Effects of human T-cell leukemia virus type 1 (HTLV-1) p13 on mitochondrial K+ permeability: A new member of the viroporin family?

Micol Silic-Benussi, Oriano Marin, Roberta Biasiotto, Donna M. D'Agostino, Vincenzo Ciminale

Research output: Contribution to journalArticle

Abstract

Human T-cell leukemia virus type-1 (HTLV-1) encodes a mitochondrial protein named p13. p13 mediates an inward K+ current in isolated mitochondria that leads to mitochondrial swelling, depolarization, increased respiratory chain activity and reactive oxygen species (ROS) production. These effects trigger the opening of the permeability transition pore and are dependent on the presence of K+ and on the amphipathic alpha helical domain of p13. In the context of cells, p13 acts as a sensitizer to selected apoptotic stimuli. Although it is not known whether p13 influences the activity of endogenous K+ channels or forms a channel itself, it shares some structural and functional analogies with viroporins, a class of small integral membrane proteins that form pores and alter membrane permeability.

Original languageEnglish
Pages (from-to)2070-2075
Number of pages6
JournalFEBS Letters
Volume584
Issue number10
DOIs
Publication statusPublished - May 2010

Keywords

  • Apoptosis
  • Calcium homeostasis
  • HTLV-1
  • Leukemia
  • Mitochondria
  • Potassium channel
  • Viroporin

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Genetics
  • Molecular Biology
  • Structural Biology

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