ライフサイエンスコーパス: NT-4

1 NGF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4)].

2 weight similar to the endogenous TrkB ligand NT-4.

3 ured elevated serum levels of NGF, NT-3, and NT-4.

4 hic factor but not by neurotrophin (NT)-3 or NT-4.

5 ic factor (BDNF), neurotrophin-3 (NT-3), and NT-4.

6 between MC load and blood levels of NGF and NT-4.

7 for the following NTs: NGF, BDNF, NT-3, and NT-4.

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

9 ngth TrkB, the cognate receptor for BDNF and NT-4.

10 NGF, NT-3 and NT-4 (10-100 ng/ml) were applied (5 days) to dissociated

11 n response to systemic administration of KA, NT-4/5 and BDNF mRNAs were dramatically upregulated in a

12 growth factor (NGF), neurotrophin-3 (NT-3), NT-4/5 and brain-derived neurotrophic factor (BDNF), hav

13 Moreover, the effects of BDNF or NT-4/5 and forskolin + PMA on NPY production were additi

14 rd to excitotoxic stimuli, and that those of NT-4/5 and NT-3 include both neurons and glia.

15 ble specific binding for [125I]labeled BDNF, NT-4/5 and NT-3 with little specific binding for CNTF an

16 BDNF and NT-4/5 are ligands of the TrkB tyrosine kinase receptor.

17 as brain-derived neurotrophic factor and/or NT-4/5 at discrete developmental times and locations.

18 The NT-4/5 effects were not seen after the critical period.

19 brain-derived neurotrophic factor (BDNF) and NT-4/5 exert their trophic effects on the nervous system

20 cnemius (MG) nerve was provided with NT-3 or NT-4/5 for 8-35 d via an osmotic minipump attached to it

21 NT-3 or NT-4/5 had no effect on the properties of treated motone

22 tential mediators of the actions of BDNF and NT-4/5 in developing visual cortex.

23 NT-4/5 induced modest recovery in group I afferent condu

24 ir responses to the deprived eye, subsequent NT-4/5 infusion could restore them.

25 th the increased labeling observed following NT-4/5 infusion.

26 received infusions of exogenous neurotrophin NT-4/5 into primary visual cortex beginning before a sho

27 Of the neurotrophins examined, NT-4/5 mRNA was most robustly expressed in the lumbosacr

28 The effects of neurotrophin-3 (NT-3) and NT-4/5 on the function of axotomized group Ia afferents

29 e-phosphorylated in response to either BDNF, NT-4/5 or NT-3.

30 esults indicate that the actions of BDNF and NT-4/5 participate in the response of the cord to excito

31 Lower doses were less effective, and NT-4/5 was without effect.

32 In contrast, both NT-3 and NT-4/5 were effective at rescuing motoneurons, with simi

33 es derived from rat fetal cortices, BDNF and NT-4/5 were equipotent in inducing NPY production but NT

34 r high-affinity receptors TrkB (for BDNF and NT-4/5) and TrkC (for NT-3).

35 neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5) upon ventral mesencephalic dopamine neurons in v

36 otrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5) via TrkB, and neurotrophin-3 (NT-3) via TrkC.

37 neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5), contribute to survival and differentiation of s

38 s of sequestration of trkB ligands (BDNF and NT-4/5), motor, but not sensory, neuron conduction was s

39 rotrophic factor (BDNF) or neurotrophin-4/5 (NT-4/5), or blockade of their endogenous actions, have b

40 otrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5).

41 rotrophic factor (BDNF) or neurotrophin-4/5 (NT-4/5).

42 Within areas affected by NT-4/5, cortical cells remained responsive to the depriv

43 Infusion of trkB-IgG, which binds BDNF and NT-4/5, inhibited the formation of OD patches within lay

44 Under none of these conditions did BDNF, NT-4/5, NT-3 or NGF induce an increase in NPY production

45 BDNF, and neurotrophin species tested (BDNF, NT-4/5, NT-3 or NGF).

46 GF or NT-3, but not brain-derived NT factor, NT-4/5, or mutant NGF, resulted in increased release of

47 pg/ml, whereas the EIA did not detect NT-3, NT-4/5, or NGF at concentrations as high as 100 ng/ml.

