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1                                              CNTFRalpha expression is essential for the normal develo
2                                              CNTFRalpha immunoreactivity (CNTFRalpha-IR) was observed
3                                              CNTFRalpha mRNA expression in retina and other tissues w
4                                              CNTFRalpha receptor expression was substantially induced
5                                              CNTFRalpha was downregulated significantly by 24-36 h in
6                                              CNTFRalpha was localized on RGCs in experimental retinas
7                                              CNTFRalpha was RH mapped to CFA 11 (Canis familiaris aut
8  ciliary neurotrophic factor receptor alpha (CNTFRalpha) and leukemia inhibitory factor receptor (LIF
9 disruption of the mouse CNTF receptor alpha (CNTFRalpha) gene leads to MN loss, demonstrating a devel
10 ional disruption of the CNTF receptor alpha (CNTFRalpha) gene to directly examine the in vivo roles p
11 alyze the expression of CNTF receptor alpha (CNTFRalpha) in mouse retina and optic nerve following in
12  Ciliary neurotrophic factor receptor alpha (CNTFRalpha) is the ligand-binding component of the CNTF
13  cells, with a "floxed" CNTF receptor alpha (CNTFRalpha) mouse line and a gene construct driving Cre
14 ioural recovery through CNTF receptor alpha (CNTFRalpha) on nigral dopamine neurons in both the MPP(+
15           Expression of CNTF receptor alpha (CNTFRalpha), an essential CNTF receptor component, is gr
16  ciliary neurotrophic factor receptor-alpha (CNTFRalpha).
17 ve system (TRPV1 and CNTF on astrocytes, and CNTFRalpha on dopamine neurons) might have relevance to
18 ither did intraneural injections of CNTF and CNTFRalpha enhance recruitment in diabetic or control ra
19                                     CNTF and CNTFRalpha synthesis and release by CE cells in 35S-meth
20  35S 61-kDa molecule that was both CNTF- and CNTFRalpha-immunoreactive in an H2O2-dependent manner, w
21  receptor complex proteins (LIFR, gp130, and CNTFRalpha) during adipocyte differentiation and the eff
22       Similar expression patterns of TR2 and CNTFRalpha were observed in most of the developing neura
23 rities in the expression patterns of TR4 and CNTFRalpha in the developing and postnatal nervous syste
24 d their respective receptors: trkB, trkA and CNTFRalpha.
25 rogate to the lost endogenous membrane-bound CNTFRalpha in CNTF signaling, suggesting the potential o
26                                       Canine CNTFRalpha shares a high degree of homology with the hum
27   The complete coding sequence of the canine CNTFRalpha cDNA was cloned, and radiation hybrid (RH) ma
28 ed by Western blot analysis RESULTS: CE cell CNTFRalpha levels decreased as corneal storage time incr
29  and spatial expression pattern of the chick CNTFRalpha protein during CNS development.
30 NTFRalpha and the formation of a 61-kDa CNTF/CNTFRalpha-IM.
31  the three CNTF receptor complex components, CNTFRalpha and LIFR, decreases during adipocyte differen
32 r= 9 days) that retained abundant endogenous CNTFRalpha, rhCNTFRalpha decreased the effectiveness of
33 ls of stored human donor corneas, endogenous CNTFRalpha levels were quantified (by Western blot analy
34  endothelial (CE) cells that lost endogenous CNTFRalpha during corneal storage METHODS: In CE cells o
35                    Fiber tracts that exhibit CNTFRalpha immunoreactivity were the lateral forebrain b
36 vation of the CreER gene construct in floxed CNTFRalpha mice depletes this essential receptor subunit
37 ption of CNTFRalpha in facial MNs of "floxed CNTFRalpha" mice by AAV-Cre vector injection leads to si
38 vely-depleted it in vivo by using a "floxed" CNTFRalpha mouse line and a gene construct (mlc1f-Cre) t
39                         Immunoreactivity for CNTFRalpha protein was preferentially observed in neurop
40 rikarya and axons were intensely labeled for CNTFRalpha.
41                               Here, we found CNTFRalpha was overexpressed in lower grade gliomas (LGG
42 ) CNTFRalpha was shown to restore functional CNTFRalpha in human corneal endothelial (CE) cells that
43 reshly dissected explant demonstrated higher CNTFRalpha levels than controls (100% vs. 142% +/- 15%;
44 lectively, these data suggest that the human CNTFRalpha gene could represent the first identified neu
45                 CNTFRalpha immunoreactivity (CNTFRalpha-IR) was observed in the somata and dendrites
46 t, a sex difference in the SNB was absent in CNTFRalpha -/- animals: male mice lacking a functional C
47                       In return, TR2 induced CNTFRalpha transcriptional activity through binding to a
48 xidative stress by a mechanism that involves CNTFRalpha and the formation of a 61-kDa CNTF/CNTFRalpha
49                  CE cells expressed a 53-kDa CNTFRalpha that, along with trace amounts of a 61-kDa CN
50 a that, along with trace amounts of a 61-kDa CNTFRalpha-IM, appeared concomitantly with the 25-kDa CN
51               CNTF-receptor complex members, CNTFRalpha, LIFRbeta and GP130, were increased in MS cor
52       To directly address the role of muscle CNTFRalpha, we selectively-depleted it in vivo by using
53                     However, the same muscle CNTFRalpha depletion unexpectedly had no detected effect
54 rograde tracing of MNs indicated that muscle CNTFRalpha contributes to MN axonal regeneration across
