The H1 linker histones: Multifunctional proteins beyond the nucleosomal
HDACs are enzymes that catalyze the deacetylation of lysine remnants located at the A/-terminal of several protein substrates, such as nucleosomal
Different EZH2-containing complexes target methylation of histone H1 or nucleosomal
Persistent hypomethylation in the promoter of nucleosomal
binding protein 1 (Nsbp1) correlates with overexpression of Nsbp1 in mouse uteri neonatally exposed to diethylstilbestrol or genistein.
Increased apoptosis, impaired clearance of apoptotic cells, impaired immune regulatory functions with consequent lower activation thresholds of T and B lymphocytes, reactive antibodies against intracellular constituents of nucleosomal
DNA proteins and ribonucleoproteins, and dysregulation of the cytokine network, particularly the overexpression of TNF-[alpha] and type 1 interferons, all together drive the inflammatory process causing the tissue damage in lupus erythematosus [27, 28, 45].
Regulated responses of this minimal transcription system by DNA-binding transcription factors or in vitro transcription from nucleosomal
DNA template require additional sets of coregulator proteins involved in chromatin remodeling/modification as well as targeted recruitment of basal transcription machinery to the promoter [2, 3].
Human monocyte cell model Deacetylated RelA-p65  of endotoxin tolerance lysine 310 and and human leukocytes from nucleosomal
histone H4 sepsis lysine 16 to promote termination of NF- [kappa]B dependent transcription.
The addition or removal of modifications in both DNA and histones needs an alteration of the compact nucleosomal
structure that is achieved by the specific remodeling ATP-dependent enzymes SWI/SNF, ISWI, and CHD.
Acetylation and deacetylation on different positions of the N-terminal tail of core histones by histone acetylases (HATs) and histone deacetylases (HDACs) change the nucleosomal
conformation of cells .
melanogaster Transposons, intergenic expression Repression of regions, nucleosomal
many genes involved in biased, preferential for CNS functions Promote GSC repeat sequences differentiation C.
Then, cofactors recruit the inhibitory nucleosomal
remodeling and deacetylation (NuRD) complex to promoter-bound Egr1 and ultimately repress Egr1-dependent transcriptional activity .