New Enzyme Identified Likely to Help in Childbirth and Muscle Diseases


Researchers at Stanford University and Texas MD Anderson Cancer Center identified an enzyme histidine methyltransferase, which is likely to boost coordination of muscles.

A team of Stanford scientists discovered the enzyme that causes modification in muscles. The enzyme is dubbed as SETD3, is formed by transferring a methyl to a histidine –what’s known as a histidine methyltransferase (SETD3). The researchers showed that the methylation accelerates the formation of new actin filaments in cells, priming them for greater strength when next flexed. The study was published on December 10, 2018, in the journal Nature.

Alex Wilkinson, a postdoctoral scholar in the lab of Or Gozani, the Dr. Morris Herzstein Professor of Biology and co-lead author of the study, said: “The histidine methylation we uncovered in this study appears to be a far more common way of regulating proteins than previously appreciated. We discovered a first-in-class enzyme, the first function for histidine methylation in animals or plants, solved a 50-year-old mystery by determining the function of actin histidine methylation and raised the curtain on a new field that may impact human health.”

The team is hopeful that they might discover an entirely new class of methyltransferases that might help in expanding the repertoire of cellular targets for drug development. The researchers conducted a series of experiments and measurements in order to characterize SETD3 and figure out its function. They tested its biological activity on actin, as well as other molecules, and crystallizing the enzyme to observe its structure.


About Author

Latisha Diaz is a general assignment reporter at Plains Gazette. She has covered sports, entertainment and many other beats in his journalism career, and has lived in City Houston for more than 8 years. Latisha has appeared periodically on national television shows and has been published in (among others) The National Post, Politico, The Atlantic, Harper’s,, Vice and