ライフサイエンスコーパス: TrkB receptor

1 were found for the full-length or truncated TrkB receptor.

2 ne downstream of BDNF, via activation of the TrkB receptor.

3 express BDNF mRNA, BDNF protein, as well as TrkB receptor.

4 ted by a feedback mechanism mediated via the TrkB receptor.

5 induced a sustained local activation of the TrkB receptor.

6 by K252b, consistent with signalling via the TrkB receptor.

7 retinas of mice lacking all isoforms of the TrkB receptor.

8 changes by disrupting BDNF signaling via the TrkB receptor.

9 smitter release, which is dependent upon the TrkB receptor.

10 d mediated by the loss of signaling from the TrkB receptor.

11 ic factor (BDNF) is a cognate ligand for the TrkB receptor.

12 precursor, and that it can potently activate TrkB receptor.

13 ice that express mutant but fully functional TrkB receptors.

14 litation by mimicking the effects of BDNF on TrkB receptors.

15 the release of BDNF, which in turn activates TrkB receptors.

16 from the SH-SY5Y and cell surface density of TrkB receptors.

17 ations do support survival via high-affinity TrkB receptors.

18 as well as survival responses, compared with TrkB receptors.

19 F activated NFAT-dependent transcription via TrkB receptors.

20 orylation of TrkC more potently than TrkA or TrkB receptors.

21 secreted BDNF interacting with extracellular TrkB receptors.

22 elease of BDNF and therefore the activity of TrkB receptors.

23 ry to determine the cellular localization of trkB receptors.

24 ibodies to the p75 neurotrophin receptor and trkB receptors.

25 on the nervous system via signaling through trkB receptors.

26 rmine the postendocytic sorting of signaling TrkB receptors.

27 al responses through direct interaction with TrkB receptors.

28 e in neuronal survival through activation of TrkB receptors.

29 or (BDNF) and tropomyosin receptor kinase B (TrkB) receptor.

30 sticity via activation of tyrosine kinase B (TrkB) receptors.

31 II (CaMKII) and tyrosine kinase receptor B (TrkB) receptors.

32 TrkB) agonist in WT mouse slices showed that TrkB receptor activation also increased evoked DA releas

33 Chronic NAS treatment triggers TrkB receptor activation and its downstream signaling in

34 ific receptor antagonist, demonstrating that TrkB receptor activation enhances extinction of cocaine-

35 esults indicate that BDNF is sufficient, and TrkB receptor activation is necessary, for the transsyna

36 These data indicate that full-length trkB receptor activation may modulate glutamatergic path

37 To determine the effects of TrkB receptor activation on synapse formation and functi

38 deprived-eye responses by interference with TrkB receptor activation or reduction of BDNF production

39 Together, infralimbic TrkB receptor activation strengthens GluN2B-containing N

40 te that theta-LTP in the NAc is dependent on TrkB receptor activation, and that BDNF rescues theta-LT

41 This retrograde effect required TrkB receptor activation, phospholipase Cgamma activity

42 tor K252a, consistent with a requirement for TrkB receptor activation.

43 spines and that this effect was dependent on TrkB receptor activation.

44 on, an effect mediated by BDNF secretion and TrkB receptor activation.

45 receptor activation, new BDNF synthesis and TrkB receptor activation.

46 ons suggest that tyrosine receptor kinase B (trkB) receptor activation promotes limbic epileptogenesi

47 actions were mediated via tyrosine kinase B (TrkB) receptor activation, established by inhibition of

48 tinction was strengthened by potentiation of TrkB receptor activity with infralimbic infusions of BDN

49 function and antiepileptogenic effects of a TrkB receptor agonist in a posttraumatic epilepsy model,

50 suggest that early treatment with a partial TrkB receptor agonist may be a promising therapeutic app

51 o the hypothesis that early treatment with a TrkB receptor agonist might prevent or reduce seizure ac

52 Here we show that R13, a small molecular TrkB receptor agonist prodrug, inhibits AEP and promotes

53 as rescued with systemic administration of a TrkB receptor agonist, 7,8-dihydroxyflavone.

54 p in 7,8-dihdyroxyflavone, a selective small TrkB receptor agonist, is critical for agonistic activit

55 7,8-DHF), a newly identified small molecular TrkB receptor agonist, rapidly activates TrkB in both pr

56 ration were rectified by administration of a TrkB receptor agonist, suggesting reduced BDNF-TrkB sign

57 ere rectified by chronic administration of a TrkB receptor agonist.

58 droxyflavone (7,8DHF), the newly synthesized TrkB receptor agonist.

