Article Dans Une Revue Journal of Virology Année : 2009

Peptidylproline cis-trans isomerase Pin1 interacts with HTLV-1 Tax and modulates its activation of NF-{kappa}B.

Junichiro Yasunaga
  • Fonction : Auteur
Takao Kinjo
  • Fonction : Auteur
Koichi Watashi
  • Fonction : Auteur
Kuan-Teh Jeang
  • Fonction : Auteur

Résumé

Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus etiologically causal of adult T-cell leukemia (ATL). The virus encodes a Tax oncoprotein which functions in transcriptional regulation, cell cycle control, and transformation. ATL is a highly virulent cancer that is resistant to chemotherapeutic treatments. To understand better this disease, it is important to comprehend how HTLV-1 promotes cellular growth and survival. Tax-activation of NF-kappaB is important for the proliferation and transformation of virus-infected cells. We show here that prolyl isomerase Pin1 is over expressed in HTLV-1 cell lines; Pin1 binds Tax and regulates Tax-induced NF-kappaB activation.

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Dates et versions

hal-00358495 , version 1 (03-02-2009)

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Citer

Jean-Marie Peloponese, Junichiro Yasunaga, Takao Kinjo, Koichi Watashi, Kuan-Teh Jeang. Peptidylproline cis-trans isomerase Pin1 interacts with HTLV-1 Tax and modulates its activation of NF-{kappa}B.. Journal of Virology, 2009, 83 (7), pp.3238-48. ⟨10.1128/JVI.01824-08⟩. ⟨hal-00358495⟩
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