An unexpected role for FosB in activation-induced cell death of T cells
The CD95 (APO-1/Fas) system plays a major role in induction of apoptosis in lymphoid and nonlymphoid tissues. The CD95 (APO-1/Fas) ligand (CD95L) is induced in response to a variety of signals including TCR/CD3 stimulation or application of chemotherapeutic drugs. Here we report that an AP-1 site lo...
Saved in:
| Main Authors: | , , |
|---|---|
| Format: | Article (Journal) |
| Language: | English |
| Published: |
5 March 2003
|
| In: |
Oncogene
Year: 2003, Volume: 22, Issue: 9, Pages: 1333-1339 |
| ISSN: | 1476-5594 |
| DOI: | 10.1038/sj.onc.1206126 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/sj.onc.1206126 Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/1206126 |
| Author Notes: | Sven Baumann, Jochen Hess, Sören T. Eichhorst, Andreas Krueger, Peter Angel, Peter H. Krammer, and Sabine Kirchhoff |
| Summary: | The CD95 (APO-1/Fas) system plays a major role in induction of apoptosis in lymphoid and nonlymphoid tissues. The CD95 (APO-1/Fas) ligand (CD95L) is induced in response to a variety of signals including TCR/CD3 stimulation or application of chemotherapeutic drugs. Here we report that an AP-1 site located in the 5′ untranslated region of the CD95L gene is required for TCR/CD3-mediated induction of the human CD95L promoter. Electrophoretic mobility shift assays using nuclear extracts of Jurkat T cells as well as TCR/CD3-restimulated primary human T cells demonstrated specific binding of AP-1, predominantly composed of c-Jun and FosB, to this sequence. Ectopic expression of transdominant negative Jun mutants strongly reduced CD95L promoter activity and activation-induced cell death (AICD), confirming the functional significance of FosB/c-Jun binding. Thus, our results demonstrate an important novel function for FosB dimerized with c-Jun in TCR/CD3-mediated AICD in human T cells. |
|---|---|
| Item Description: | Gesehen am 14.04.2021 |
| Physical Description: | Online Resource |
| ISSN: | 1476-5594 |
| DOI: | 10.1038/sj.onc.1206126 |