ライフサイエンスコーパス: LIFR

1 LIFR beta was expressed by more cells than CNTFR alpha;

2 LIFR is downregulated in human breast carcinomas and inv

3 LIFR was localized on RGCs and Muller cells in normal an

4 ciliary neurotrophic factor (CNTF) bind to a LIFR.gp130 receptor complex to activate Jak/signal trans

5 In this investigation, we used a LIFR antagonist to help resolve signaling responses and

6 r leukemia inhibitory factor receptor alpha (LIFR) were used to identify signaling molecules and regi

7 receptor complex components, CNTFRalpha and LIFR, decreases during adipocyte differentiation.

8 (CNTER alpha) and beta components (gp130 and LIFR beta) of the tripartite CNTF receptor.

9 Since adipocytes express both gp130 and LIFR proteins and are responsive to other IL-6 family cy

10 Our results demonstrate that gp130 and LIFR stimulate MAPK activity through box 3-independent m

11 th reduced phosphorylation of both gp130 and LIFR.

12 s, including TNC, PTPRZ1, FAM107A, HOPX, and LIFR.

13 of human NPC biopsies revealed that LIF and LIFR were overexpressed in tumor cells and that LIF expr

14 oop enhanced OSM's interaction with OSMR and LIFR as shown by kinetic and equilibrium binding analysi

15 etent cytoplasmic domain regions of OSMR and LIFR were defined by the analysis of progressive carboxy

16 Anti-LIFR or anti-gp130 antibodies immunoprecipitated the 100

17 which is essential for OSM's binding to both LIFR and OSMR.

18 In contrast, signaling by LIFR did not display the same requirement for receptor d

19 Similarly, expression of chimeric LIFR constructs lacking box 3 maximally stimulated MAPK

20 n the expression of the LIF receptor complex LIFR/IL6ST (gp130).

21 xon detected in JEG-3 cells failed to detect LIFR transcripts.

22 Finally, LIFR deficiency rescues the SOCS3-deficient placental de

23 onsisting of CNTFR.gp130.LIFR or IL-6R.gp130.LIFR, respectively.

24 nduced STAT3 phosphorylation via IL-6R.gp130.LIFR.

25 kine selectively signals via the CNTFR.gp130.LIFR complex, albeit with a much lower affinity compared

26 CNTF-dependent proliferation of CNTFR.gp130.LIFR expressing cells indicated that only CV-1 was as bi

27 receptor complexes consisting of CNTFR.gp130.LIFR or IL-6R.gp130.LIFR, respectively.

28 on and STAT3 phosphorylation via CNTFR.gp130.LIFR, only CV-3 induced STAT3 phosphorylation via IL-6R.

29 phosphorylation and activation of the gp130.LIFR combination, but the gp130.OSMRbeta complex is acti

30 The formation of gp130/LIFR complex triggers the auto/trans-phosphorylation of

31 features, characterized by a low LIF, a high LIFR/OSMR ratio, and high MYC expression.

32 criptional induction, thus leading to a high LIFR/OSMR ratio.

33 ication of an enhancer in a functional human LIFR gene promoter and alternative promoter usage by thi

34 placenta-specific enhancer activity in human LIFR gene.

35 emonstrate a complex regulation of the human LIFR gene, including alternative promoter usage and tiss

36 These findings identify LIFR as a metastasis suppressor that functions through t

37 h factor receptor genes (EGFR, FGFR1, IGF1R, LIFR, and NGFR) also showed recurrent gains, and these w

38 nt ability to repress new targets, including LIFR, a well-characterized metastasis suppressor.

39 itive feedback loop involving autocrine LIF, LIFR, and STAT4 drove sustained IL-6 transcription.

40 The mRNAs for LIF/LIFR, IL-6/IL-6R, and their common signal-transduction m

41 itial finding to discover a role for the LIF/LIFR/mTORC1 signaling axis in NPC tumor cell growth as w

42 The apparent absence of LIFR explains why other gp130 binding cytokines do not a

43 SM with gp130 and OSMRbeta, co-activation of LIFR and OSMR resulted in a predominant LIF-like respons

44 ccurs as a result of specific degradation of LIFR via a lysosome-mediated pathway.

