By comparison, small molecule Hdac inhibitors have short half-lives in serum and might only temporally change chromatin structure and gene expression in relatively short-term cell culture assays.
These histone modifications may serve as a binding platform for non-histone proteins, whose activities change chromatin structure and function.
As such, methylation marks change chromatin structure by different mechanisms, involving the recruitment or inhibition of recruitment of distinct enzymatic complexes [ 25, 26].
To obtain a comprehensive view of how VPA treatment might change chromatin structure, we constructed DHSS libraries from VPA- (200 mg/kg, i.p).
Generally, certain histone modifications such as acetylation or phosphorylation are thought to change chromatin structure by altering the net positive charge of the histone proteins, thereby rendering the underlying DNA sequence information more accessible [24].
Some histone modifications act in cis to change chromatin structure directly, whereas others act in trans to affect the recruitment of a protein complex that regulates gene expression [ 36].
Aberrant methylation can change chromatin structure, rendering DNA binding sites accessible or inaccessible to transcription factors leading to activation or silencing of genes important in cell differentiation and maintenance.
This repression mechanism is one of the best examples in biology to learn how changes in chromatin structure cause changes in gene expression.
Genes that are located in similar regions of chromatin may be concomitantly influenced by changes in chromatin structure or by changes in chromosome regions.
It is also thought that changes in chromatin structure accompany developmental changes in order to establish and/or maintain tissue specific gene expression states [ 2, 3].
