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

FEBS Letters

Vieillard, Vincent³  Ghysdael, Jacques¹  Cremer, Isabelle² 

[1] Régulations Cellulaires et Oncogénèse, CNRS UMR 146, Institut Curie, 91405 Orsay, France;Laboratoire d'Immunologie Cellulaire et Clinique, INSERM U255, Université Paris-6, 75005 Paris, France;Laboratoire d'Immunologie Cellulaire et Tissulaire, INSERM U543, Hôpital Pitié-Salpétrière, 75013 Paris, France

关键词: Signal transduction;    Interferon-α/β;    Regulated upon activation normal T cell expressed and secreted;    Signal transducer and activator of transcription-1;    IFN;    interferon;    RANTES;    regulated upon activation normal T cell expressed and secreted;    Stat;    signal transducer and activator of transcription;    Jak;    Janus kinase;    ISRE;    interferon-stimulated response element;    EMSA;    electrophoretic mobility shift assay;   

DOI  :  10.1016/S0014-5793(01)03276-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown