ライフサイエンスコーパス: NF-IL6

1 NF-IL6 is an important transcriptional regulator of gene

2 NF-IL6 is first detectable after 3 h of infection and co

3 NF-IL6 production could not be induced by UV-inactivated

4 NF-IL6 utilizes two distinct regions to bind to the hypo

5 NF-IL6-mediated transcriptional activation is enhanced 3

6 taining cytokine and hypoxia-sensitive AP-1, NF-IL6, and NF-kappaB sites, was insufficient for induct

7 ctors activating protein-1, serum protein-1, NF-IL6, or cyclic adenosine monophosphate responsive ele

8 (NFkappaB) and nuclear factor interleukin 6 (NF-IL6 or C/EBP) activation and bacteremia, inflammatory

9 on with the nuclear factor of interleukin 6 (NF-IL6, also known as CCAAT enhancer binding protein (C/

10 also known as nuclear factor-interleukin-6 (NF-IL6), is a transcription factor that plays an importa

11 ncer action of nuclear factor-interleukin-6 (NF-IL6).

12 ve human transcription factors: NFAT1, ALL1, NF-IL6, ESX, and HSF-1.

13 re, RARs and RXRs do not bind in vitro to an NF-IL6 binding site.

14 g of NF-kappaB; however, binding of AP-1 and NF-IL6 was inhibited.

15 g sites including AP-2, Sp1, CRE, PEA-3, and NF-IL6.

16 elements, IRF-1 located at -730 to -719, and NF-IL6 at -520 to -512, were also studied by deletion an

17 nt- binding protein, ICER IIgamma, ATF3, and NF-IL6 in hepatocytes.

18 tion via the cyclic AMP response element and NF-IL6 sites of the COX-2 promoter.

19 Interaction between HSF1 and NF-IL6 could thus be an important mechanism in HSF1 regu

20 tors ATF3, gadd153/Chop10, ICER IIgamma, and NF-IL6.

21 The NF-kappaB and NF-IL6 elements have previously been shown to play an im

22 on sites for factors including NF-kappaB and NF-IL6 involved in responses to various cytokine and hor

23 for the transcription factors NF-kappaB and NF-IL6.

24 tein (AP)-1, nuclear factor (NF)-kappaB, and NF-IL6 in respiratory syncytial virus (RSV)-induced inte

25 uced in activated monocytes/macrophages, and NF-IL6 is the only CCAAT/enhancer-binding protein (C/EBP

26 tivation of hepatic and splenic NFkappaB and NF-IL6 positively correlates with tissue cytokine mRNA e

27 ar factor (NF)-IL6/CREB, NFB1, NFkappaB, and NF-IL6], consistent with the activation of an upstream s

28 ation of transcriptional factors NF-kappa B, NF-IL6, cyclic adenosine monophosphate responsive elemen

29 e human homolog of chicken NF-M, C/EBP-beta (NF-IL6).

30 n a concentration-dependent decrease in both NF-IL6/CREB binding to the IL-1beta promoter and IL-1bet

31 ffect COX-2 promoter activity, mutating both NF-IL6 sites substantially inhibits COX-2 promoter activ

32 NF-IL6 and to the synergistic activation by NF-IL6 and Spi.1.

33 inhibitory to transcriptional activation by NF-IL6 and to the synergistic activation by NF-IL6 and S

34 uences in producing HIV-1 gene activation by NF-IL6.

35 ces in vitro and promoter transactivation by NF-IL6 in cells.

36 In HepG2 cells, NF-IL6 elicits a relatively low level of gene activation

37 Additionally, TAD-deficient NF-IL6 functions as a dominant negative for Spi-1-mediat

38 promoter (-59/+12) in the absence of direct NF-IL6 binding to DNA.

39 B and CCAAT/enhancer-binding protein (C/EBP; NF-IL6) sites in the IL-6 promoter are important for coo

40 In addition, the cytokine response elements (NF-IL6 binding sites) in opioid receptor genes are not f

41 ontain potential cytokine response elements (NF-IL6 binding sites).

42 t in the absence of NF-IL6 binding elements, NF-IL6 can elicit LTR-mediated gene expression in cotran

43 urkat) and hepatoma cells (HepG2), exogenous NF-IL6 can activate HIV-1 gene expression even in the ab

44 Spi-1 (also called PU.1) and the bZIP factor NF-IL6 (also called C/EBPbeta) have been shown to be inv

45 nds to the basic zipper transcription factor NF-IL6 required for activation of c-fms and IL-1beta.

46 f the immune regulatory transcription factor NF-IL6.

47 aptamers" targeting the transcription factor NF-IL6.

48 on by cytokine-induced transcription factor, NF-IL6, using a number of immune cell lines which respon

49 o interact with other transcription factors, NF-IL6 is involved in transcriptional regulation of a wi

50 ng was done to investigate the mechanism for NF-IL6 production.

51 ing the requirement of viral replication for NF-IL6 synthesis.

52 hancer binding protein recognition sites for NF-IL6.

