ライフサイエンスコーパス: GDNF

1 GDNF also stimulated cell proliferation in serum-free co

2 GDNF content in myotubes and GDNF in conditioned culture

3 GDNF expression and EGC apoptosis were determined by imm

4 GDNF has been shown to be a potent survival factor for m

5 GDNF is synthesized and secreted by neuronal target tiss

6 GDNF localization was examined by immunocytochemistry.

7 GDNF mRNA expression was not higher in reactive astrocyt

8 GDNF protein content in cells and in culture medium was

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

10 GDNF supported only modest and transient survival of pos

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

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

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

14 In addition, GDNF induced a downward shift in the dose-response curve

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

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

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

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

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

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

21 ens (i.e., pleiotrophin, heregulin, FGF1 and GDNF) were found to have a higher affinity for 6-O sulfa

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

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

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

25 imals were sacrificed and contusion size and GDNF protein expression measured.

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

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

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

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

30 eir interaction with growth factors, such as GDNF, members of the FGF and TGFbeta superfamilies, EGF

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 s respond synergistically to coactivation by GDNF and EphA ligands, and these cooperative interaction

46 to the striatum was followed 1 week later by GDNF (9mug) or its vehicle.

47 uld be prevented by NGF and ARTN, but not by GDNF or NRTN.

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

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

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

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

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

53 nd this fusion protein is designated cTfRMAb-GDNF.

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

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

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

57 re treated with either saline or the cTfRMAb-GDNF fusion protein every other day for 3 weeks, startin

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

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

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

61 thetic and sensory neurons to target-derived GDNF was attributable to the differential expression and

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

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

64 Ret in both the axons and cell bodies during GDNF stimulation.

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

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

67 ns may further reveal the role of endogenous GDNF in human brain diseases.

68 s regulating normal production of endogenous GDNF in skeletal muscle.

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

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

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

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

73 muscle and 38% of colon afferents exhibited GDNF-induced potentiation.

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

75 Cultures of DPCs expressed GDNF as well as its receptors, GFRalpha1 and RET.

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

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

78 glial cell line-derived neurotrophic factor (GDNF) and fibroblast growth factor 2 (FGF2) are critical

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

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

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

82 glial cell line-derived neurotrophic factor (GDNF) could improve human islet survival and posttranspl

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

84 glial cell line-derived neurotrophic factor (GDNF) families of growth factors regulate the sensitivit

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

86 glial-cell line-derived neurotrophic factor (GDNF) family member artemin was found to be significantl

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

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

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

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

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

92 glial cell line-derived neurotrophic factor (GDNF) gene.

93 Glial cell line-derived neurotrophic factor (GDNF) has been identified as a potent survival factor fo

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

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

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

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

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

99 glial cell line-derived neurotrophic factor (GDNF) into the ventral tegmental area (VTA) rapidly redu

100 Glial cell line-derived neurotrophic factor (GDNF) is a neuronal growth factor critical for the devel

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

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

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

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

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

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

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

108 glial cell line-derived neurotrophic factor (GDNF) on dental pulp cells (DPCs).

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

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

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

112 Glial cell line-derived neurotrophic factor (GDNF) protects dopamine (DA) neurons from 6-hydroxydopam

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 ited glial cell derived neurotrophic factor (GDNF)-promoted neurogenesis.

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

130 including glial derived neurotrophic factor (GDNF).

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

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

133 Ret, the receptor tyrosine kinase for GDNF, underwent rapid proteasomal degradation in the axo

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

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

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

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

138 Furthermore, GDNF expression was upregulated upon radiation therapy i

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

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

141 buse liability, the study further highlights GDNF as a promising target for treatment of alcohol use/

142 ion of GDNF to a BBB molecular Trojan horse, GDNF trophic effects in brain in experimental PD are obs

143 However, GDNF blocked acquisition and expression of alcohol-CPP.

144 ot significantly affect DPC growth; however, GDNF dose-dependently increased viable cell number under

145 An adenoviral vector harboring human GDNF was injected unilaterally into FL-SMC of the rat im

146 at there are possibly five isoforms of human GDNF gene with different pre- and pro-regions by inter-

147 To study human GDNF and GDNFOS regulation in neurodegenerative diseases

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

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

150 ess of promoter type, a specific decrease in GDNF protein expression was observed in the MBP-halphasy

151 al pathologies via iNOS-mediated decrease in GDNF.

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

153 rn blotting showed a substantial increase in GDNF protein.

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

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

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

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

158 evels of beta-catenin also express increased GDNF.

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

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

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

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

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

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

165 Conversely, intravenous GDNF had no therapeutic effect.

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

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

168 In contrast, the mature GDNF peptide and the isoform mRNA levels were not change

169 In the MTG of AD patients, the mature GDNF peptide was down-regulated; however, the transcript

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

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

172 sed ERK activity due to abnormal mesenchymal GDNF expression.

173 The benefits conferred by MSC GDNF release could potentially apply to all degenerating

174 ediated neuroprotective effect is due to MSC GDNF release and that such protection is diminished when

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

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

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

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

179 Although ELISA results showed no GDNF in differentiated NG108-15 cells grown alone, immun

180 Furthermore, skin afferents showed no GDNF-induced potentiation of TRPA1, but 43% of muscle an

181 n of several neurotrophic factors and normal GDNF signaling.

