Analysis of Histone Modification in Stroke

Histones are basic proteins found in eukaryotic cell nuclei. Their termini contain multiple potential post-translational modification sites, including acetylation, methylation, phosphorylation, ubiquitination, SUMOylation, and ADP ribosylation, to regulate DNA packaging and chromatin organization. An increasing number of studies have shown that histone modifications, such as acetylation and methylation, play an important role in the pathogenesis of ischemic stroke. Studies have found that histone H3 and H4 acetylation levels are generally reduced in animal models of stroke, which is associated with severe brain damage. Because epigenetic changes can be reversed, histone deacetylase inhibitors can effectively protect the brain from ischemic damage, opening up new avenues for the study of ischemic stroke.

Fig. 1. Histone deacetylase inhibitors can effectively protect the brain from ischemic damage. Fig. 1. The involvement of histone acetyltransferases and histone deacetylases in regulation of protein synthesis and apoptosis in the ischemic brain. (Uzdensky et al., 2021)

Our Services

Ace Therapeutics provides comprehensive services to assist clients in analyzing the role of histone modifications in the pathogenesis of ischemic stroke and in the development of stroke therapeutics. By mapping the distribution and abundance of specific histone modifications (e.g., acetylation and methylation marks), we help clients identify key genes and pathways regulated by histone modifications.

Analysis of Histone Acetylation in Stroke

We use antibody microarrays and immunofluorescence microscopy to detect the acetylation levels of acH3K9 and H4 in animal models of ischemic stroke. In addition, we can analyze the expression of a variety of related proteins and investigate their role in the post-stroke period by genetic manipulation. We aim to help clients develop and validate inhibitors of different histone deacetylases (HDACs) to protect the rodent brain from ischemic damage.

Type of Histone Acetylation Potential Targets of Inhibitors
Histone acetyltransferases HAT1 and PCAF
HDACs Class I: HDAC1, HDAC2, HDAC3 and HDAC8.
Class II: HDAC4, HDAC5, HDAC6, HDAC7, HDAC9 and HDAC10.
Class III: sirtuins.
Class IV: HDAC11.

Analysis of Histone Methylation in Stroke

We offer comprehensive services to analyze the role of histone methylation and related histone methyltransferase (HMT) inhibitors in the pathogenesis of ischemic stroke.

  • Knockdown or pharmacological inhibition studies of HMT inhibitors, including G9a, G9a-like protein, SUV39H1, SUV39H2, enhancer of zeste homolog 2 (EZH2), and SUV420H2.
  • Detection of Jumonji-domain histone demethylase (JHDM) expression levels.
  • Detection of H3K27me3 expression levels.

Ace Therapeutics is committed to providing experimental data on the role of histone acetylation and methylation in stroke. We aim to help clients develop new therapeutic strategies for stroke. If you are interested in our services, please do not hesitate to contact us!

Reference
  1. Uzdensky, A. B., & Demyanenko, S. (2021). Histone acetylation and deacetylation in ischemic stroke. Neural Regeneration Research, 16(8), 1529-1530.
All of our services are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.
0
Inquiry Basket