Biochemical and Biophysical Research Communications, Vol.310, No.2, 312-317, 2003
Expression of histone acetyltransferases was down-regulated in poly(ADP-ribose) polymerase-1-deficient murine cells
NF-kappaB-dependent, as well as human immunodeficiency virus type-1 (HIV-1) long terminal repeat (LT R)-dependent, reporter gene expression was significantly impaired in cells derived from poly(ADP-ribose) polymerase-1 (PARP-1)-knockout (PARP-1 -/-) mice. In addition, the level of protein acetylation was markedly lower in PARP-1 -/- cells than control (PARP-1 +/+) cells. Surprisingly, the expression levels of historic acetyltransferases (HATs), p300, cAMP response element-binding protein-binding protein (CBP), and p300/CBP-associated factor (PCAF), were significantly reduced in PARP-1 -/- cells, as compared with PARP-1 +/+ cells. These results suggest that PARP-I is required for the proper expression of particular HATs. Since p300 and CBP are coactivators of NF-kappaB, we propose here that PARP-1 participates in NF-kappaB-dependent transcription by means of maintaining the expression of HATs. (C) 2003 Elsevier Inc. All rights reserved.
Keywords:poly(ADP-ribose) polymerase-1;poly(ADP-ribosyl)ation;NF-kappa B;human immunodeficiency virus type-1;histone acetyltransferase;p300;CBP;PCAF