Image of L3MBTL2 detected in Nucleoplasm from The Human Protein Atlas.

“Using the gene editing tool CRISPR, Lu and his team were able to look at how different genes affect the stress response, and they homed in on L3MBTL2 because it appears to play a protective role for cells. When L3MBTL2 was removed from cells and Lu’s team induced a stress response by exposing the cells to arsenic—a toxic element commonly found in the environment—the cells died. When they overexpressed the gene—or made more of the proteins that the gene consists of—the cells had a higher threshold for stress and didn’t self-destruct.

From a public health perspective, the findings are especially intriguing as Lu noted that the ER produces secretory proteins, including insulin and beta-amyloid, which are implicated in diabetes and Alzheimer’s disease, respectively. Understanding how L3MBTL2 affects ER-related stress responses may lead to new insights into how these diseases develop.”

More on When Cells Reach their Breaking Point by Chris Sweeney via Harvard T.H. Chan School of Public Health.

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