ライフサイエンスコーパス: TrkB receptor

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

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

3 changes by disrupting BDNF signaling via the 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 smitter release, which is dependent upon the TrkB receptor.

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

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

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

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

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

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

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

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

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

17 F activated NFAT-dependent transcription via TrkB receptors.

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

19 secreted BDNF interacting with extracellular TrkB receptors.

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

21 ry to determine the cellular localization of trkB receptors.

22 ibodies to the p75 neurotrophin receptor and trkB receptors.

23 on the nervous system via signaling through trkB receptors.

24 al responses through direct interaction with TrkB receptors.

25 e in neuronal survival through activation of TrkB receptors.

26 ice that express mutant but fully functional TrkB receptors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 7,8-DHF), a newly identified small molecular TrkB receptor agonist, rapidly activates TrkB in both pr

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

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

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

50 TrkB receptor agonists would therefore be useful as phar

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

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

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

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

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

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

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

58 2 induced acute, transient activation of the TrkB receptor and subsequent CREB phosphorylation in hip

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 Conversely, TrkB receptors are predominantly sorted to the degradati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 TrkB receptor immunoreactivity was localized to postsyna

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 the organism by signaling through different TrkB receptor isoforms.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 Activation of TrkB receptors triggers a signaling cascade involving JN

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 TrkB receptors were observed opposed to cortical termina

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

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

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

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

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

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