Highly mutated protein in skin cancer plays central role in skin cell renewal
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IMAGE: When KMT2D was depleted (right) from human skin cells, undifferentiated stem cells could not multiply normally, causing different layers of skin epidermis to become thickened and disorganized. view more 

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Credit: The lab of Brian C. Capell, M.D., Ph.D., Perelman School of Medicine, University Pennsylvania

PHILADELPHIA – Approximately once a month, our skin completely renews itself. If this highly coordinated process goes awry, it can lead to a variety of skin diseases, ranging from skin cancer to psoriasis. Cells lining such organs as skin and the gut, lungs, and many other organs (collectively called epithelial tissue) rely on a delicate balance of self-renewal, proliferation, and differentiation. However, disruption of this equilibrium may drive cancer and other disorders.

Researchers from the Perelman School of Medicine at the University Pennsylvania have shown for the first time that a key protein called KMT2D involved in the epigenetic regulation of gene expression guides this renewal. They published their work this month in Genes & Development. Epigenetics involves chemical modifications to DNA and its supporting proteins that affect the availability of genes to be “read” and made into proteins.

“We have known that KMT2D is one of the most frequently mutated genes in all of skin

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