Mutational analysis of mononucleotide repeats in HDAC4, 5, 6, 7, 9 and 11 genes in gastric and colorectal carcinomas with microsatellite instability.

摘要

Histone acetylation in conjunction with deacetylation serves as a crucial modulation process of chromatin structure and is one of the main epigenetic mechanisms for gene regulation [1]. The status of histone acetylation is controlled by histone acetyl-transferases and histone deacetylase (HDAC). HDACs are responsible for the deacetylation of lysine residues on the N-terminal region of the core histones (H2A, H2B, H3 and H4). Human HDACs consist of 11 proteins in four families (class I: HDAC1, 2, 3 and 8; class IIa: HDAC4, 5, 7 and 9; class IIb: HDAC6 and 10; class IV: HDAC 11) [1]. HDAC-mediated deacetylation alters activities of many transcription factors, including p53, nuclear factor kB, and HIF1alpha, subsequently regulating many cellular events, including organ development, angiogenesis, apoptosis and cell proliferation [1].