59 TrkB receptor agonists would therefore be useful as phar

60 ograde and anterograde trafficking routes of TrkB receptor along the axon in rat hippocampal neurons.

61 ated in part through local activation of the TrkB receptor and also by recruitment of Sca-1+CD11b+ pr

62 val effect of BDNF via its interactions with TrkB receptor and exerts an additional BDNF-independent

63 and PI3-K/Akt signaling is downstream of the TrkB receptor and involves docking proteins insulin rece

64 This effect involves signaling through the TrkB receptor and is blocked by the N-methyl-d-aspartate

65 t partly from differential activation of the TrkB receptor and its down-stream signals.

66 icited transient and sustained activation of TrkB receptor and its downstream signaling, respectively

67 own that BDNF leads to the downregulation of TrkB receptor and some of its downstream responses, wher

68 2 induced acute, transient activation of the TrkB receptor and subsequent CREB phosphorylation in hip

69 BDNF) and neurotrophin-4/5 (NT4) act via the TrkB receptor and support survival of primary somatic an

70 ed neurotrophin (NT)-4 signaling through the TrkB receptor and that early-life OVA exposure significa

71 ere was an intense labeling of the truncated TrkB receptor and the p75(NTR) in the area surrounding t

72 failed to induce autophosphorylation of the TrkB receptor and to increase neurite outgrowth in npc(n

73 rophic factor (BDNF)-dependent activation of TrkB receptors and downregulation of KCC2 expression, wh

74 lonal antibodies have been shown to activate TrkB receptors and exert neuroprotective and neurotrophi

75 l link of synapsin phosphorylation via BDNF, TrkB receptors and MAP kinase with downstream facilitati

76 secondary signaling molecules downstream of TrkB receptors and promote neuronal survival and neurite

77 Hence, 7,8-DHF interacts robustly with the TrkB receptor, and its agonistic effect may be mediated

78 Extinction induced activation of the BDNF TrkB receptor, and signaling pathways associated with BD

79 ntial splicing--gp145trkB or the full-length trkB receptor, and trkB.T1 and trkB.T2, two cytoplasmica

80 brane region, which is distinct from that in TrkB receptors, and is both necessary and sufficient for

81 evidenced by significant reductions in BDNF, TrkB receptors, and phosphorylated TrkB.

82 e microinjected BDNF or the highly selective TrkB receptor antagonist [N2-2-2-oxoazepan-3-yl amino] c

83 istration of a BDNF receptor antagonist (the TrkB receptor antagonist ANA-12) reversed the diminished

84 tions of a BDNF tropomyosin-receptor-kinase (TrkB) receptor antagonist reduced retinal function and p

85 n-derived neurotrophic factor (BDNF) and its TrkB receptor are known to protect NB cells from chemoth

86 Full-length kinase domain-containing TrkB receptors are expressed at low and seemingly unchan

87 en they reach the cell bodies, the activated TrkB receptors are in a complex with ligand.

88 er afferent cells after SCI and (2) TrkA and TrkB receptors are phosphorylated in DRG after SCI.

89 Conversely, TrkB receptors are predominantly sorted to the degradati

90 These results indicate that TrkB receptors are required for the early growth of ovar

91 eport that neurotrophins (NTs) signaling via TrkB receptors are required for the growth of newly form

92 Further, in P301S retinas, TrkB receptors are selectively upregulated, but uncouple

93 or (BDNF) and its tyrosine protein kinase B (TrkB) receptors are known to potentiate glutamatergic an

94 In addition, the TrkB receptor-associated signaling molecule pERK5 accumu

95 ces BDNF signaling by selectively modulating TrkB receptors at active neurons or synapses without aff

96 BDNF released by cortical neurons activates TrkB receptors at striatal dendrites to promote striatum

97 Here we show that the TrkB receptor binds and phosphorylates APP, reducing amy

98 Here we show that the TrkB receptor binds and phosphorylates APP, reducing amy

99 The intracerebroventricular infusion of trkB receptor body (trkB-Fc) inhibited development of ki

100 We also have found that ligands for the trkB receptor (brain-derived neurotrophic factor and neu

101 (NT4/5) exert their action through a common trkB receptor but independently support gustatory sensor

102 ine, and retinal ganglion cells, express the TrkB receptor, but rod photoreceptors do not.

103 mission and plasticity primarily through the TrkB receptor, but the molecules involved in BDNF-mediat

104 drugs activate tropomyosin-related kinase B (TRKB) receptor, but it remains unclear whether these com

105 ults indicate that both p75 neurotrophin and trkB receptors can mediate internalization and retrograd

106 We find that TrkB receptor colocalizes to NHE6-associated endosomes.

107 e normal levels of full-length and truncated TrkB receptor, constitutive and neurotrophin-4/5-induced

108 aggregates impair the transport of Rab7 and TrkB receptor-containing endosomes, as well as autophago

109 anisms through which neurotrophins acting at trkB receptors contribute to synaptic plasticity.

