The phrase "altering chromatin structure" is correct and usable in written English.
It can be used in scientific or academic contexts, particularly in discussions related to genetics, molecular biology, or epigenetics.
Example: "The research focused on the mechanisms involved in altering chromatin structure to regulate gene expression."
Alternatives: "modifying chromatin configuration" or "changing chromatin arrangement".
Covalent modifications (for example, methylation, phosphorylation and acetylation) on histone residues that facilitate epigenetic regulation of gene expression by altering chromatin structure or recruiting chromatin modifiers.
Proteins containing an RCC1 domain are believed to be involved in altering chromatin structure and modifying gene expression.
Some co-activator and co-repressor proteins have also been shown to be required for the regulation of gene expression by many transcription factors through altering chromatin structure.
First, we examined the fitness pleiotropy of genes that encode chromatin regulatory factors, that likely influence transcription by altering chromatin structure.
In normal stem cells, epigenetic repression of developmental genes is largely regulated by polycomb proteins which act together in multi-factorial complexes to modify histones, altering chromatin structure and inhibiting transcriptional activation [39].
By altering chromatin structure globally (e.g., chromatin condensation and heterochromatin formation) and locally (e.g., mobilization of nucleosomes), CM dictates access to DNA, thereby playing vital roles in the regulation of all DNA-templated processes, such as transcription and DNA recombination, replication, and repair [1].
The development of cancer is closely associated with the stepwise accumulation of not only somatic mutations, but also epigenetic alterations that alter chromatin structure and lead to dysregulated gene expression.
Based on this we hypothesize that epigenetic alterations occurring through changes in DNA methylation and altered chromatin structure promote TTP gene silencing in cervical tumors.
Consistent with this model, loss of Set2/H3K36me leads to abrogated DNA damage signalling activation, altered chromatin structure and inappropriate repair.
