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1 eurotrophin receptor p75 (p75(NTR)), the pro-BDNF receptor.
2 ctor BDNF, Numb binds to activated TrkB, the BDNF receptor, and functions both as an endocytic regula
3 1 at trkB brain-derived neurotrophic factor (BDNF) receptors, and BDNF neuroprotection is enhanced by
4                          Administration of a BDNF receptor antagonist (the TrkB receptor antagonist A
5 be determined whether transport of TrkB, the BDNF receptor, depends on HTT and whether such transport
6                               Mutants in the BDNF receptor gene trkB and antibodies to its second rec
7 ith neuroticism, and a locus overlapping the BDNF receptor gene, NTRK2.
8 [NTRK2, a brain-derived neurotrophic factor (BDNF) receptor gene, rs1211166, P = 1.04E-06] in the Pha
9 sting involvement of trkB (the high-affinity BDNF receptor) in BDNF-induced differentiation.
10      Intriguingly, the activity of TrkB, the BDNF receptor, is required in the cell body for the indu
11 wing for inducible, reversible disruption of BDNF receptor kinase activity by administration of 1NMPP
12 TrkB, the brain-derived neurotrophic factor (BDNF) receptor, selectively from D1+ or D2+ neurons oppo
13  the TrkB brain-derived neurotrophic factor (BDNF) receptor specifically localized to intracellular l
14                      Activation of TrkB, the BDNF receptor, stimulates GCPs to secrete BDNF, thereby
15 RKB), the brain-derived neurotrophic factor (BDNF) receptor that promotes neuronal plasticity and ant
16 e pan-neurotrophin receptor p75(NTR) and the BDNF receptor TrkB (tropomyosin receptor kinase B) are n
17 and (4) prevents decreased activation of the BDNF receptor TrkB (tropomyosin-related kinase B), all a
18 ly, we found that systemic administration of BDNF receptor TrkB agonist, LM22A-4, dampens habitual al
19  immunoreactivity for activated forms of the BDNF receptor TrkB and beta1-integrins, two synaptic rec
20 t increases in cAMP can rapidly activate the BDNF receptor TrkB and induce BDNF-dependent long-lastin
21 ignaling, we measured the mRNA levels of the BDNF receptor TrkB and of P/Q-type Ca(2+) channel alpha-
22 4R mutants, mouse mutants that expresses the BDNF receptor TrkB at a quarter of the normal amount sho
23 tiviral vectors were used to overexpress the BDNF receptor trkB in layer V corticospinal motor neuron
24 hat bind to PSD-95 promoted signaling by the BDNF receptor TrkB in the hippocampus and reduced depres
25         Here, we show that inhibition of the BDNF receptor TrkB increases voluntary ethanol consumpti
26 ults, we hypothesized that activation of the BDNF receptor TrkB is necessary for the effects of BDNF
27            Here we report that the number of BDNF receptor TrkB on the surface of hippocampal neurons
28 ing evidence suggests that activation of the BDNF receptor TrkB promotes epileptogenesis caused by st
29  1, a protein that couples activation of the BDNF receptor TrkB to downstream signaling pathways regu
30  to ethanol results in the activation of the BDNF receptor TrkB, leading to the activation of the mit
31  removal of the endogenous BDNF by using the BDNF receptor TrkB-Fc fusion protein inhibited the forma
32 e and precursor BDNF protein, as well as the BDNF receptor TrkB.
33 corpuscles, a mechanoreceptor expressing the BDNF receptor TrkB.
34                       Here, we show that the BDNF receptor TrkB.T1 is expressed by pancreatic beta-ce
35  LR animals a downregulation of the inactive BDNF receptor TrkB.T1, associated with an activation of
36 vation of brain-derived neurotrophic factor (BDNF) receptor TrkB, facilitation of mammalian target of
37 on of the brain-derived neurotrophic factor (BDNF) receptor trkB.T1, a truncated isoform of BDNF.
38 heat-shock cognate protein-70 as well as the BDNF receptor (trkB) and protein kinases, as determined
39 mortem human subjects with major depression, BDNF receptor (TRKB) expression, but not BDNF, was reduc
40 of females, though the HVC of both sexes has BDNF receptors (TrkB).
41 tive, green fluorescent protein (GFP)-tagged BDNF receptors (TrkB-GFP) in live cells during retrograd
42 tudy, we found that 5-HT treatment increases BDNF receptor, TrkB (tropomyosin related kinase B), leve
43 re associated with reduced activation of the BDNF receptor, TrkB, and that pharmacologic activation o
44                                          The BDNF receptor, TrkB, is critical to limbic epileptogenes
45 ls about the subcellular localization of the BDNF receptor, TrkB, relative to synaptic and nonsynapti
46 noadhesin chimera (TrkB-IgG) that mimics the BDNF receptor, TrkB, to selectively block BDNF in the hi
47 ophin independence, transcripts encoding the BDNF receptor, TrkB, were expressed at very low levels.
48 d subsequent activation of the high-affinity BDNF receptor, TrkB.
49               For example, activation of the BDNF receptor tropomyosin receptor kinase B (TrkB) in th
50                             Furthermore, the BDNF receptor tropomyosin receptor kinase B (TrkB) was e
51  to locally knock down the expression of the BDNF receptor tropomyosin-receptor-kinase type B in rats
52 ternatively spliced truncated isoform of the BDNF receptor tropomyosin-related kinase B.T1 (trkB.T1).
53 NF scavenger or by intracellular blockade of BDNF receptor [tropomyosin-related kinase B (TrkB)] sign
54 t can be reversed by directly activating the BDNF receptor, tropomyosin receptor kinase B.
55 on of the brain-derived neurotrophic factor (BDNF) receptor tropomysin-related kinase B (TrkB).
56 to induce long-term depression, and with the BDNF receptor tyrosine kinase TrkB to elicit long-term p
57                 SE-induced activation of the BDNF receptor tyrosine kinase, TrkB, is one signaling pa
58                                          The BDNF receptor tyrosine kinase, TrkB, underlies nervous s
59 ncated, kinase-deficient isoform (T1) of the BDNF receptor tyrosine receptor kinase B (trkB).
60 se is accompanied by the upregulation of the BDNF receptor, tyrosine kinase B (TrkB).
61 ice (TrkB-PV(-/-)) in which the gene for the BDNF receptor, tyrosine kinase B receptor (trkB), has be
62                                Activation of BDNF receptors using a pharmacological agonist was also
63 r tyrosine kinase B (trkB) demonstrated that BDNF receptors were present on corticospinal neuronal so
64 of these neurons were positive for TrkB, the BDNF receptor with a tyrosine kinase activity.