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1                                              LIFR beta was expressed by more cells than CNTFR alpha;
2                                              LIFR is downregulated in human breast carcinomas and inv
3                                              LIFR is frequently downregulated in HCC.
4                                              LIFR upregulation is associated with SUCLG2, which incre
5                                              LIFR was localized on RGCs and Muller cells in normal an
6          While GIO-6 signals via gp130:IL-6R:LIFR and gp130:IL-6R:OSMR complexes, GIL-6 selectively a
7 ciliary neurotrophic factor (CNTF) bind to a LIFR.gp130 receptor complex to activate Jak/signal trans
8             In this investigation, we used a LIFR antagonist to help resolve signaling responses and
9 r leukemia inhibitory factor receptor alpha (LIFR) were used to identify signaling molecules and regi
10 tification of 3a as a potent FXR agonist and LIFR antagonist with excellent ADME properties.
11 and immune proteins (e.g., PD-L1, CCL28, and LIFR).
12 ormancy phenotype in breast cancer cells and LIFR loss is correlated with poor patient survival.
13  receptor complex components, CNTFRalpha and LIFR, decreases during adipocyte differentiation.
14 (CNTER alpha) and beta components (gp130 and LIFR beta) of the tripartite CNTF receptor.
15      Since adipocytes express both gp130 and LIFR proteins and are responsive to other IL-6 family cy
16       Our results demonstrate that gp130 and LIFR stimulate MAPK activity through box 3-independent m
17 th reduced phosphorylation of both gp130 and LIFR.
18 s, including TNC, PTPRZ1, FAM107A, HOPX, and LIFR.
19  of human NPC biopsies revealed that LIF and LIFR were overexpressed in tumor cells and that LIF expr
20 oop enhanced OSM's interaction with OSMR and LIFR as shown by kinetic and equilibrium binding analysi
21 etent cytoplasmic domain regions of OSMR and LIFR were defined by the analysis of progressive carboxy
22                                         Anti-LIFR or anti-gp130 antibodies immunoprecipitated the 100
23 which is essential for OSM's binding to both LIFR and OSMR.
24                    In contrast, signaling by LIFR did not display the same requirement for receptor d
25            Similarly, expression of chimeric LIFR constructs lacking box 3 maximally stimulated MAPK
26 ification of compound 2o as a first-in-class LIFR/GPBAR1 modulator that reverses liver fibrosis in vi
27 n the expression of the LIF receptor complex LIFR/IL6ST (gp130).
28 xon detected in JEG-3 cells failed to detect LIFR transcripts.
29 radien-3,17-dione derivatives acting as dual LIFR inhibitors and GPBAR1 agonists.
30 des a mechanism whereby ADT upregulates EGFR-LIFR signaling that activates SUCLG2, which subsequently
31                                     Finally, LIFR deficiency rescues the SOCS3-deficient placental de
32 or complexes, whereas the trimeric LIF-GP130-LIFR complex remained stable through an additional membr
33 onsisting of CNTFR.gp130.LIFR or IL-6R.gp130.LIFR, respectively.
34 nduced STAT3 phosphorylation via IL-6R.gp130.LIFR.
35 kine selectively signals via the CNTFR.gp130.LIFR complex, albeit with a much lower affinity compared
36  CNTF-dependent proliferation of CNTFR.gp130.LIFR expressing cells indicated that only CV-1 was as bi
37 receptor complexes consisting of CNTFR.gp130.LIFR or IL-6R.gp130.LIFR, respectively.
38 on and STAT3 phosphorylation via CNTFR.gp130.LIFR, only CV-3 induced STAT3 phosphorylation via IL-6R.
39  phosphorylation and activation of the gp130.LIFR combination, but the gp130.OSMRbeta complex is acti
40                       The formation of gp130/LIFR complex triggers the auto/trans-phosphorylation of
41 ras that specifically target the IL-6R:gp130:LIFR complex.
42  from CNTF to activate cells via IL-6R:gp130:LIFR complexes.
