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A mechanism that improves functioning of proteins impaired in patients with acute forms of leukaemia has been unveiled by researchers at the Memorial Sloan-Kettering Cancer Center (MSKCC) in New York.
The protein, called AML1, plays a crucial role in the development of the blood system and in the production of platelets and immune cells.
Investigators identified the methyltransferase enzyme that controls the activity of normal AML1 protein – also called RUNX1. They demonstrated its ability to regulate the function of proteins that control cell fate by turning genes on or off.
The researchers found that cellular pathways that regulate activity of normal AML1 protein through a process called arginine methylation cannot similarly regulate the activity of AML1-ETO, a protein associated with causing acute leukaemia.
Methylation is the process by which methyltransferases catalyze the attachment of a methyl group to DNA or protein in order to regulate gene expression or protein function.
Demethylase enzymes that remove methyl groups from proteins have only recently been discovered.
“By manipulating the activity of these enzymes, it may be possible to promote the activity of the normal protein, and thereby lessen the impact of the protein that promotes leukaemia,” said the study’s co-author Stephen D. Nimer, of Hematology Service at MSKCC.
There are currently no available drugs that target protein methylation, although two drugs that target DNA methylation are FDA approved for treating patients with myelodysplastic syndromes.
Sources: The Times Of India