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Alternative splicing is a posttranscriptional mechanism that explains how individual genes can produce more than one transcript due to the inclusion or exclusion of specific regions originating multiple protein isoforms with diverse features. More than 90% of human genes undergo alternative splicing. This high prevalence raises the question of how developmental stage- and tissue-specific splicing influence protein function and how this regulation occurs.
In the lab we are interested on how alternative splicing regulates the expression of trafficking and membrane dynamics proteins in normal development and diseases, especially in heart and skeletal muscles. A second angle of the lab is how alternative splicing impacts the functions of these proteins and thus in internal cell architecture and physiology. Third, we aim to understand how chromatin dynamics influences alternative splicing outcomes.


UNC AFFILIATIONS:

Cell Biology & Physiology, McAllister Heart Institute

CLINICAL/RESEARCH INTERESTS:

Cardiovascular Biology, Cardiovascular disease, Cell Biology, Cell Signaling, Genetics, Molecular Biology