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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
16 elements, IRF-1 located at -730 to -719, and NF-IL6 at -520 to -512, were also studied by deletion an
22 on sites for factors including NF-kappaB and NF-IL6 involved in responses to various cytokine and hor
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
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
33 inhibitory to transcriptional activation by NF-IL6 and to the synergistic activation by NF-IL6 and S
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
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.
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
55 of the transcription start site of the human NF-IL6 gene to evaluate the predictions of two computati
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
63 genes driven by either wild-type or mutated NF-IL6 binding sites show a virus-induced increase in NF
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
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
76 that synthetic retinoids with properties of NF-IL6 antagonism but lacking transactivation capabiliti
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
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
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
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
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-
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
106 ion from the basal LTR elements; response to NF-IL6 is restored with either the Sp1 binding sequences
108 umor antigen (T antigen)-binding domain with NF-IL6, a member of the CAAT/enhancer-binding protein (C
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