48 the idea that BDNF, NT-3, and in particular, NT-4/5, play a role in the normal function of the adult

49 conclude that NT-3, and to a limited extent NT-4/5, promotes recovery of axotomized group Ia afferen

50 Following exposure to BDNF or NT-4/5, TrkB is autophosphorylated on five cytoplasmic t

51 (trkB.FL) is capable of initiating BDNF and NT-4/5-induced signal transduction, the functional role

52 ne proteins serves as receptors for BDNF and NT-4/5.

53 tibular neurons were present in mice lacking NT-4/5.

54 only the rat aggregates responded to BDNF or NT-4/5.

55 rd glia, but was less widespread compared to NT-4/5.

56 Neurotrophin-4 (NT-4), a neuronal signaling molecule, is also expressed

57 , neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4) activated the FL receptor, as determined by tyrosi

58 In genotype 1 and 6 HCV, nt 4 also base pairs with nt 14 of miR-122.

59 TrkB signaling mediated by BDNF but not NT-4 also suppresses these sympathetic terminations.

60 although not all motoneurons coexpress both NT-4 and BDNF mRNAs.

61 ovaries of these mice or those lacking both NT-4 and BDNF suffer a stage-selective deficiency in ear

62 the other factors tested, we also found that NT-4 and GDNF increased the number of surviving neurons

63 B for brain-derived neurotrophic factor, and NT-4 and TrkC for NT-3 on skin MCs; and of TrkA and TrkC

64 Both neurotrophin-4/5 (NT-4) and brain-derived neurotrophic factor (BDNF), the

65 e taste buds is regulated by neurotrophin-4 (NT-4) and brain-derived neurotrophic factor (BDNF).

66 DNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), and glial cell line-derived neurotrophic factor (

67 DNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), and their receptors because of their potential ro

68 BDNF and NT-4 appear to mediate this suppressing effect in the up

69 following: (1) expression of trkB, BDNF, and NT-4 are not modulated by an excess of serotonin during

70 brain-derived neurotrophic factor (BDNF) and NT-4) at promoting neurite outgrowth from cerebellar neu

71 eurons of gene-targeted mouse mutants at the NT-4, BDNF, NT-3, and TrkA loci.

72 ression suggest that a significant number of NT-4/BDNF actions in the developing mammalian ovary are

73 Expression of the neurotrophins NT-4, brain-derived neurotrophic factor (BDNF), and NT-3

74 g densities (2-28 cells/mm2) BDNF, NT-3, and NT-4 (but not NGF) increased total neuronal survival, an

75 ransported [125I]BDNF, [125I]NT-3, and [125I]NT-4, but not [125I]NGF.

76 This effect of BDNF is mimicked by NT-4, but not NGF, and blocked by the Trk tyrosine kinas

77 GDNF, BDNF, and NT-4, but not NT-3 or NGF, stimulate geniculate axon out

78 sence of the TrkB receptor ligands, BDNF and NT-4, but not the TrkC receptor ligand, NT-3.

79 s for tropomyosin-related kinase B, BDNF and NT-4, can mediate diverse biological responses.

80 DNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), ciliary neuronotrophic factor (CNTF), leukaemia i

81 Levels of NGF-beta and NT-4 correlated with tryptase levels, suggesting a link

82 Because the release of BDNF and NT-4 could be abnormal in MAOA knock-out (KO) mice, we t

83 To examine whether neurotrophin-4 (NT-4)-deficient mice, which have only 45% of the normal

84 kB receptor ligands BDNF and neurotrophin-4 (NT-4) developed a full complement of Purkinje cell inhib

85 yet innervate their gustatory targets; thus, NT-4 does not function as a target-derived growth factor

86 ammalian neurotrophins - NGF, BDNF, NT-3 and NT-4 - each bind and activate one or more of the Trk fam

87 ), neurotrophin-3 (NT-3), or neurotrophin-4 (NT-4), each at 100 ng/ml] showed a two- to threefold inc

88 The NT-4 effects involve a potentiation of presynaptic trans

89 ry neurons are equally dependent on BDNF and NT-4 expression for survival, regardless of what periphe

90 In the absence of NT-4 function, BDNF-dependent, TrkB-expressing neurons f

91 We show that NT-4 functions early in gangliogenesis, upstream of BDNF

92 NT-4 had no significant effects on the numbers of TH, VI

93 The results suggest that BDNF and NT-4 have a role in the promotion of activity-dependent

94 BDNF or NT-4 improves, but NT-3 or CNTF reduces, survival of iso

95 s suppressing effect in the upper dermis and NT-4 in the epidermis.