43 L-6 as the first truly selective IL-6R:gp130:LIFR cytokine, whereas GIO-6 is a CNTF-free alternative
44  GIL-6 selectively activates the IL-6R:gp130:LIFR receptor complex.
45 features, characterized by a low LIF, a high LIFR/OSMR ratio, and high MYC expression.
46 criptional induction, thus leading to a high LIFR/OSMR ratio.
47 ication of an enhancer in a functional human LIFR gene promoter and alternative promoter usage by thi
48 placenta-specific enhancer activity in human LIFR gene.
49 emonstrate a complex regulation of the human LIFR gene, including alternative promoter usage and tiss
50 ied compound 3a as the first-in-class hybrid LIFR inhibitor and FXR agonist that protects against the
51                      These findings identify LIFR as a metastasis suppressor that functions through t
52                                  We identify LIFR as the receptor for ILEI, which mediates signaling
53 h factor receptor genes (EGFR, FGFR1, IGF1R, LIFR, and NGFR) also showed recurrent gains, and these w
54 nt ability to repress new targets, including LIFR, a well-characterized metastasis suppressor.
55 rs from HDACi-treated patients had increased LIFR levels and reduced proliferation rates compared to
56 ls for breast cancer, epigenetically induced LIFR and activated a pro-dormancy program in breast canc
57 re augmented in newly generated mice lacking LIFR in either CD11c(+) or hematopoietic cells.
58 itive feedback loop involving autocrine LIF, LIFR, and STAT4 drove sustained IL-6 transcription.
59                            The mRNAs for LIF/LIFR, IL-6/IL-6R, and their common signal-transduction m
60 itial finding to discover a role for the LIF/LIFR/mTORC1 signaling axis in NPC tumor cell growth as w
61 lls via VEGF-A:VEGFR2, CXCL12:CXCR4, and LIF:LIFR pathways.
62 CC patient-derived xenograft tumors with low LIFR expression and high LCN2 expression.
63                                     Notably, LIFR, an immune receptor that enhanced IL-6 transcriptio
64                      The apparent absence of LIFR explains why other gp130 binding cytokines do not a
65 SM with gp130 and OSMRbeta, co-activation of LIFR and OSMR resulted in a predominant LIF-like respons
66 arrow DC progenitor expressed low amounts of LIFR and developed into pDCs less efficiently after bein
67 ccurs as a result of specific degradation of LIFR via a lysosome-mediated pathway.
68 ytes would promote the beneficial effects of LIFR signaling in limiting demyelination.
69 ys post-OBX, when up-regulated expression of LIFR also was detected on globose basal cells (GBCs), a
70 ing cells showed reestablished expression of LIFR protein and function.
71 the transient up-regulation of expression of LIFR, IL-6, and IL-6R in ensheathing cells by 3 days pos
72          Hepatocyte-specific inactivation of LIFR accelerated NASH progression in mice, supporting an
73 er, which coincides with decreased levels of LIFR at the plasma membrane.
74                     Mechanistically, loss of LIFR activates NF-kB signaling through SHP1, leading to
75                          Conversely, loss of LIFR in nonmetastatic breast cancer cells induces migrat
76 CNTF induced the tyrosine phosphorylation of LIFR and gp130, as well as of proteins with the molecula
77 ngs demonstrate the therapeutic potential of LIFR/GPBAR1 hybrid molecules in human fibrotic disorders
78 establish SOCS3 as an essential regulator of LIFR signaling in trophoblast differentiation.
79                  Reduction of either ILEI or LIFR protein levels results in reduced tumor growth, few
80 ) that interacts with its receptors (OSMR or LIFR) in complex with GP130 on glioblastoma cells and ac
81 y specimens poorly expressed LIF, precluding LIFR lysosomal degradation and OSMR transcriptional indu
82 xpression of CNTF receptor complex proteins (LIFR, gp130, and CNTFRalpha) during adipocyte differenti
83  either leukemia inhibitory factor receptor (LIFR) (type I) or oncostatin M receptor (OSMR) (type II)
84 (gp130)/leukemia inhibitory factor receptor (LIFR) alpha and gp130/OSM receptor beta (OSMRbeta).