53 Hepatic NF-IL6 activation was observed at 3, 4, and 6 hours afte

54 The HSF1/NF-IL6 interaction involves a sequence of HSF1 containin

55 of the transcription start site of the human NF-IL6 gene to evaluate the predictions of two computati

56 This manuscript identifies NF-IL6 as another transcription factor, in addition to A

57 fect of RSV infection on nuclear factor-IL6 (NF-IL6) expression, a human basic domain-leucine zipper-

58 or-kappa B (NF-kappa B), nuclear factor-IL6 (NF-IL6), cyclic adenosine monophosphate responsive eleme

59 tightly to the nuclear factor for human IL6 (NF-IL6), a basic leucine zipper transcription factor inv

60 nding sites show a virus-induced increase in NF-IL6-dependent transcription.

61 of RAR and RXR is obligatory for inhibiting NF-IL6 activity.

62 n the abundance or size of the single 1.8-kb NF-IL6 mRNA.

63 genes driven by either wild-type or mutated NF-IL6 binding sites show a virus-induced increase in NF

64 In these experiments, isolated NFkappaB, NF-IL6, and CRE promoter sites were less effective than

65 r-luciferase construct showed that NFkappaB, NF-IL6, and CRE promoter sites mediate gene transcriptio

66 tional regulatory factor NF-kappa B (but not NF-IL6, cyclic adenosine monophosphate responsive elemen

67 ences retain a significant fraction (42%) of NF-IL6 responsiveness in the absence of upstream regulat

68 HepG2 cells, we find that in the absence of NF-IL6 binding elements, NF-IL6 can elicit LTR-mediated

69 ction by antagonizing the enhancer action of NF-IL6, a basic domain leucine zipper transcription fact

70 mutant RB enhanced both binding activity of NF-IL6 to its cognate DNA sequences in vitro and promote

71 Furthermore, binding of NF-IL6 (C/EBPbeta) and c-Jun to the SPRR1A promoter was

72 cible mechanism for translational control of NF-IL6 synthesis and identify this transcription factor

73 ponsible, at least in part, for induction of NF-IL6 mRNA following activation of U937 promonocytic ce

74 The interdiction of NF-IL6-dependent signal transduction pathway by RARs may

75 549) synthesize a single 45.7-kDa isoform of NF-IL6 rapidly and in a time-dependent manner.

76 that synthetic retinoids with properties of NF-IL6 antagonism but lacking transactivation capabiliti

77 nd regulatory domains and the bZip region of NF-IL6.

78 enhancer binding protein beta (C/EBPbeta, or NF-IL6) is expressed in macrophages, where it participat

79 be the preferred transcription factor (over NF-IL6) for cooperative interaction with NF-kappaB in RS

80 There was robust NF-IL6 protein synthesis within RSV-infected (24 h) cell

81 the highest specificity in binding to target NF-IL6.

82 lix (wHTH) DNA binding domains, arguing that NF-IL6 vigorously activates the il1b core promoter via p

83 ive synthetic retinoids, we demonstrate that NF-IL6 antagonism and transactivation are separable func

84 We also show that NF-IL6 acts as a transcriptional enhancer of MRP-8, and

85 The NF-IL6 antagonism function of RAR is a complex of the co

86 The NF-IL6 site is also important for COX-2 transcription in

87 lso found that an ETS site (-75/-72) and the NF-IL6 site were responsible for COX-2 activity induced

88 stration of in vitro interaction between the NF-IL6 bZIP and Spi-1 winged helix-turn-helix (wHTH) DNA

89 Furthermore, the NF-IL6 transactivation domain (TAD) is functionally indi

90 However, the NF-IL6 gene is expressed in a variety of nonmyeloid cell

91 with increased C/EBP binding activity in the NF-IL6 site of EP4 promoter region and C/EBPbeta protein

92 romoters, showed that the Spi-1, but not the NF-IL6, binding site is absolutely required for function

93 ibutes independently to transcription of the NF-IL6 gene in U937 cells.

94 We show that increased transcription of the NF-IL6 gene is responsible, at least in part, for induct

95 fied a 104-bp minimal promoter region of the NF-IL6 gene that is sufficient for basal and activation-

96 Mutation of the NF-IL6 site had minimal effect in the presence of intact

97 romoter mapping experiments suggest that the NF-IL6 site in the COX-2 promoter is important for media

98 ition blocks IL-1beta-induced binding to the NF-IL6 element of the COX-2 promoter and inhibits transc

99 ot only the binding activity of C/EBP to the NF-IL6 site in the EP4 promoter, which was prevented by

100 Using the NF-IL6 transcription factor we show that the assay can d

101 In addition, even though NF-IL6 induces a relatively low gene activity from the b

102 Thus, NF-IL6 is a potential therapeutic target for the treatme

103 addition, HSF2 is not capable of binding to NF-IL6.

104 r the first time that HSF1 binds directly to NF-IL6 in vivo and antagonizes its activity.

105 ed for the responsiveness of Sp1 elements to NF-IL6 in this cellular background.

106 ion from the basal LTR elements; response to NF-IL6 is restored with either the Sp1 binding sequences

107 Although mutating the two NF-IL6 sites individually did not affect COX-2 promoter

108 umor antigen (T antigen)-binding domain with NF-IL6, a member of the CAAT/enhancer-binding protein (C