55 Walking track analysis indicated that muscle CNTFRalpha is also required for normal recovery of motor
56        Together the data suggest that muscle CNTFRalpha may contribute to neuromuscular maintenance,
57                            Therefore, muscle CNTFRalpha is an interesting new example of a muscle gro
58                Interestingly, combination of CNTFRalpha methylation and IDH mutation significantly (p
59 NTF receptor tripartite complex comprised of CNTFRalpha, LIF receptor, and gp130.
60                               The density of CNTFRalpha-IR in neuropil also tended to be highest in i
61  reveals significant regional differences of CNTFRalpha protein expression between chick and mammals.
62 viously found that adult onset disruption of CNTFRalpha in facial MNs of "floxed CNTFRalpha" mice by
63                 The cellular distribution of CNTFRalpha in the canine retina was studied by in situ h
64 d CLF can account for many of the effects of CNTFRalpha on developing motoneurons.
65               We conclude that expression of CNTFRalpha protein is androgen-regulated in spinal moton
66 nsferase demonstrated that the 5th intron of CNTFRalpha has an enhancer activity which could be induc
67                  Despite decreased levels of CNTFRalpha expression in fully differentiated 3T3-L1 adi
68 vo resulted in modest decreases in levels of CNTFRalpha mRNA and protein in skeletal muscle.
69             It is suggested that the loss of CNTFRalpha from axons renders RGCs unresponsive to CNTF,
70         However, the molecular mechanisms of CNTFRalpha regulation and its clinical significance in g
71              Importantly, DNA methylation of CNTFRalpha might serve as a potential epigenetic therano
72 ndent of IDH mutation status, methylation of CNTFRalpha was significantly correlated with down-regula
73 ine the expression and hormone regulation of CNTFRalpha protein in the spinal nucleus of the bulbocav
74                     Furthermore, the role of CNTFRalpha in glioma proliferation and apoptosis through
75               Interestingly, two variants of CNTFRalpha, 69 and 65 kD, were identified by immunoblott
76 le Cre gene construct to produce adult-onset CNTFRalpha disruption in facial MNs without the traumati
77 oneurons, was not affected in either CNTF or CNTFRalpha knockout males.
78          An acute blockade of trkB, trkC, or CNTFRalpha prevented the androgenic sparing of SNB moton
79 over, blockade of the CNTF-specific receptor CNTFRalpha induced sensory nerve degeneration and retard
80  ciliary neurotrophic factor alpha-receptor (CNTFRalpha) is required for motoneuron survival during d
81                Although CNTF alpha-receptor (CNTFRalpha) mRNA and protein are localized predominantly
82 -binding alpha-subunit of the CNTF receptor (CNTFRalpha) is expressed in a variety of neuronal popula
83 -binding alpha-subunit of the CNTF receptor (CNTFRalpha) is released from injured tissues.
84 f or the alpha-subunit of the CNTF receptor (CNTFRalpha) to assess whether CNTF and/or its receptors
85     CE ciliary neurotrophic factor receptor (CNTFRalpha) and CNTF (0.83 nM) responsiveness in connexi
86 of the ciliary neurotrophic factor receptor (CNTFRalpha) gene for the human TR4 orphan receptor (TR4)
87          The localization of CNTF receptors (CNTFRalpha) to the sarcolemma in C57BL/6, ob/ob and db/d
88 significantly correlated with down-regulated CNTFRalpha gene expression and longer LGG patient surviv
89                               In the retina, CNTFRalpha was highly expressed by photoreceptors, but b
90             Here, the recombinant human (rh) CNTFRalpha was shown to restore functional CNTFRalpha in
91                  Here we show that this same CNTFRalpha depletion does not affect ChAT labeling in no
92                                      Soluble CNTFRalpha also partially restored the branching of diab
93  neurotrophic factor receptor alpha subunit (CNTFRalpha) and CNTF play important roles in neuron surv
94        CNTF and CNTF receptor alpha subunit (CNTFRalpha) in CE cells and cell-conditioned medium (H2O
95              These findings demonstrate that CNTFRalpha is expressed by rods and cones in the normal
96 n inhibitor (CGX) of molecules that bind the CNTFRalpha, which is required for CNTF signaling, did no
97 rmatics analysis revealed a CpG shore of the CNTFRalpha gene regulated its mRNA expression in TCGA da
98 rtantly, in mice lacking the LIFRbeta or the CNTFRalpha there is a significant loss of MNs during emb
99 ports subsets of axial motor neurons through CNTFRalpha; and Artemin acts as the first survival facto
100 ct photoreceptor rescue effect by binding to CNTFRalpha in these cells.
101                             CLC/CLF binds to CNTFRalpha and enhances the survival of developing moton
102 demonstrated that hypomethylation leading to CNTFRalpha up-regulation, together with autocrine expres
103                      The MNs survive without CNTFRalpha, even when challenged by facial nerve crush o

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