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Effects of human T‐cell leukemia virus type 1 (HTLV‐1) p13 on mitochondrial K + permeability: A new member of the viroporin family?
Author(s) -
Silic-Benussi Micol,
Marin Oriano,
Biasiotto Roberta,
D'Agostino Donna M.,
Ciminale Vincenzo
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.02.030
Subject(s) - virology , leukemia , chemistry , mitochondrion , biology , microbiology and biotechnology , biochemistry , genetics
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.