A non-classical ISRE/ISGF3 pathway mediates induction of RANTES gene transcription by type I IFNs

22Citations
Citations of this article
12Readers
Mendeley users who have this article in their library.

Abstract

RANTES (regulated upon activation normal T cell expressed and secreted) is a chemoattractant cytokine important in the generation of inflammatory responses and human immunodeficiency virus resistance. In hematopoietic cells, RANTES is over-expressed by type I interferons (IFN-α and IFN-β). The upstream region of the RANTES gene promoter contains a distal low affinity IFN-stimulated response element (ISRE). Specific mutagenesis in this ISRE-like motif abolished the activation of RANTES transcription by type I IFNs. Examination of the ISRE binding factors strongly suggested that signal transducer and activator of transcription (Stat)-2 and p48/IFN-stimulated gene factor 3γ (ISGF3γ) are not required for the induction of RANTES by type I IFNs. The specific requirement of Stat-1 was demonstrated using Stat-1-deficient U3A cells. These results revealed a non-classical ISRE/ISGF3 signal transduction pathway for the induction of RANTES by type I IFNs. © 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

Cite

CITATION STYLE

APA

Cremer, I., Ghysdael, J., & Vieillard, V. (2002). A non-classical ISRE/ISGF3 pathway mediates induction of RANTES gene transcription by type I IFNs. FEBS Letters, 511(1–3), 41–45. https://doi.org/10.1016/S0014-5793(01)03276-8

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free