182 The findings of novel GDNF and GDNFOS isoforms and differences in tissue expre

183 The remaining 5% of GDNF+ cells are cholinergic and somatostatin+ interneuro

184 protection is diminished when the action of GDNF is blocked.

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

186 Administration of GDNF improved saliva production and enriched the number

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

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

189 e MBP-halphasyn transgenic mice, analysis of GDNF expression levels in human MSA samples demonstrated

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

191 Deletion of GDNF expression by perineurial macrophages, or inhibitio

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

193 The effect of GDNF was abolished in the presence of inhibitors to GFRa

194 In vivo effects of GDNF were assessed in streptozotocin-induced diabetic nu

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

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

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

198 In conclusion, following fusion of GDNF to a BBB molecular Trojan horse, GDNF trophic effec

199 transport across the BBB following fusion of GDNF to the heavy chain of a chimeric monoclonal antibod

200 Cellular identification of GDNF by unequivocal histochemical methods demonstrated t

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

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

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

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

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

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

207 esults provide insight into the mechanism of GDNF protection of DA neurons, and may help avoid incorr

208 from prepubertal rabbits in the presence of GDNF and FGF2 and found they proliferated indefinitely a

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

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

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

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

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

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

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

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

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

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

219 eletal muscle cells reduced the secretion of GDNF by skeletal muscle.

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

221 o be transcribed from the opposite strand of GDNF gene.

222 eurons may be regulating their own supply of GDNF secreted by skeletal muscle and that activation of

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

224 s down-regulated; however, the transcript of GDNF isoform from human exon 2 was up-regulated, whereas

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

226 a-BTX reversed the action of neural cells on GDNF secretion by skeletal muscle.

227 ration of rabbit germ cells was dependent on GDNF.

228 ronal differentiation, such as BMP4, POU4F3, GDNF, OTX2, NEFM, CNTN4, OTP, SIM1, FYN, EN1, CHAT, GSX2

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

230 these results demonstrate that NAc-produced GDNF serves as a retrograde enhancer that upregulates th

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

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

233 d in the hairy hindpaw skin and its receptor GDNF family receptor alpha3 (GFRalpha3) was increased in

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

235 Addition of recombinant GDNF to cultures in serum-containing medium did not sign

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

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

238 e role that motor neurons play in regulating GDNF secretion by skeletal muscle.

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

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

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

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

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

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

245 Striatal GDNF mRNA was present in neonates but markedly increased

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

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

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

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

250 In the present study, GDNF was re-engineered to enable receptor-mediated trans

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

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

253 The tethered GDNF protein remained functional and capable of activati

254 curred under serum-free conditions, and that GDNF significantly reduced the number of dead cells by i

255 This study also demonstrated that GDNF counteracted TNFalpha-induced DPC cytotoxicity, sug

256 This study demonstrates that GDNF is a mitogenic factor promoting self-renewal that i

257 In conclusion, our findings indicate that GDNF promotes cell survival and proliferation of DPCs an

258 preference (CPP) paradigm, we observed that GDNF on its own does not induce CPP, suggesting that the

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

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

261 one, immunocytochemical analysis showed that GDNF was localized in NG108-15 cells co-cultured with C2

262 Recent work has shown that GDNF attracts motor neuron growth cones, and interacts s

263 Our study shows that GDNF has beneficial effects on human islet survival and

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

265 l and proliferation of DPCs and suggest that GDNF may play a multifunctional role in the regulation o

266 Our findings suggest that GDNF reduces alcohol-drinking behaviors by reversing an

267 ha-induced DPC cytotoxicity, suggesting that GDNF may be cytoprotective under disease conditions.

268 stration of alcohol, further suggesting that GDNF suppresses, rather than substitutes for, the reinfo

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

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

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

272 the NGF receptor TrkA, and half express the GDNF family ligand (GFL) receptor Ret.

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

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

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

276 Genetic and pharmacologic inhibition of the GDNF receptors GFRA1 and RET abrogated the migratory eff

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

278 growth factor 2 (FGF2) and mediators of the GDNF/RET and WNT11 signaling pathway were also decreased

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

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

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

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

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

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

285 -anchored GFRalpha1 signaling in response to GDNF, a diffusible chemoattractant in the limb, indicati

286 leagues link maladaptive stress responses to GDNF through a comprehensive investigation of the neurot

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

288 DA overflow, which was reversed by intra-VTA GDNF infusion.

289 iproliferative effects of tamoxifen, whereas GDNF stimulation had a protective effect against the dru

290 To determine whether GDNF promotes retrograde survival over long axonal dista

291 degradation of Ret in axons dictates whether GDNF family ligands act as retrograde survival factors.

292 We therefore tested whether GDNF in the VTA reverses alcohol withdrawal-associated D

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

294 root ganglion (DRG) sensory neurons in which GDNF promoted survival equally well from either distal a

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

296 lets precultured in medium supplemented with GDNF restored more diabetic mice to normoglycemia and fo

297 for 2 to 10 days in medium supplemented with GDNF showed lower beta-cell death, increased Akt phospho

298 med cell death and continuous treatment with GDNF maintains hyperinnervation of skeletal muscle in ad

299 tured in medium supplemented with or without GDNF (100 ng/mL) and in vitro islet survival and functio

300 tured in medium supplemented with or without GDNF.