Hehlgans, Thomas and Seitz, Carola and Lewis, Claire and Maennel, Daniela N. (2001) Hypoxic upregulation of TNF receptor type 2 expression involves NF-IL-6 and is independent of HIF-1 or HIF-2. JOURNAL OF INTERFERON AND CYTOKINE RESEARCH, 21 (9). pp. 757-762. ISSN 1079-9907
Full text not available from this repository. (Request a copy)Abstract
Tumor necrosis factor (TNF) exerts its biologic activity via two distinct membrane receptors, TNF receptor type 1 (p55TNFR) and TNF receptor type 2 (p75TNFR). Whereas the p55TNFR gene is rather constitutively expressed, transcription of p75TNFR is strongly modulated by a number of stimulatory agents. Experimental evidence suggested the involvement of p75TNFR in endothelial cell activation. Therefore, we have tested the transcriptional activity of p75TNFR under conditions of hypoxia and reoxygenation. Northern blot analysis revealed that p75TNFR mRNA is upregulated in NIH3T3 cells under hypoxia and reoxygenation. This observation directly originates from transcriptional activation of the p75TNFR gene, as shown by reporter gene analysis. Cotransfection experiments clearly showed that the transcriptional induction of the p75TNFR gene is independent of the hypoxia-induced factors, HIF-1 alpha and HIF-2 alpha. Using deletion mutants of the 5'-flanking region of the p75TNFR gene, we were able to identify a putative DNA binding site for the transcription factor nuclear factor-interleukin-6 (NF-IL-6) to be responsible for the transcriptional upregulation of the p75TNFR gene under conditions of hypoxia and reoxygenation.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | TUMOR-NECROSIS-FACTOR; DNA-BINDING ACTIVITY; INDUCIBLE FACTOR-I; GENE-EXPRESSION; CEREBRAL-ISCHEMIA; MOLECULAR-CLONING; VIRAL-PROTEINS; MESSENGER-RNA; UP-REGULATION; FACTOR-ALPHA; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Pathologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 13 Dec 2021 09:05 |
| Last Modified: | 13 Dec 2021 09:05 |
| URI: | https://pred.uni-regensburg.de/id/eprint/41157 |
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