Cutting and his colleagues don't know how exactly the loss of MSRA reduces risk for fatal intestinal obstruction, but they suspect that MSRA's ability to alter the activity of specific intestinal enzymes may be the key. They suspect that with reduced levels of MSRA, the enzymes are free to do their job breaking down proteins that make up meconium so that meconium can pass through the intestines and be evacuated normally at birth.
The researchers' work on MSRA could shed light on how meconium normally gets broken down in the intestines. Moreover, use of the techniques pioneered by Cutting and his colleagues may lead to identification of modifier genes that play roles in other complications of CF, like lung function, and in other diseases caused by a single gene, like Huntington's disease.
|Contact: Audrey Huang|
Johns Hopkins Medical Institutions