A group of researchers led by the University of Colorado at Boulder have solved the crystal structure of a molecule switch that can trigger heart disease and cancer, paving the way for future drug designs to mitigate these diseases.
The key component of the switch is a protein called MEF2 that binds to the DNA and is involved in muscle cell, T cell and nerve cell development. In cases involving human hearts, it can lower gene activity that causes enlarged hearts, known as hypertrophic cardiomyopathy, said Assistant Professor Lin Chen of CU-Boulders chemistry and biochemistry department who is leading the study.
MEF2 works in part by recruiting proteins known as histone deacetylases, or HDACs, that can modify DNA structure to suppress specific gene expression. MEF2 does so by either binding directly to HDACs or to an adaptor protein known as Cabin1 that in turn binds to HDACs.
Lin Chen | EurekAlert!
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