Cellular and Molecular Life Sciences CMLS

, Volume 58, Issue 5, pp 728–736

Histone acetylation and disease

Authors

  • S. Timmermann
    • CNRS UPR 9079, IFC-01 André Lwoff, 7, rue Guy Moquet, 94801 Villejuif (France), Fax +33 1 49 58 33 07, e-mail: ahbellan@vjf.cnrs.fr
  • H. Lehrmann
    • CNRS UPR 9079, IFC-01 André Lwoff, 7, rue Guy Moquet, 94801 Villejuif (France), Fax +33 1 49 58 33 07, e-mail: ahbellan@vjf.cnrs.fr
  • A. Polesskaya
    • CNRS UPR 9079, IFC-01 André Lwoff, 7, rue Guy Moquet, 94801 Villejuif (France), Fax +33 1 49 58 33 07, e-mail: ahbellan@vjf.cnrs.fr
  • A. Harel-Bellan
    • CNRS UPR 9079, IFC-01 André Lwoff, 7, rue Guy Moquet, 94801 Villejuif (France), Fax +33 1 49 58 33 07, e-mail: ahbellan@vjf.cnrs.fr

DOI: 10.1007/PL00000896

Cite this article as:
Timmermann, S., Lehrmann, H., Polesskaya, A. et al. CMLS, Cell. Mol. Life Sci. (2001) 58: 728. doi:10.1007/PL00000896

Abstract.

Differential acetylation of histones and transcription factors plays an important regulatory role in developmental processes, proliferation and differentiation. Aberrant acetylation or deacetylation leads to such diverse disorders as leukemia, epithelial cancers, fragile X syndrome and Rubinstein-Taybi syndrome. The various groups of histone acetyltransferases (CBP/p300, GNAT, MYST, nuclear receptor coactivators and TAFII250) and histone deacetylases are surveyed with regard to their possible or known involvement in cancer progression and human developmental disorders. Current treatment strategies are discussed, which are still mostly limited to histone deacetylase inhibitors such as trichostatin A and butyrate.

Key words. HAT; HDAC; histone acetylation; butyrate; TSA; dietary fiber; leukemia; fragile X syndrome.

Copyright information

© Birkhäuser Verlag, 2001