التفاصيل البيبلوغرافية
العنوان: |
Extracellular Tat activates c‐fos promoter in low serum‐starved CD4 + T cells |
المؤلفون: |
Gibellini, Davide, Re, Maria Carla, Ponti, Cristina, Celeghini, Claudio, Melloni, Elisabetta, La Placa, Michele, Zauli, Giorgio |
المصدر: |
British Journal of Haematology ; volume 112, issue 3, page 663-670 ; ISSN 0007-1048 1365-2141 |
بيانات النشر: |
Wiley |
سنة النشر: |
2001 |
المجموعة: |
Wiley Online Library (Open Access Articles via Crossref) |
الوصف: |
The regulatory human immunodeficiency virus‐1 (HIV‐1) Tat protein shows pleiotropic effects on the survival and growth of both HIV‐1‐infected and uninfected CD4 + T lymphocytes. In this study, we have demonstrated that low concentrations (10 ng/ml) of extracellular Tat protein induce the expression of both c‐fos mRNA and protein in serum‐starved Jurkat CD4 + lymphoblastoid T cells. Using deletion mutants, we demonstrates that the SRE, CRE and, to a lesser extent, also the SIE domains (all placed in the first 356 bp of c‐fos promoter) play a key role in mediating the response to extracellular Tat. Moreover, the ability of Tat to activate the transcriptional activity of c‐fos promoter was consistently decreased by pretreatment with the ERK/MAPK kinase inhibitor PD98058. Activation of c‐fos is functional as demonstrated by induction of the AP‐1 transcription factor, which is involved in the regulation of critical genes for the activation of T lymphocytes, such as interleukin 2. The Tat‐mediated induction of c‐fos and AP‐1 in uninfected lymphoid T cells may contribute to explain the immune hyperactivation that characterizes the progression to autoimmuno deficiency syndrome and constitutes the optimal environment for HIV‐1 replication, occurring predominantly in activated/proliferating CD4 + T cells. |
نوع الوثيقة: |
article in journal/newspaper |
اللغة: |
English |
DOI: |
10.1046/j.1365-2141.2001.02576.x |
الإتاحة: |
https://doi.org/10.1046/j.1365-2141.2001.02576.xTest |
حقوق: |
http://onlinelibrary.wiley.com/termsAndConditions#vorTest |
رقم الانضمام: |
edsbas.8773FEDA |
قاعدة البيانات: |
BASE |