Anti-Histone H3 polyclonal antibody

The dynamics of eukaryotic nucleosomes are essential in gene activity and well regulated by various factors. Here, we elucidated the internal dynamics at multiple timescales for the human histones hH3 and hH4 in the Widom 601 nucleosome core particles (NCP), suggesting that four dynamic networks are formed by the residues exhibiting larger-scale mu s-ms motions that extend from the NCP core to the histone tails and DNA. Furthermore, despite possessing highly conserved structural features, histones in the telomeric NCP exhibit enhanced mu s-ms dynamics in the globular sites residing at the identified dynamic networks and in a neighboring region. In addition, higher mobility was observed for the N-terminal tails of hH3 and hH4 in the telomeric NCP. The results demonstrate the existence of dynamic networks in nucleosomes, through which the center of the core regions could interactively communicate with histone tails and DNA to potentially propagate epigenetic changes. Shi et al. use solid-state nuclear magnetic resonance spectroscopy to reveal the internal dynamics of human histones hH3 and hH4 in the Widom 601 and the telomeric nucleosome core particles. This work has implications for the propagation of epigenetic changes via the center of the nucleosome core communicating with histone tails and DNA.

Previous studies have suggested that histone methylation can modulate carcinogenesis and cancer progression. For instance, the histone methyltransferase SET and MYND domain containing 2 (SMYD2) is overexpressed in several types of cancer tissue. The aim of the present study was to determine whether SMYD2 could serve a therapeutic role in ovarian clear cell carcinoma (OCCC). Reverse transcription-quantitative PCR was used to examine SMYD2 expression in 23 clinical OCCC specimens. Moreover, OCCC cell proliferation and cell cycle progression were also examined following small interfering RNA-mediated SMYD2 silencing or treatment with a selective SMYD2 inhibitor. SMYD2 was significantly upregulated in clinical OCCC specimens, compared with normal ovarian tissue. In addition, SMYD2 knockdown decreased cell viability as determined via a Cell Counting Kit-8 assay. Moreover, the proportion of cells in the sub-G(1) phase increased following SMYD2 knockdown, suggesting increased apoptosis. Treatment with the SMYD2 inhibitor LLY-507 suppressed OCCC cell viability. These results suggested that SMYD2 could promote OCCC viability, and that SMYD2 inhibition induced apoptosis in these cells. Thus, SMYD2 inhibitors may represent a promising molecular targeted approach for OCCC treatment.