G9a
| Identifiers | |
|---|---|
| EC number | 2.1.1.- |
| CAS number | |
| Alt. names | |
| IntEnz | IntEnz view |
| BRENDA | BRENDA entry |
| ExPASy | NiceZyme view |
| KEGG | KEGG entry |
| MetaCyc | metabolic pathway |
G9a is a protein that in humans is encoded by the EHMT2 gene. G9a is a histone methyltransferase enzyme that specifically methylates the lysine 9 position of histone H3, a process that is associated with the transcriptional repression of genes. The activity of G9a is crucial for various biological processes, including embryonic development, cell differentiation, and the regulation of viral infections.
Function[edit | edit source]
G9a is primarily known for its role in epigenetics, where it modifies chromatin structure to regulate gene expression. The methylation of histone H3 at lysine 9 by G9a creates a marker that is recognized by other proteins involved in gene repression. This modification can lead to the formation of heterochromatin, a tightly packed form of DNA which often silences gene expression.
In addition to its role in chromatin dynamics, G9a has been implicated in other cellular processes such as DNA repair and cell cycle regulation. The enzyme's activity is regulated by various factors, including its interaction with other proteins and post-translational modifications.
Clinical Significance[edit | edit source]
Alterations in G9a activity and expression levels have been linked to several human diseases, particularly cancer. Overexpression of G9a has been observed in various types of cancer, where it can promote tumor growth and survival by silencing tumor suppressor genes. Consequently, G9a is considered a potential target for cancer therapy, with inhibitors of G9a being explored as therapeutic agents.
In addition to cancer, dysregulation of G9a activity has been associated with neurological disorders and developmental abnormalities. Research is ongoing to further understand the role of G9a in these conditions and to develop strategies for therapeutic intervention.
See Also[edit | edit source]
References[edit | edit source]
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