scholarly journals Interleukin-6 induction by tumor necrosis factor and interleukin-1 in human fibroblasts involves activation of a nuclear factor binding to a kappa B-like sequence.

1990 ◽  
Vol 10 (7) ◽  
pp. 3818-3823 ◽  
Author(s):  
Y H Zhang ◽  
J X Lin ◽  
J Vilcek
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Human Fibroblasts ◽  
Nf Kappa B ◽  
Mobility Shift ◽  
Dnase I Footprinting ◽  
Chloramphenicol Acetyltransferase Gene ◽  
Necrosis Factor

Using variable-length deletion constructs of the 5'-flanking region of the human interleukin-6 (IL-6) gene linked to the chloramphenicol acetyltransferase gene, we showed that the region from positions -109 to -50 mediated the bulk of the response to tumor necrosis factor (TNF) or interleukin-1 (IL-1), while it was less responsive to forskolin. DNA mobility shift assays and DNase I footprinting analysis identified a nuclear protein from TNF- or IL-1-treated fibroblasts that bound to a region comprising a kappa B-like element located between positions -72 and -63 on the IL-6 gene. On the basis of these and other experiments, we conclude that TNF and IL-1 apparently activate IL-6 gene expression by closely related mechanisms involving activation of a NF-kappa B-like factor, whereas the pathway of IL-6 induction by forskolin is, in part, different.

Interleukin-6 induction by tumor necrosis factor and interleukin-1 in human fibroblasts involves activation of a nuclear factor binding to a kappa B-like sequence

1990 ◽  
Vol 10 (7) ◽  
pp. 3818-3823
Author(s):  
Y H Zhang ◽  
J X Lin ◽  
J Vilcek
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Human Fibroblasts ◽  
Nf Kappa B ◽  
Mobility Shift ◽  
Dnase I Footprinting ◽  
Chloramphenicol Acetyltransferase Gene ◽  
Necrosis Factor

Using variable-length deletion constructs of the 5'-flanking region of the human interleukin-6 (IL-6) gene linked to the chloramphenicol acetyltransferase gene, we showed that the region from positions -109 to -50 mediated the bulk of the response to tumor necrosis factor (TNF) or interleukin-1 (IL-1), while it was less responsive to forskolin. DNA mobility shift assays and DNase I footprinting analysis identified a nuclear protein from TNF- or IL-1-treated fibroblasts that bound to a region comprising a kappa B-like element located between positions -72 and -63 on the IL-6 gene. On the basis of these and other experiments, we conclude that TNF and IL-1 apparently activate IL-6 gene expression by closely related mechanisms involving activation of a NF-kappa B-like factor, whereas the pathway of IL-6 induction by forskolin is, in part, different.

Characterization of a tumor necrosis factor-responsive element which down-regulates the human osteocalcin gene

1993 ◽  
Vol 13 (6) ◽  
pp. 3714-3721
Author(s):  
Y P Li ◽  
P Stashenko
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Consensus Sequence ◽  
Simian Virus 40 ◽  
Transcriptional Level ◽  
Nf Kappa B ◽  
Mobility Shift ◽  
Promoter Deletion Analysis ◽  
Responsive Element ◽  
Necrosis Factor

Tumor necrosis factor (TNF) down-regulates the production of bone matrix proteins by osteoblasts, thereby inhibiting bone formation. Osteocalcin, the major noncollagenous protein in bone, is inhibited by TNF at the transcriptional level. Mapping studies were undertaken to characterize the TNF-responsive element (TNFRE) in the osteocalcin promoter. Deletion analysis localized the TNFRE to the -522/-511 region, which contains a 9-bp palindromic motif (AGGCTGCCT). Promoter segments containing this sequence down-regulated a heterologous simian virus 40 promoter. Site-specific mutagenesis of the TNFRE eliminated TNF down-regulation. Mobility shift assays demonstrated that a constitutively expressed nuclear factor bound to the TNFRE; this factor was tentatively identified as the p50 homodimer of NF-kappa B. TNF stimulation induced a second TNFRE-binding protein which displaced the constitutive factor. The TNF-induced protein was not inhibitable by the NF-kappa B consensus sequence and was unreactive with anti-NF-kappa B antiserum. DNase footprinting demonstrated that both factors protected the -522/-501 portion of the promoter, consistent with the results of mapping studies and competitive mobility shift assays. It is hypothesized that the generalized catabolic activities of TNF in infectious and malignant diseases may be regulated via this novel element.

NF-IL6 and AP-1 cooperatively modulate the activation of the TSG-6 gene by tumor necrosis factor alpha and interleukin-1

1994 ◽  
Vol 14 (10) ◽  
pp. 6561-6569
Author(s):  
L Klampfer ◽  
T H Lee ◽  
W Hsu ◽  
J Vilcek ◽  
S Chen-Kiang
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Human Fibroblasts ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Normal Human ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) activate transcription of the TSG-6 gene in normal human fibroblasts through a promoter region (-165 to -58) that encompasses an AP-1 and a NF-IL6 site. We show by deletion analysis and substitution mutagenesis that both sites are necessary for activation by TNF-alpha. Activation by IL-1 requires the NF-IL6 site and is enhanced by the AP-1 site. These results suggest that the NF-IL6 and AP-1 family transcription factors functionally cooperate to mediate TNF-alpha and IL-1 signals. Consistent with this possibility, IL-1 and TNF-alpha markedly increase the binding of Fos and Jun to the AP-1 site, and NF-IL6 activates the native TSG-6 promoter. Activation by NF-IL6 requires an intact NF-IL6 site and is modulated by the ratio of activator to inhibitor NF-IL6 isoforms that are translated from different in-frame AUGs. However, the inhibitor isoform can also bind to the AP-1 site and repress AP-1 site-mediated transcription. The finding that the inhibitor isoform antagonizes activation of the native TSG-6 promoter by IL-1 and TNF-alpha suggests that NF-IL6 has a physiologic role in these cytokine responses. Thus, the functionally distinct NF-IL6 isoforms cooperate with Fos and Jun to positively and negatively regulate the native TSG-6 promoter by TNF-alpha and IL-1.

scholarly journals Bioassay for Interleukin-1, Interleukin-6, and Tumor Necrosis Factor-Like Activities in Canine Sera.

1994 ◽  
Vol 56 (1) ◽  
pp. 103-107 ◽  
Author(s):  
Kazuto YAMASHITA ◽  
Toru FUJINAGA ◽  
Mitsuyoshi HAGIO ◽  
Toru MIYAMOTO ◽  
Yasuharu IZUMISAWA ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Necrosis Factor

scholarly journals Dorsal root sensitivity to interleukin-1 beta, interleukin-6 and tumor necrosis factor in rats

2002 ◽  
Vol 11 (5) ◽  
pp. 467-475 ◽  
Author(s):  
Cüneyt Özaktay ◽  
John Cavanaugh ◽  
Ibrahim Asik ◽  
Joyce DeLeo ◽  
James Weinstein
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Dorsal Root ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Necrosis Factor
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