110 These results imply that activation of trkB receptors contributes to the development of kindlin

111 that neurotrophin signaling mediated by the TrkB receptor controls striatal size by promoting the su

112 over, the results suggest that activation of trkB receptors could contribute to the hyperexcitability

113 use line with Tropomyosin receptor kinase B (TrkB) receptor deletion from D1-expressing cells (D1-Cre

114 plication suggest the involvement of a local TrkB-receptor-dependent mechanism for synapse-specific r

115 The two best-characterized truncated trkB receptors, designated as trkB.T1 and trkB.T2, conta

116 Actions of the truncated TrkB receptor did not involve unmasking of endogenous Tr

117 BDNF signaling through TrkB receptors differentially modulates cocaine self-adm

118 These results suggest that TrkB receptors do not regulate dendritic growth per se b

119 edd4-2 does not bind or ubiquitinate related TrkB receptors, due to the lack of a consensus PPXY moti

120 IL, and this effect is abolished by blocking TrkB receptors during extinction, highlighting a potenti

121 Activating TrkB receptors during the critical period (P33-P40) in d

122 c blockade of tropomyosin receptor kinase B (TrkB) receptors during extinction, via the TrkB antagoni

123 h acts through tropomyosin-related kinase B (TrkB) receptors during mammalian development, also enhan

124 BDNF, via the tropomyosin-related kinase B (TRKB) receptor, elicits specific cellular responses is o

125 DNF and prevents its binding to the neuronal TrkB receptor, eliminated the neurotrophic effect of CM-

126 Neutralizing the BDNF or blocking the TrkB receptor enhanced the glutamate-induced cytotoxicit

127 NF target, the tropomyosin-related kinase B (TrkB) receptor, enhances the amplitude and prolongs the

128 s are consistent with a difference in a post TrkB-receptor event(s) mediating BDNF action in the cult

129 tracellular domain of the human neurotrophin TRKB receptor expressed in Chinese hamster ovary cells i

130 Ovarian BDNF acts on TrkB receptors expressed exclusively in oocytes to enhan

131 As trkB.T1 is the sole isoform of trkB receptors expressed on astrocytes, we examined the

132 tropomyosin-related receptor kinase type B (trkB) receptors expressed on astrocytes.

133 Hence, in ferrets, we examined BDNF and TrkB receptor expression in identified AVPNs using in si

134 g in various neuronal systems, and increased TrkB receptor expression in phrenic motoneurons enhances

135 neurites and a 30% increase in neurotrophin trkB receptor expression, indicating that PACAP induced

136 ociated virus (AAV)-mediated upregulation of TrkB receptor expression, is associated with increased e

137 nftm1Jae/J) and in glioma cells silenced for TrkB receptor expression, oleandrin was not effective, i

138 f presynaptic tropomyosin receptor kinase B (TrkB) receptors, facilitating presynaptic homeostatic co

139 eurons responsible for movement suppression, TrkB receptors failed to properly engage postsynaptic si

140 isual cortex requires phosphorylation of the TrkB receptor for BDNF [M.

141 ironment is accompanied by activation of the TrkB receptor for brain-derived neurotrophic factor (BDN

142 gainst OGD, whereas downstream activation of TrkB receptors for BDNF is necessary for neuroprotection

143 LM22A-4 (LM), a partial agonist at the BDNF TrkB receptor, for 7 d starting at postnatal day 13 (P13

144 a suggest that naturally occurring truncated trkB receptors function as inhibitory modulators of neur

145 Alternative splicing of the avian trkB receptor generates an extracellular deletion (ED) i

146 Neurotrophins acting at the trkB receptor have been shown to be important modulators

147 properties, neurons were exposed to soluble trkB receptor-IgG fusion protein, which is known to inhi

148 adult rat hippocampal formation, full-length trkB receptor immunoreactivity (trkB-IR) was localized u

149 TrkB receptor immunoreactivity was localized to postsyna

150 h activated (phosphorylated) forms of BDNF's TrkB receptor in adult rat hippocampus; these increases

151 the first time, a role for the neurotrophin TrkB receptor in atherosclerotic lesion development.

152 t regions of the extracellular domain of the TRKB receptor in binding BDNF.

153 PTP1B interacts with activated TrkB receptor in mouse brain and human SH-SY5Y neuroblas

154 ynaptic potentiation, while knockdown of the TrkB receptor in postsynaptic myocytes had no effect.

