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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
5 be determined whether transport of TrkB, the BDNF receptor, depends on HTT and whether such transport
7 [NTRK2, a brain-derived neurotrophic factor (BDNF) receptor gene, rs1211166, P = 1.04E-06] in the Pha
10 TrkB, the brain-derived neurotrophic factor (BDNF) receptor, selectively from D1+ or D2+ neurons oppo
11 the TrkB brain-derived neurotrophic factor (BDNF) receptor specifically localized to intracellular l
13 e pan-neurotrophin receptor p75(NTR) and the BDNF receptor TrkB (tropomyosin receptor kinase B) are n
14 immunoreactivity for activated forms of the BDNF receptor TrkB and beta1-integrins, two synaptic rec
15 t increases in cAMP can rapidly activate the BDNF receptor TrkB and induce BDNF-dependent long-lastin
16 4R mutants, mouse mutants that expresses the BDNF receptor TrkB at a quarter of the normal amount sho
17 tiviral vectors were used to overexpress the BDNF receptor trkB in layer V corticospinal motor neuron
19 ults, we hypothesized that activation of the BDNF receptor TrkB is necessary for the effects of BDNF
21 ing evidence suggests that activation of the BDNF receptor TrkB promotes epileptogenesis caused by st
22 1, a protein that couples activation of the BDNF receptor TrkB to downstream signaling pathways regu
23 to ethanol results in the activation of the BDNF receptor TrkB, leading to the activation of the mit
24 removal of the endogenous BDNF by using the BDNF receptor TrkB-Fc fusion protein inhibited the forma
26 LR animals a downregulation of the inactive BDNF receptor TrkB.T1, associated with an activation of
27 vation of brain-derived neurotrophic factor (BDNF) receptor TrkB, facilitation of mammalian target of
28 on of the brain-derived neurotrophic factor (BDNF) receptor trkB.T1, a truncated isoform of BDNF.
29 heat-shock cognate protein-70 as well as the BDNF receptor (trkB) and protein kinases, as determined
30 mortem human subjects with major depression, BDNF receptor (TRKB) expression, but not BDNF, was reduc
32 tive, green fluorescent protein (GFP)-tagged BDNF receptors (TrkB-GFP) in live cells during retrograd
33 tudy, we found that 5-HT treatment increases BDNF receptor, TrkB (tropomyosin related kinase B), leve
34 re associated with reduced activation of the BDNF receptor, TrkB, and that pharmacologic activation o
36 ls about the subcellular localization of the BDNF receptor, TrkB, relative to synaptic and nonsynapti
37 noadhesin chimera (TrkB-IgG) that mimics the BDNF receptor, TrkB, to selectively block BDNF in the hi
38 ophin independence, transcripts encoding the BDNF receptor, TrkB, were expressed at very low levels.
41 to locally knock down the expression of the BDNF receptor tropomyosin-receptor-kinase type B in rats
42 ternatively spliced truncated isoform of the BDNF receptor tropomyosin-related kinase B.T1 (trkB.T1).
43 NF scavenger or by intracellular blockade of BDNF receptor [tropomyosin-related kinase B (TrkB)] sign
46 to induce long-term depression, and with the BDNF receptor tyrosine kinase TrkB to elicit long-term p
50 ice (TrkB-PV(-/-)) in which the gene for the BDNF receptor, tyrosine kinase B receptor (trkB), has be
51 r tyrosine kinase B (trkB) demonstrated that BDNF receptors were present on corticospinal neuronal so
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