Paper Title
H3K4me3 Knock Down regulates PTIP and Kcnip2 Genes in Cardiomyocytes

Abstract
Hist one H3 lysine 4 trimethylation was identified as an epigenetic mark critical to transcription activation and had determined to control cardiac gene expression. In myocardial fibrosis, there is a loss of H3K4me3 linked with cardinal changes in the expression of genes pertaining to cardiac function such as PTIP (Pax Trans activation domain Interacting Protein) and Kcnip2 (Kv Channel Interacting Protein 2). PTIP is an integral part of the H3K4 methyl transferase complex that ensures the maintenance of vital H3K4me3 marks for stable gene expression in cardiac tissue. Down regulation of H3K4me3 disrupts pathways associated with the PTIP and results in instability in gene expression, contributing to the advancement of the disease course of fibrosis. Critical downregulation of the Kcnip2 potassium current effector modulator that is specifically crucial for cardiac repolarization led to a prolonged action potential duration and arrhythmic tendencies, caused increased myocardial stress and fibrosis. Together, these results yield significance about the role of H3K4me3 in maintaining transcriptional integrity in cardiac cells, with its knockdown causing fibrosis and electrical instability, offering insights into therapeutic targets for myocardial fibrosis and cardiac dysfunction. Keywords - H3K4me3, Histone H3 lysine 4 trimethylation, Epigenetic mark, Myocardial fibrosis, PTIP (Pax Transactivation domain Interacting Protein), Kcnip2 (Kv Channel Interacting Protein 2).