilitate re-innervation

234 ore, this co-dependence precludes the use of GDNF as a tool to study a putative functional cross-talk

235 Sertoli cells produce GDNF and other growth factors and are commonly thought t

236 lycerophosphatidylinositol-anchored receptor GDNF family receptor alpha1 (GFRalpha1) and the receptor

237 itol (GPI)-anchored, ligand binding receptor GDNF family receptor alpha1 (GFRalpha1) and the receptor

238 ut not in mice lacking GDF15 or its receptor GDNF family receptor alpha-like (GFRAL).

239 d, conversely, administration of recombinant GDNF and Artemin protein substantially ameliorated impai

240 and short-term electrical stimulation reduce GDNF secretion, while treatment with carbachol or long-t

241 However, reduced GDNF expression does not play a major role in SMA pathol

242 The reduced GDNF in patients with IBD indicates a disease-relevant c

243 Ureteric bud growth and branching requires GDNF signaling from the surrounding mesenchyme to cells

244 This feature restricts GDNF activity to systems in which GFRa1 and RET are both

245 ic IB4+ neurons expressing the GFRalpha1-RET GDNF receptor complex.

246 region ternary complexes of GDF15/GFRAL/RET, GDNF/GFRalpha1/RET, NRTN/GFRalpha2/RET and ARTN/GFRalpha

247 Although SPRY1 antagonizes Ret-GDNF signaling, which modulates renal branching, its rol

248 luding PAX2, HNF1B, EYA1, SIX1, SIX2, SALL1, GDNF, WNT4, and WT1.

249 trahippocampal implants continued to secrete GDNF that produced high hippocampal GDNF tissue levels i

250 ssion of repair cell markers, including Shh, GDNF, and BDNF.

251 Specifically, GDNF has been characterized as a survival factor for spi

252 TLR3 activator-stimulated GDNF expression was selectively JNK-dependent, followed

253 Striatal GDNF mRNA was present in neonates but markedly increased

254 We have studied in detail striatal GDNF production in normal mouse and after damage of DA n

255 However, the source of striatal GDNF is not well known.

256 ryonic development and reduction of striatal GDNF levels in adult mice via AAV-Cre delivery.

257 In the current study, GDNF production by skeletal muscle myotubes following tr

258 zed in neurons, but numerous reports suggest GDNF production in glial cells, particularly in the inju

259 In summary, GDNF-transfected macrophages represent a promising thera

260 ronal growth, differentiation, and survival, GDNF is currently being used in clinical trials as a tre

261 Sustained GDNF treatment of one medial rectus muscle resulted in a

262 After sustained GDNF treatment, few changes were seen in mean myofiber c

263 ame multiply innervated after this sustained GDNF treatment.

264 The tethered GDNF protein remained functional and capable of activati

265 ces neuronal death significantly better than GDNF, suggesting therapeutic potential.

266 We hypothesized that GDNF is involved in the loss of DSG2, resulting in impai

267 Here we report that GDNF-family receptor alpha-like (GFRAL), an orphan membe

268 We previously reported that GDNF is protective against high fat diet (HFD)-induced h

269 This revealed that GDNF and BMP8B broadly support human SPG culture, while

270 and RET-deficient Caco2 cells revealed that GDNF specifically recruits DSG2 to the cell borders, res

271 d immunosorbent assays (ELISA) revealed that GDNF, covalently tethered onto polycaprolactone (PCL) el

272 Our studies show that GDNF and its receptor agonists could be useful for enhan

273 tinct GFRalpha family co-receptor, such that GDNF, NRTN and ARTN bind GFRalpha1, -alpha2, and -alpha3

274 The GDNF and the TNFR decoy receptor were re-engineered for

275 ing the mechanoreceptor marker NF200 and the GDNF coreceptor GFRalpha1.

276 (GDNF) binds the GFRalpha1 receptor, and the GDNF-GFRalpha1 complex binds to and activates the transm

277 Both the GDNF and the TNFR are large molecules that do not cross

278 To dissect the GDNF-GFRalpha1-RET signaling complex, agents that bind a

279 or contributors are trophic factors from the GDNF family and a cytokine, interferon-gamma.

280 ionale to explore whether alterations in the GDNF-Ret pathway contribute to pathophysiological condit

281 These data indicate that modulation of the GDNF pathway may have potential therapeutic benefit for

282 e periphery require the translocation of the GDNF receptor complex into lipid rafts.

283 Stimulation of the GDNF-producing striatal PV+ ensemble in PD patients coul

284 es in mice suggest that perturbations of the GDNF-Ret signaling pathway are a major genetic cause of

285 Overall, the GDNF-Ret pathway exerts two critical and distinct functi

286 Knockdown of Cbl-3/c using siRNA reduced the GDNF-induced ubiquitination and degradation of Ret51 in

287 form conditional gene targeting, testing the GDNF coreceptors Gfra1 and Ret for effects on teratoma s

288 ransport as IgG fusion proteins, wherein the GDNF or the TNFR are fused to the heavy chain of a chime

289 Therefore, GDNF released from peptidergic CGRP/somatostatin+ nocice

290 Despite a timed GDNF expression period, a subset of animals displayed ax

291 al root avulsion injuries, we combined timed GDNF gene therapy delivered to the proximal nerve roots

292 eimplantation of lumbar ventral roots, timed GDNF-gene therapy enhanced motoneuron survival up to 45

293 find that GDF15 binds with high affinity to GDNF family receptor alpha-like (GFRAL), a distant relat

294 GDNF binds to GDNF family receptor alpha1 (GFRa1), and the resulting c

295 In the adult tooth, GDNF is highly expressed by many cell types throughout t

296 Exploiting a transgenic GDNF overexpression model, which expands and normalizes

297 In vitro, GDNF accelerated autophagic cargo clearance in primary m

298 ice showed a mild branching defect in vitro, GDNF was able to support survival and downstream signali

299 ous system; however, the mechanisms by which GDNF is synthesized and released by skeletal muscle are

300 function in GDNF/RET-deficient cells, while GDNF stimulation rescued mitochondrial defects in parkin

301 s from children with HSCR were cultured with GDNF and evaluated for neurogenesis.