155 , largely depending on the expression of the TrkB receptor in PV(+) interneurons.

156 Selective deletion of the gene for the TrkB receptor in striatal progenitors, using the Dlx5/6-

157 produced normally refined RFs, and blocking TrkB receptors in light-exposed animals resulted in enla

158 The predominance of truncated TrkB receptors in oocytes and their developmental patter

159 ese data suggest that BDNF signaling through TrkB receptors in the amygdala is required for the acqui

160 t spinal A2a receptor agonists transactivate TrkB receptors in the rat cervical spinal cord near phre

161 (BDNF) signaling through tyrosine kinase B (TrkB) receptors in NACsh neurons is necessary for cocain

162 neurotrophin, possibly mediated by truncated trkB receptors, in the regulation of hippocampal plastic

163 ng of perisomatic inhibition was occluded by TrkB receptor inhibition and resulted from a coordinated

164 The TrkB receptor is critical for the control of energy bala

165 Thus, a functional TrkB receptor is expressed by both the human and rat agg

166 We demonstrate that a functional trkB receptor is expressed by motor neuron progenitors i

167 nic neurons (AVPNs) produce BDNF and contain TrkB receptors is not known.

168 indicate that the lipid raft localization of TrkB receptors is regulated by Fyn and represents an imp

169 show that the tropomyosin receptor kinase B (TrkB) receptor is a direct PTP1B substrate and implicate

170 unknown, we have examined the expression of trkB receptor isoforms during development of the rat for

171 the organism by signaling through different TrkB receptor isoforms.

172 BDNF antibody or K252a, an inhibitor of BDNF TrkB receptors, led to a local SWA decrease during the f

173 flammation and activity increase full-length TrkB receptor levels in the dorsal horn.

174 Activity-blocked explants treated with the TrkB receptor ligands BDNF and neurotrophin-4 (NT-4) dev

175 The added TrkB receptor ligands did not induce axonal sprouting to

176 results are consistent with the concept that TrkB receptor ligands promote inhibitory synaptogenesis.

177 ic synapses developed in the presence of the TrkB receptor ligands, BDNF and NT-4, but not the TrkC r

178 Taken together, these data suggest that the TrkB receptor may be a critical component in the multi-s

179 ults suggest that neurotrophin activation of TrkB receptors may physiologically control neuronal exci

180 nosine receptor agonists) that transactivate TrkB receptors may provide an effective therapeutic stra

181 ynaptically expressed, tropomyosin kinase B (TrkB) receptor-mediated, and augmented in the presence o

182 eurotrophic factor (BDNF), via activation of TrkB receptors, mediates vital physiological functions i

183 e ligand for the tyrosine kinase receptor B (TrkB) receptor, mediates neuronal survival, differentiat

184 Relatedly, presynaptic levels of TrkB-receptors mediating retrograde trophic signaling-we

185 Chronic block of TrkB receptors mimics the MeCP2 deficiency in wildtype g

186 both the full-length and the truncated BDNF TrkB receptor mRNA were unaltered.

187 g-induced down-regulation of the full-length TrkB receptor needed to activate intracellular pathways.

188 cognate tropomyosin receptor kinase type B (trkB) receptor occurs in substantia nigra pars compacta

189 a manner that depended on activation of the TrkB-receptor of BDNF.

190 nd the increased expression of the truncated TrkB receptor on SCs.

191 These results indicate that TrkB receptors on geniculocortical afferents are potenti

192 ovel role for neurotrophin signaling through TrkB receptors on muscle fibers in the ongoing maintenan

193 rophic factor (BDNF), which is recognised by TrkB receptors on the plasma membrane, endocytosed, and

194 tly acts through tyrosine receptor kinase B (TrkB) receptor on striatal neurons.

195 BDNF does not lead to the downregulation of TrkB receptor or of the biological responses leading to

196 Blockade of infralimbic TrkB receptors or GluN2B-containing NMDARs disrupted con

197 he longest neurite per cell were mediated by trkB receptors or mTor signaling.

