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1 ents (gp130 and LIFR beta) of the tripartite CNTF receptor.
2 lpha) is the ligand-binding component of the CNTF receptor.
3 lf is not the only endogenous ligand for the CNTF receptor.
4 lly characterize cells containing functional CNTF receptors.
5 ne therapy remained unchanged after deleting CNTF receptor alpha (CNTFRa) in retinal ganglion cells (
7 nd adult-onset conditional disruption of the CNTF receptor alpha (CNTFRalpha) gene to directly examin
8 ohistochemistry to analyze the expression of CNTF receptor alpha (CNTFRalpha) in mouse retina and opt
9 signaling in SVZ NSP cells, with a "floxed" CNTF receptor alpha (CNTFRalpha) mouse line and a gene c
10 ns and leads to behavioural recovery through CNTF receptor alpha (CNTFRalpha) on nigral dopamine neur
11 as the rat ages there is significantly less CNTF receptor alpha (CNTFRalpha) protein in the uninjure
14 ibody targeted to the gp130 component of the CNTF receptor) and AG490 (an inhibitor of the JAK/STAT p
17 s cells via the non-signaling alpha-receptor CNTF receptor (CNTFR) and the two signaling beta-recepto
18 als, the ligand-binding alpha-subunit of the CNTF receptor (CNTFRalpha) is expressed in a variety of
19 w that the CNTF-binding alpha-subunit of the CNTF receptor (CNTFRalpha) is released from injured tiss
20 ther CNTF itself or the alpha-subunit of the CNTF receptor (CNTFRalpha) to assess whether CNTF and/or
22 rate that the expression of two of the three CNTF receptor complex components, CNTFRalpha and LIFR, d
23 rt the idea that a ligand for the tripartite CNTF receptor complex plays a role in ENS development.
24 on fat cells, we examined the expression of CNTF receptor complex proteins (LIFR, gp130, and CNTFRal
27 TF receptor alpha (CNTFRalpha), an essential CNTF receptor component, is greatly increased in skeleta
28 es miR-383-5p levels, which then disinhibits CNTF receptor components to sensitize neurons to the lig
29 observed that protein levels of CNTF and the CNTF receptor components were increased in the SON and N
31 irectly targets ciliary neurotrophic factor (CNTF) receptor components, and miR-383-5p inhibition sen
33 amine the in vivo roles played by endogenous CNTF receptors in adult motor neuron survival and ChAT m
34 ervations suggest that signaling through the CNTF receptor is involved in sexually dimorphic developm
39 FRalpha, the ligand-binding component of the CNTF-receptor multiprotein complex, which can function a
41 at, although neither motor neuron nor muscle CNTF receptors play a significant, nonredundant role in
42 d motor neurons, indicating that these adult CNTF receptors play no essential survival role in this m
46 ion with our previous study, that endogenous CNTF receptor signaling can protect MNs against toxic in
48 Together, the data suggest that endogenous CNTF receptor signaling in type B stem cells inhibits ad
50 that endogenous ciliary neurotrophic factor (CNTF) receptor signaling may inhibit neuronal differenti
51 sted that functional differences in the CNTF/CNTF receptor system between chicks and mammals exist.
52 tural features with CNTF and signals via the CNTF receptor tripartite complex comprised of CNTFRalpha