ライフサイエンスコーパス: COUP-TFI

1 COUP-TFI expression in cortex, and in ventral telencepha

2 COUP-TFI is expressed mainly in the nervous system, and

3 in upstream promoter-transcription factor 1 (COUP-TFI), plays a critical role in glial cell developme

4 orphan/nuclear receptors, ERRalpha-1, EAR-2, COUP-TFI (EAR-3), and RARgamma, bind to the silencer (S1

5 Since EAR-2, COUP-TFI, and RARgamma are expressed at high levels, it

6 In this study, the interaction of EAR-2, COUP-TFI, and RARgamma with S1 was confirmed by DNA mobi

7 ymal cell line was stably transfected with a COUP-TFI expression vector.

8 that members of the ETS family can activate COUP-TFI gene expression.

9 In addition, COUP-TFI and CHL1 exhibit dynamic expression patterns th

10 In addition, COUP-TFI is coexpressed with some ETS factors in the mou

11 receptors including RORalpha2, RORgamma and COUP-TFI are also potentiated by CaMKIV.

12 ed intron-binding proteins from rat brain as COUP-TFI, EAR2, and NURR1.

13 s missense mutations in NR2F1, also known as COUP-TFI, or deletions encompassing NR2F1.

14 DBC1 stabilized the interaction between COUP-TFI and NCoR by interacting directly with both prot

15 activation of the NGFI-A promoter induced by COUP-TFI.

16 tein 8) was identified as being repressed by COUP-TFI in a manner that required several of the compon

17 these three mechanisms of transactivation by COUP-TFI.

18 xpression of GRIP1 or SRC-1 does not convert COUP-TFI from a transcriptional repressor into a transcr

19 Also, endogenous EAR2 and EAR3/COUP-TFI from JAR cell and human testis and TR4 from tes

20 yses in CV-1 cells showed that EAR2 and EAR3/COUP-TFI repressed the hLHR promoter activity by up to 7

21 d three nuclear orphan receptors, EAR2, EAR3/COUP-TFI, and TR4.

22 was reversed by coexpression of EAR2 or EAR3/COUP-TFI, indicating their competitive binding for this

23 ons of the four transcription factors, Emx2, COUP-TFI, Pax6, and Sp8, thus far implicated in arealiza

24 min upstream promoter transcription factors (COUP-TFI and II), is initially activated in the cardiac

25 Four transcription factors, COUP-TFI, Emx2, Pax6, and Sp8, with graded expression ac

26 ly, our studies highlight a central role for COUP-TFI in the induction of the TNFAIP8 promoter by TNF

27 t cancer cells with an expression vector for COUP-TFI resulted in a dose-dependent inhibition of E2-i

28 k ovalbumin upstream transcription factor I (COUP-TFI) and close homolog of L1 (CHL1), have been clon

29 in upstream promoter transcription factor I (COUP-TFI) plays key roles in development and homeostasis

30 in upstream promotor-transcription factor I (COUP-TFI), an orphan member of the nuclear receptor supe

31 in upstream promoter transcription factor I (COUP-TFI), apolipoprotein regulatory protein 1 (ARP-1) a

32 in upstream promoter-transcription factor I (COUP-TFI, or NR2F1) is an orphan nuclear receptor that p

33 We identified COUP-TFI and -TFII as factors that bind to the TGF-beta-

34 In this study, we identified COUP-TFI as a regulatory factor for early neocortical re

35 ter increase in hair cell differentiation in COUP-TFI(-/-) cochlear cultures than in wild-type cultur

36 h regulation of hair cell differentiation in COUP-TFI(-/-) mice and confirmed misregulation of Notch

37 air cell and support cell differentiation in COUP-TFI(-/-) mice, and suggest that COUP-TFI is require

38 poptotic protein DBC1 was also identified in COUP-TFI complexes.

39 a hypersensitivity to Notch inactivation in COUP-TFI(-/-) cochlea, particularly at the apical turn.

40 duced thalamocortical projection reported in COUP-TFI knock-out mice.

41 tions between the cortex and the thalamus in COUP-TFI null mice indicate COUP-TFI plays a critical ro

42 nuclear receptors, which minimally includes COUP-TFI and ARP1, are highly expressed in brain and are

43 the thalamus in COUP-TFI null mice indicate COUP-TFI plays a critical role in regulating early regio

44 The COUP-TFI knockout (COUP-TFI(-/-)) has a significant increase in hair cell (

45 t for the first time that COUP-TFII, but not COUP-TFI, is reduced in three antiestrogen/TAM-R cell li

46 Together, these studies identify a novel COUP-TFI complex that functions as a repressor of transc

47 t GRIP1 and SRC-1 potentiate the activity of COUP-TFI and that COUP-TFI associates with these coactiv

48 Phenotype analysis of COUP-TFI and COUP-TFII single-gene conditional knockout

49 nverse correlation between the expression of COUP-TFI and that of aromatase in breast tumor tissue.

50 NA and protein levels upon overexpression of COUP-TFI in these cells.

51 e spatial and temporal expression pattern of COUP-TFI suggested a role in specification of the neocor

52 Here we show that the same region of COUP-TFI, located between amino acids 184 and 423, is in

53 of-function, that high levels of postmitotic COUP-TFI (Nr2f1) expression are necessary and sufficient

54 Postnatally, COUP-TFI is most prominently expressed in layer 4, in bo

55 The orphan nuclear receptor COUP-TFI (Nr2f1) regulates many aspects of mammalian dev

56 this screen as the orphan nuclear receptors COUP-TFI and COUP-TFII.

57 Here we tested the hypothesis that reduced COUP-TFI and COUP-TFII correlate with TAM resistance.

58 However, in eye-specific COUP-TFI/TFII double-knockout mice, progenitor cells at

59 These results also substantiate COUP-TFI as an important regulator of neuronal developme

60 potentiate the activity of COUP-TFI and that COUP-TFI associates with these coactivators in vivo usin

61 Furthermore, we demonstrate that COUP-TFI null mutant mice exhibit delayed axon myelinati

62 ffinity purification procedure revealed that COUP-TFI associated with a number of transcriptional reg

63 In vitro experiments revealed that COUP-TFI interacted directly with NCoR but in a manner d

64 Here, we show that COUP-TFI (Nr2f1) and COUP-TFII (Nr2f2) are highly expres

65 Our results substantiate that COUP-TFI, an intrinsic factor, may work in concert with

66 Taken together, these results suggest that COUP-TFI is an important regulator of oligodendrocyte di

67 tion in COUP-TFI(-/-) mice, and suggest that COUP-TFI is required for Notch regulation of hair cell a

68 tion and transfection analysis suggests that COUP-TFI acts as an upstream regulator of SCIP/Oct-6/Tst

69 The COUP-TFI knockout (COUP-TFI(-/-)) has a significant incr

70 here that three ETS response elements in the COUP-TFI promoter mediate its transcription.

71 ates a defect of convergent-extension in the COUP-TFI(-/-) duct.

72 In addition, excess proliferation in the COUP-TFI(-/-) sensory epithelium indicates that the orig

73 red several of the component proteins of the COUP-TFI complex.

74 hat other ETS factors also transactivate the COUP-TFI promoter.