85 imer of leukemia inhibitory factor receptor (LIFR) and gp130.
86 dentify leukemia inhibitory factor receptor (LIFR) as a breast cancer metastasis suppressor downstrea
87 e human leukemia inhibitory factor receptor (LIFR) gene and now show detailed characterization of the
88  of the leukemia inhibitory factor receptor (LIFR) gene results in disrupted placental architecture,
89 e gp130/leukemia inhibitory factor receptor (LIFR) heterodimer.
90         Leukemia inhibitory factor receptor (LIFR) promotes a dormancy phenotype in breast cancer cel
91  (EGFR)-leukemia inhibitory factor receptor (LIFR) signaling induced SUCLG2 expression in prostate ca
92 tion of leukemia inhibitory factor receptor (LIFR) signaling is a candidate therapeutic strategy for
93 ha) and leukemia inhibitory factor receptor (LIFR) was studied in normal, 6-h, 1-, and 3-day optic ne
94 vels of leukemia inhibitory factor receptor (LIFR), a subunit of the receptor complex for CLCF1, were
95 on with Leukemia Inhibitory Factor receptor (LIFR), type II OSM receptor complex is composed of gp130
96 ess the leukemia inhibitory factor receptor (LIFR), which promotes fibrosis, and a bile acid-activate
97 ect the leukemia inhibitory factor receptor (LIFR).
98 30) and leukemia inhibitory factor receptor (LIFR).
99 and the leukemia inhibitory factor receptor (LIFR).
100 ypes I [leukemia inhibitory factor receptor (LIFR)] and II [OSM receptor (OSMR)] receptors, high STAT
101 ia inhibitory factor (LIF) and its receptor (LIFR) and interleukin 6 (IL-6) and its receptor (IL-6R)
102 ter fibroblast activation, and LIF receptor (LIFR) and STAT4 formed a molecular complex that, togethe
103 TF, and CT-1) also utilize the LIF receptor (LIFR) as a component of their receptor complex.
104  differentiation in vitro, and LIF receptor (LIFR) deficiency results in loss of giant cell different
105 that the reduced expression of LIF receptor (LIFR) observed in hepatoma cells is mediated by altered
106 or (a heterodimer of gp130 and LIF receptor (LIFR)) and the OSM-specific receptor (a heterodimer of g
107 mLIF) act in mouse cells via a LIF receptor (LIFR)-glycoprotein 130 (gp130) heterodimer.
108 red with healthy pancreas, but its receptors LIFR and gp130 were expressed only in intratumoral nerve
109                                    Restoring LIFR expression in highly malignant tumor cells suppress
110 undergo epigenetic alterations that suppress LIFR gene expression and modify the responsiveness to th
111                                          The LIFR is upregulated by nuclear EGFR, which acts as a tra
112 o induce ligand-dependent degradation of the LIFR, in a proteasome-independent manner, which coincide
113 scriptional regulator, directly binds to the LIFR promoter, and drives NE differentiation and glycoly
114       In GIL-6 and GIO-6, we transferred the LIFR binding site from LIF or OSM to IL-6, respectively.
115 ntensity of nuclear EGFR associated with the LIFR and SUCLG2 in castration-resistant prostate cancer
116 the framework of interleukin (IL-)6 with the LIFR-binding site from CNTF to activate cells via IL-6R:
117 d remethylation of the CpG island within the LIFR promoter that is active in normal liver cells corre
118                                         This LIFR.gp130 complex is also a functional receptor for LIF
119 units, but only human OSM also acted through LIFR.
120 itor cells, some of which is attributable to LIFR signaling.
121 oximately 1,000 nonmetastatic breast tumors, LIFR expression status correlated with metastasis-free,
122                However, in other cell types, LIFR signaling is under tight negative regulation by the
123  of cytokine receptor action exists in which LIFR ranks as dominant member.

 
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