Study in Disease Models & Mechanisms also found an miRNA that controls lamin expression.
A group of scientists at the University of California have found that while the protein lamin is necessary in the initial stages of myelin formation, too much lamin promotes myelin breakdown.
The investigators also discovered a signal that fine-tunes lamin expression. The miR-23signal turned down lamin gene expression, preventing demyelination due to lamin overexpression. This kept the myelin sheaths around nerve cells functional, properly insulating the cells.
The report will be published in the March/April issue of Disease Models & Mechanisms.