96 related neurotrophin ligand, neurotrophin-4 (NT-4), in the regulation of revascularization of the adu

97 urotrophic factor (BDNF) and neurotrophin-4 (NT-4) inhibit agrin-induced AChR clustering on cultured

98 This BDNF/NT-4 inhibition is likely to be an intrinsic mechanism f

99 concentrations of agrin can occlude the BDNF/NT-4 inhibition of AChR clustering.

100 or by anti-TrkB antibodies mimicked the BDNF/NT-4 inhibition of agrin-induced AChR clustering.

101 lation of acetylcholine channels by secreted NT-4 is spatially restricted to <60 micron from the site

102 ve-muscle coculture in which neurotrophin-4 (NT-4) is overexpressed in a subpopulation of postsynapti

103 These findings indicate that NT-4 knock-out mice have a selective vagal afferent loss

104 Neither BDNF, NT-3, NT-4, LIF, IGF-1 or IGF-2 - singly or in combination - c

105 ceptor displayed a similar loss of NT-3- and NT-4-mediated activation, in addition to a diminished re

106 y was to examine the timing and mechanism of NT-4-mediated regulation of geniculate neuron number dur

107 Thus, NT-4 might represent a member of a new class of candidat

108 mbar motoneurons (approximately 63%) express NT-4 mRNA as assessed by counting motoneurons in the L4

109 not apparent until postnatal day 5 (P5) and NT-4 mRNA first appears at P9.

110 e at which cells exit the cell cycle between NT-4 mutant and wild type ganglia.

111 We discovered that NT-4 mutant mice lose 33% of their geniculate neuronal c

112 NT-4 mutants had a substantial organ-specific reduction

113 Meal pattern analyses revealed that NT-4 mutants had increased meal durations with solid foo

114 Immunoassays (ELISA) detected BDNF, NT-4, NGF, and NT-3 in the culture media from HTM cells.

115 Taste bud loss was not as profound in the NT-4 null mice compared to BDNF-null mice.

116 f two other members of this family, BDNF and NT-4, on sensory neuron development are less clear.

117 All potentiation effects of NT-4 overexpression were abolished by the extracellular

118 Therefore, compared to BDNF, NT-4 plays distinct roles in gustatory development; diff

119 Thus, during early embryonic development, NT-4 produced in the ganglion and along the projection p

120 dogenous TrkB agonist ligand neurotrophin-4 (NT-4) profoundly decreases food intake and body weight i

121 We found that NT-4 protein and mRNA were present in both type I and ty

122 ls of trkB mRNA and BDNF and neurotrophin-4 (NT-4) proteins are normal in the thalamus and the cortex

123 , taste buds are more sensitive to BDNF than NT-4 removal.

124 nding indicates that cell death initiated by NT-4-removal occurs through a different cell death pathw

125 s to a combination of antibodies to BDNF and NT-4 resulted in reduced inhibitory synapse formation, s

126 ), neurotrophin-3 (NT-3), or neurotrophin-4 (NT-4) results in a 30-50% reduction in neuronal survival

127 ly restricted to <60 micron from the site of NT-4 secretion.

128 ry pathway without affecting neurotrophin-4 (NT-4) secretion.

129 the nodose ganglion, whereas the profile for NT-4 suggests a p75 receptor-mediated transport mechanis

130 Application of antibodies to BDNF and NT-4 to cerebellar explants exposed to picrotoxin to inc

131 transported [125I]NT-3, [125I]NGF, and [125I]NT-4 to the central terminal field, the nucleus tractus

132 owth factor (NGF), and [125I]neurotrophin-4 (NT-4) to perikarya in the ipsilateral nodose ganglion, a

133 ranule neurons are present, however, BDNF or NT-4 treatment leads to Purkinje cell loss.

134 DNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), tyrosine kinase (trk) A, trkB, trkC, or p75.

135 rmation within the Matrigel plug by BDNF and NT-4 was comparable to that induced by VEGF-A.

136 l encephalomyopathies; it is noteworthy that NT-4 was not up-regulated in muscle fibers from healthy

137 G, indicating that postsynaptic secretion of NT-4 was responsible for the synaptic modification.

138 only by NGF, whereas the transport of [125I]NT-4 was significantly reduced by each of the neurotroph

139 The neurotrophins, BDNF, NT-3 and NT-4, were applied to cerebellar explants during activit

140 we determined that BDNF and neurotrophin-4 (NT-4), which both bind to the TrkB high-affinity recepto

141 icted to synapses on myocytes overexpressing NT-4 without affecting nearby synapses formed by the sam