
UCLA researchers characterized the mechanism of the mammalian EAK-7 gene, or mEAK-7
On May 14, 2018, University of California, Los Angeles (UCLA) researchers characterized the mechanism of the mammalian EAK-7 gene, or mEAK-7, which regulates the molecular process, or ‘metabolic pathway,’ that dictates cell growth and human development.
The disruption of those processes is part of what causes cancer and other diseases, as well as some neurological disorders. Findings from the study could be a preliminary step toward new therapies that would work by slowing or blocking mEAK-7’s molecular process, which in turn could potentially control the spread and growth of the cells responsible for those diseases. The research was published in the journal Science Advances.
The researchers began studying EAK-7, the worm gene, in 2013, when Krebsbach was a faculty member at the University of Michigan. Knowing about its important role in worms, the team wanted to understand if it played a role in human biology, and whether it could provide insight on why certain human cells become stem cells. Joe Nguyen, the study’s lead author, said the team essentially stumbled on the link between EAK-7 and its human counterpart after their initial hypothesis about that connection proved incorrect.
Once they identified mEAK-7 in human cells, they screened several types of human cells — including embryonic stem cells and fibroblasts, the cells that form connective tissues and aid in wound healing — to better understand how the gene worked.
To support their findings, the scientists tested the significance of mEAK-7’s role in cell proliferation and migration by inhibiting the gene in living human cells. When they mutated mEAK-7 or removed it from those cells, there was a dramatic reduction of those processes. They also tested a scenario in which mEAK-7 was overexpressed in cells and found that the proliferation of those cells increased significantly.
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Source: University of California, Los Angeles
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