45 ytes would promote the beneficial effects of LIFR signaling in limiting demyelination.

46 ys post-OBX, when up-regulated expression of LIFR also was detected on globose basal cells (GBCs), a

47 ing cells showed reestablished expression of LIFR protein and function.

48 the transient up-regulation of expression of LIFR, IL-6, and IL-6R in ensheathing cells by 3 days pos

49 er, which coincides with decreased levels of LIFR at the plasma membrane.

50 Conversely, loss of LIFR in nonmetastatic breast cancer cells induces migrat

51 CNTF induced the tyrosine phosphorylation of LIFR and gp130, as well as of proteins with the molecula

52 establish SOCS3 as an essential regulator of LIFR signaling in trophoblast differentiation.

53 y specimens poorly expressed LIF, precluding LIFR lysosomal degradation and OSMR transcriptional indu

54 xpression of CNTF receptor complex proteins (LIFR, gp130, and CNTFRalpha) during adipocyte differenti

55 either leukemia inhibitory factor receptor (LIFR) (type I) or oncostatin M receptor (OSMR) (type II)

56 (gp130)/leukemia inhibitory factor receptor (LIFR) alpha and gp130/OSM receptor beta (OSMRbeta).

57 imer of leukemia inhibitory factor receptor (LIFR) and gp130.

58 dentify leukemia inhibitory factor receptor (LIFR) as a breast cancer metastasis suppressor downstrea

59 e human leukemia inhibitory factor receptor (LIFR) gene and now show detailed characterization of the

60 of the leukemia inhibitory factor receptor (LIFR) gene results in disrupted placental architecture,

61 e gp130/leukemia inhibitory factor receptor (LIFR) heterodimer.

62 tion of leukemia inhibitory factor receptor (LIFR) signaling is a candidate therapeutic strategy for

63 ha) and leukemia inhibitory factor receptor (LIFR) was studied in normal, 6-h, 1-, and 3-day optic ne

64 ect the leukemia inhibitory factor receptor (LIFR).

65 ypes I [leukemia inhibitory factor receptor (LIFR)] and II [OSM receptor (OSMR)] receptors, high STAT

66 ia inhibitory factor (LIF) and its receptor (LIFR) and interleukin 6 (IL-6) and its receptor (IL-6R)

67 ter fibroblast activation, and LIF receptor (LIFR) and STAT4 formed a molecular complex that, togethe

68 TF, and CT-1) also utilize the LIF receptor (LIFR) as a component of their receptor complex.

69 differentiation in vitro, and LIF receptor (LIFR) deficiency results in loss of giant cell different

70 that the reduced expression of LIF receptor (LIFR) observed in hepatoma cells is mediated by altered

71 or (a heterodimer of gp130 and LIF receptor (LIFR)) and the OSM-specific receptor (a heterodimer of g

72 mLIF) act in mouse cells via a LIF receptor (LIFR)-glycoprotein 130 (gp130) heterodimer.

73 red with healthy pancreas, but its receptors LIFR and gp130 were expressed only in intratumoral nerve

74 Restoring LIFR expression in highly malignant tumor cells suppress

75 undergo epigenetic alterations that suppress LIFR gene expression and modify the responsiveness to th

76 o induce ligand-dependent degradation of the LIFR, in a proteasome-independent manner, which coincide

77 d remethylation of the CpG island within the LIFR promoter that is active in normal liver cells corre

78 This LIFR.gp130 complex is also a functional receptor for LIF

79 units, but only human OSM also acted through LIFR.

80 itor cells, some of which is attributable to LIFR signaling.

81 oximately 1,000 nonmetastatic breast tumors, LIFR expression status correlated with metastasis-free,

82 However, in other cell types, LIFR signaling is under tight negative regulation by the

83 of cytokine receptor action exists in which LIFR ranks as dominant member.