198 ition, we found that a transient increase in TrkB receptor phosphorylation in the vHipp contributes t

199 otrophic factor (BDNF) signaling through the TrkB receptor plays a critical role in the control of en

200 neurotrophic factor (BDNF) signaling through TrkB receptors plays a well established role in cocaine

201 The expression pattern of TrkB receptor protein suggests that TrkB plays a broad r

202 rs, we have examined the distribution of the TrkB receptor proteins in the adult rat brain by using i

203 antation of the TrkA recycling sequence into TrkB receptors reroutes the TrkB receptor to the recycli

204 We propose that the failure of TrkB receptor signaling at synapses in AS is directly li

205 s, by disrupting KChIP binding, by restoring TrkB receptor signaling or by lowering mutant-Htt (mHtt)

206 y-dependent BDNF secretion and/or potentiate TrkB receptor signaling would therefore be of considerab

207 ssion and secretion of BDNF, which activates TrkB receptor signaling, is known to play a critical rol

208 ith brain-derived neurotrophic factor (BDNF) TrkB receptor signaling, which is known to be essential

209 This association was negatively modulated by TrkB receptor signaling.

210 ent of brain-derived nerve growth factor and TrkB receptor signaling.

211 tes GABAA receptor-mediated activity through TrkB receptor signalling that triggers a kinase-dependen

212 actor (BDNF) and tyrosine receptor kinase B (TrkB) receptor signalling in the NTS on baroreflex contr

213 Acute BDNF-induced activation of TrkB receptors significantly increased tyrosine phosphor

214 transmission in hippocampal neurons through trkB receptor stimulation and postsynaptic phosphorylati

215 s well as human) were devoid of a functional TrkB receptor, strongly suggesting a neuronal expression

216 trophic factor (BDNF), through activation of TrkB receptors, strongly inhibited the basal activity of

217 The dendritic localization of trkB receptors supports the hypothesis that dendrites, a

218 ing via gene transfer of a dominant negative TrkB receptor suppresses adipose NK cells.

219 extracellular domain of the full-length rat TrkB receptor to create a DeltaIgTrkB that is constituti

220 epidermal growth factor receptor (EGFR) and TrkB receptor to investigate the MVB sorting pathway in

221 ng sequence into TrkB receptors reroutes the TrkB receptor to the recycling pathway.

222 ing release of BDNF that binds high-affinity TrkB receptors to activate MAPK and by recruiting CaMKII

223 rtical slices with full-length and truncated TrkB receptors to examine their roles in regulating cort

224 d that Slitrk5 mediates optimal targeting of TrkB receptors to Rab11-positive recycling endosomes thr

225 We show that newly synthesized TrkB receptors traffic through the secretory pathway and

226 The expression of novel TrkB receptor transcripts has been characterized to unde

227 Activation of TrkB receptors triggers a signaling cascade involving JN

228 levels of a functionally inactive truncated TrkB receptor (TrkBtrunc) had a greater chance of surviv

229 BDNF and NT4 both signal through the p75 and TrkB receptors, trophin-specific activation of different

230 lin was protein kinase A (PKA) dependent but TrkB (receptor tyrosine kinase B) independent and was ac

231 The TrkB receptor tyrosine kinase (RTK) is a high affinity r

232 BDNF signaling thru TrkB receptor tyrosine kinase is one molecular mechanism

233 Like ROS, the neurotrophin receptor, TrkB receptor tyrosine kinase, has diverse effects in th

234 The neurotrophin receptor, TrkB receptor tyrosine kinase, is critical to central ne

235 ion, and synaptic modulation mediated by the TrkB receptor tyrosine kinase.

236 We suggest that NMDA activates the TrkB receptor via a BDNF autocrine loop, resulting in ne

237 Activation of TrkB receptor was analyzed at two potential tyrosine pho

238 When a dominant negative mutant of the trkB receptor was expressed in developing embryos, sever

239 mma and Grb2-associated binder 1 (Gab1) with TrkB receptors was attenuated, resulting in reduced acti

240 To address the specific role of the TrkB receptor, we created a novel lentiviral vector expr

241 ound nanoparticles and chimeric, EGF-binding TrkB receptors, we elucidate Trk-endosomal events involv

242 n spine cytoskeletal reorganization, and its TrkB receptor were comparable between genotypes.

243 In trigeminal ganglia, neurons expressing trkB receptor were increased threefold, whereas trkA-pos

244 TrkB receptors were observed opposed to cortical termina

245 its activation of tyrosine-related kinase B (TrkB) receptors were normal.

246 abotropic glutamate (mGluR1 alpha and 5) and TrkB receptors which interact with inputs from the corte

247 ation of the tyrosine phosphatase Shp-2 with TrkB receptors, which inhibits BDNF-induced TrkB autopho

248 TrkB receptors, which mediate effects of BDNF on TBS-LTP

249 e-3-carboxamide (HIOC) selectively activates TrkB receptor with greater potency than NAS.

250 ia HDAC inhibition or by directly activating trkB receptors with 7,8-dihydroxyflavone, a newly identi

251 in BDNF-signaling markers, but not 5-HTTs or TrkB receptors, within both brain regions.