Premium
Trichostatin A activates p18 INK4c gene: differential activation and cooperation with p19 INK4d gene
Author(s) -
Yokota Tomoya,
Matsuzaki Youichirou,
Sakai Toshiyuki
Publication year - 2004
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.2004.08.025
Subject(s) - trichostatin a , jurkat cells , histone deacetylase inhibitor , microbiology and biotechnology , gene , histone deacetylase , biology , chemistry , genetics , histone , t cell , immune system
We have reported that histone deacetylase (HDAC) inhibitors activate a member of the INK4 family, the p19 INK4d gene, causing G1 phase arrest. We report here that HDAC inhibitor, Trichostatin A, activates another member of the INK4 family, the p18 INK4c gene, through its promoter in Jurkat cells. Interestingly, the activation patterns of the p18 INK4c gene were different from those of p19 INK4d . Furthermore, mouse embryo fibroblasts lacking p18 Ink4c or p18 Ink4c /p19 Ink4d were resistant to the growth inhibitory effects of TSA as compared to their wild‐type counterpart. Our findings suggest that p18 INK4c is involved in TSA‐mediated cell growth inhibition and cooperates with p19 INK4d .