The prolyl isomerase Pin1 stabilizes the human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein and promotes malignant transformation

Biochem Biophys Res Commun. 2009 Apr 3;381(2):294-9. doi: 10.1016/j.bbrc.2009.02.024. Epub 2009 Feb 11.

Abstract

The HTLV Tax protein is crucial for viral replication and malignant transformation. We investigated the possible role of peptidyl prolyl isomerase Pin1 in the positive regulation of the human T-cell leukemia virus type 1 Tax. Pin1 is highly expressed in adult T-cell leukemia (ATL) cells expressing Tax protein and forced expression of Pin1 in turn increases the Tax protein expression. Pin1 prolonged the protein half-life of Tax by suppressing the ubiquitination and subsequent lysosomal degradation of Tax. Pin1 interacts with phosphorylated Tax on its Ser160-Pro motif at the mitotic phase. Finally, we found that Pin1 plays a supporting role in Tax-mediated cell transformation. Our current study demonstrates an important role for Pin1 in the post-translational regulation of Tax and suggests that the targeting of Pin1 may offer a new insight into the pathogenesis of HTLV-1 related diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Motifs
  • Animals
  • Cell Line
  • Cell Transformation, Viral*
  • Gene Products, tax / metabolism*
  • HTLV-I Infections / metabolism*
  • HTLV-I Infections / virology*
  • Human T-lymphotropic virus 1 / genetics
  • Human T-lymphotropic virus 1 / metabolism*
  • Humans
  • Mice
  • Mitosis
  • NIMA-Interacting Peptidylprolyl Isomerase
  • Peptidylprolyl Isomerase / metabolism*
  • Protein Stability
  • Transcriptional Activation
  • Ubiquitination

Substances

  • Gene Products, tax
  • NIMA-Interacting Peptidylprolyl Isomerase
  • PIN1 protein, human
  • Peptidylprolyl Isomerase
  • Pin1 protein, mouse