ライフサイエンスコーパス: transcription factor AP-1

1 ascade, which is essential for activation of transcription factor AP-1.

2 ity, increased c-fos and c-jun mRNAs and the transcription factor AP-1.

3 olving the opioid-mediated activation of the transcription factor AP-1.

4 and the reporter activity of the downstream transcription factor AP-1.

5 ed by estrogen in a process dependent on the transcription factor AP-1.

6 f TREM-1 in mouse macrophages partly via the transcription factor AP-1.

7 cade involving jun N-terminal kinase and the transcription factor AP-1.

8 un and Nrf2, two components of the oncogenic transcription factor AP-1.

9 of interleukin (IL)-8 via activation of the transcription factor AP-1.

10 diated via the JNK signaling pathway and the transcription factor AP-1.

11 monstrated that Lys-des-Arg-BK activates the transcription factor AP-1.

12 zipper) with Jun family members to form the transcription factor AP-1.

13 ansducin and accompanied by induction of the transcription factor AP-1.

14 levels and suppression of activation of the transcription factor AP-1.

15 functions as a subunit of the heterodimeric transcription factor AP-1.

16 phatidylcholine hydrolysis and activates the transcription factor AP-1.

17 and stimulation of transcription mediated by transcription factor AP-1.

18 c-Jun forms as a heterodimer with c-Fos, the transcription factor AP-1.

19 ect on activation of another redox-sensitive transcription factor, AP-1.

20 N-terminal kinase, and of the Jun-containing transcription factor AP-1, a regulator of cellular stres

21 regulation of the best known immediate early transcription factor, AP-1; a heterodimer of the basic l

22 ho were involved in the shear stress-induced transcription factor AP-1 acting on the 12-O-tetradecano

23 Activation of the transcription factor AP-1 (activator protein-1) is requi

24 iated suppression of another CCL2-regulating transcription factor, AP-1 (activator protein-1).

25 Transcription factor AP-1 and alpha2beta1 integrin, whic

26 eptors includes up-regulation of the nuclear transcription factor AP-1 and AP-1 transcriptional activ

27 Lead activated the transcription factor AP-1 and increased AP-1-dependent l

28 cJun is a major component of the transcription factor AP-1 and mediates a diverse set of

29 aling pathways such as the activation of the transcription factor AP-1 and modulation of Wnt signalin

30 through an IL-11-dependent pathway involving transcription factor AP-1 and STAT3.

31 ) was down-regulation of the activity of the transcription factor AP-1 and subsequent coordinate redu

32 ephosphorylation of the c-Fos subunit of the transcription factor AP-1 and thereby inhibited TLR4-tri

33 G) ratios, and activation of stress-response transcription factors (AP-1 and NF-kappaB) were measured

34 el to DNA nucleated the concerted binding of transcription factors AP-1 and C/EBP beta to the 5'-regu

35 ces matching the consensus binding sites for transcription factors AP-1 and C/EBP.

36 Within minutes, low-dose UVB upregulated the transcription factors AP-1 and NF-kappa B, which are kno

37 antly inhibits both DA-induced activation of transcription factors AP-1 and NF-kappaB and subsequent

38 vents in the cell nucleus, the activation of transcription factors AP-1 and NF-kappaB by ultraviolet

39 The redox-sensitive transcription factors AP-1 and NF-kappaB have been impli

40 /TIMP-1 RNA abundance with activation of the transcription factors AP-1 and NF-kappaB in the lungs of

41 tumor necrosis factor (TNF-alpha) stimulate transcription factors AP-1 and NF-kappaB through activat

42 DNA binding of transcription factors AP-1 and NF-kappaB was not affecte

43 es such as c-jun and c-fos and activates the transcription factors AP-1 and NF-kappaB.

44 stitutive activation of the immunoregulatory transcription factors AP-1 and NF-kappaB.

45 optosis in vivo is mediated by activation of transcription factors AP-1 and NF-kappaB.

46 ctivation of c-Jun N-terminal kinase and the transcription factors AP-1 and NFAT but does not affect

47 emic area showed enhanced DNA binding of the transcription factors AP-1 and nuclear factor (NF)-kappa

48 we examine the role of the redox-responsive transcription factors AP-1 and nuclear factor-kappaB (NF

49 TNF-alpha messenger RNA (mRNA) levels and transcription factors AP-1 and nuclear factor-kappaB (NF

50 y we determined that inflammation responsive transcription factors AP-1 and SAF-1 synergistically reg

51 pounds that blocks the activation of two key transcription factors, AP-1 and NF-kappa B.

52 The transcription factors, AP-1 and nuclear factor kappaB (N

53 o found that NAC increased two IL-4 relevant transcription factors (AP-1) and NFATc.

