Recombinant human KMT3C / SMYD2 protein (Active)

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

KMT3C also known as SMYD2 is a lysine methyltransferase enzyme that possesses a unique SET domain responsible for catalyzing the methylation of lysine residues on histone and non-histone proteins. The enzyme has a molecular mass of approximately 52 kDa. SMYD2 shows expression in various tissues including heart skeletal muscle and also liver. It methylates histone H3 on lysine 36 (H3K36) and several non-histone proteins influencing gene expression regulation and protein function.

Biological function summary

KMT3C/SMYD2 plays important roles in gene regulation and cellular processes. It functions as a part of a protein complex affecting transcriptional activation and repression via chromatin remodeling. The methylation activity of SMYD2 extends to p53 an important tumor suppressor linking it to the regulation of cell cycle and apoptosis. This enzymatic activity impacts cellular growth and differentiation interfacing with the larger network of cellular gene expression control and protein function modulation.

Pathways

Research shows KMT3C/SMYD2 being active in the p53 and AKT signaling pathways fundamental to cell survival proliferation and apoptosis. In the context of the p53 pathway SMYD2 methylates p53 which may impact its tumor suppressor functions. SMYD2 also interacts with proteins like RB1 and HDAC1 integrating into broader cell regulatory networks. These interactions facilitate SMYD2's influence on pathways that govern important cellular processes such as growth and DNA damage response.

Associated diseases and disorders

Mutations and overexpression of KMT3C/SMYD2 associate with various cancers including breast and esophageal cancer. In the case of breast cancer SMYD2 modulates p53 and RB1 activity contributing to tumorigenesis. Furthermore its interaction with HDAC1 connects it with epigenetic dysregulation seen in cancer progression. Altered activity or expression of SMYD2 disrupts normal cellular function providing a link between its biological activity and oncogenic processes.