The study focused on a signaling pathway regulated by the MLL1 gene. Histone modification is one of the important regulatory mechanisms in biological epigenetics. Histone methylation involved by histone transferase not only plays a key role in the self-renewal and maintenance of hematopoietic stem cells, but also regulates many occurrences and development of leukemia. Related protein expression and activity.
The MLL gene is an important member of the trxG family. MLL gene rearrangement can be seen in more than 70% of childhood leukemias, and MLL gene rearrangement can be seen in approximately 10% of adult acute myeloid leukemia (AML) patients. The C-terminus of MLL has a SET domain with H3K4 methyltransferase activity.
When the MLL1 gene is impaired, it can cause leukemia, a blood cancer that often occurs in very young patients. The researchers found that the normal version of the MLL1 gene controls many other genes and maintains hematopoiesis in this way.
"When this gene is damaged or broken, this control can be confusing, causing normal blood cells to become leukemia cells," Ernst said.
In this new article, the researchers found that MLL1 methyltransferase activity is not a necessary condition for hematopoietic stem cell maintenance and MLL-AF9 fusion oncogene-driven leukemia formation, but is related to its partner gene MOF, and MOF will be small. The acetyl "chemical modification" was added to the vicinity of the MLL1-controlled gene. This acetyl modification acts as a switch to turn on the gene. When this function is compromised, MLL1 is unable to maintain normal blood stem cells.
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