54 of transcription, does not affect binding of transcription factor AP-1, and appears to involve a mech

55 tionally regulated by UV irradiation through transcription factor AP-1, and mediates altered collagen

56 ression through an AP-1 site and its cognate transcription factor AP-1, and requires the involvement

57 nts, inhibited the TNF-induced activation of transcription factor AP-1, and suppressed the TNF-induce

58 ivity, inhibition of DNA binding activity of transcription factor AP-1, and suppression of in vivo tr

59 al transduction, growth factors activate the transcription factor AP-1, and we show that this in turn

60 hat FGF-2 stimulates DNA binding activity of transcription factor AP-1 but not NF-kappaB and that AP-

61 ated protein kinase (MAP kinase) pathway and transcription factors (AP-1), but are toxic at high conc

62 ade specifically inhibited activation of the transcription factor AP-1 by TGF-beta1, whereas PD98059

63 lso suppressed TNF-induced activation of the transcription factor AP-1, c-jun N-terminal kinase and M

64 xhibit decreased DNA binding activity of the transcription factor, AP-1, compared with monocytes.

65 T(reg) cells downregulated expression of the transcription factor AP-1 complex and suppressed other T

66 The transcription factor AP-1, composed of Fos-Jun dimers, m

67 uch as Pin1 and Men1, that regulate the host transcription factor AP-1 controlling host inflammation,

68 regulated kinase, and p38, and activation of transcription factors AP-1, CREB, NF-kappaB, and STAT1 a

69 vated the binding of three oxidant-sensitive transcription factors: AP-1, CREB, and nuclear respirato

70 c-jun protein expression, and an increase in transcription factor AP-1 DNA binding activity.

71 were peripheral myelin protein 22, decorin, transcription factor AP-1, dystroglycan 1, myelin protei

72 clase Rutabaga, the Ig-CAM Fasciclin II, the transcription factor AP-1 (Fos/Jun), and the adhesion pr

73 ombin-induced CD44 expression is mediated by transcription factor AP-1 in a NADPH oxidase-dependent m

74 irradiation is mediated via induction of the transcription factor AP-1 in human skin fibroblasts.

75 nscription and mobilization of the mitogenic transcription factor, AP-1, in response to DOR1 signalin

76 n and functional assays, have implicated the transcription factor, AP-1, in the regulation of program

77 Because the transcription factor AP-1 is important for tumor promote

78 Transcription factor AP-1 is known to make specific cont

79 e transcriptional level, and that binding of transcription factor AP-1 is not affected.

80 In contrast, the transcription factor AP-1 is not required for activation

81 hat tumor promoter induced activation of the transcription factor AP-1 is required for induced neopla

82 iously reported that a JunD homodimer of the transcription factor AP-1 is specifically activated by T

83 As a transcription factor, AP-1 is commonly found as a hetero

84 on the integrity of NF-E2 recognition sites, transcription factor AP-1-like protein-binding motifs, l

85 on at the IFNB1 promoter through activity at transcription factor AP-1-like sites.

86 P) kinase pathway and the binding of nuclear transcription factors (AP-1, NF-kappaB, and C/EBP) and s

87 Consensus binding sequences for the transcription factors AP-1, NF-kappaB and Sp1 were modif

88 overexpression of Fra-1, a component of the transcription factor AP-1, offers prognostic potential.

89 omplex formed between NFAT and the mitogenic transcription factor AP-1 on the interleukin-2 enhancer.

90 racellular signal-regulated kinase), and the transcription factors AP-1 or NF-kappaB.

91 We demonstrate that HCV-induced transcription factors AP-1, Sp1, NF-kappaB and STAT-3 ar

92 n part by antagonizing the activities of the transcription factors AP-1, STAT and NF-kappaB.

93 exclude the inhibitory effect and shown that transcription factors AP-1, Stat5, and Creb cooperate in

94 chanism of action involves the activation of transcription factor AP-1 that turns on neuronal growth

95 We focus on the role of the transcription factor AP-1 to both induce the expression

96 Transcription factor AP-1 transduces environmental signa

97 Furthermore, transcription factor AP-1 was a main factor in IL-5-indu

98 The transcription factor AP-1 was involved in the down-regul

99 while antigen receptor-induced activation of transcription factor AP-1 was severely impaired.

100 T cell anergy, in which the activity of the transcription factor AP-1 was substantially diminished.F

101 TNF-induced activation of another nuclear transcription factor, AP-1, was suppressed by IL-13.

102 nduces cFos phosphorylation, stimulating the transcription factor AP-1, which in turn enhances transc

103 c-Jun is a component of the transcription factor AP-1, which is activated by a wide

104 The transcription factor AP-1, which is composed of Fos and

105 ated ras proteins are potent inducers of the transcription factor AP-1, which is composed of heterodi

106 Jun N-terminal kinase (JNK) regulates the transcription factor AP-1, which is implicated in the co

107 tive in the trnsactivational activity of the transcription factor, AP-1, which is required for optima

108 activity of As3+, we examined its effect on transcription factor AP-1, whose activity is stimulated