The basis for the research in my laboratory lies in my strong interest in understanding the transcriptional processes that are disrupted in heart disease including changes in response to obesity. We identified a novel transcriptional signaling pathway in the heart that mediates the heart’s ability to regulate whole body metabolism. Through a combination of pharmacological and genetic gain- and loss-of-function studies in mice, we found the heart is capable of regulating whole body metabolism through a mechanism that is governed by MED13 and miR-208a. MED13 is a particularly interesting component of the Mediator complex because it functions as a molecular bridge between the core complex and kinase submodule, providing a mechanism for spatial and temporal control of Mediator-dependent regulation of transcription. We primarily utilize mutant mouse models to study the proteomic, molecular, bioinformatic and biochemical methods to study the molecular signaling events controlling cardiac transcriptional response to stress. The full article can be found here.
In the current study, we focus on two aspects of the MED13 signaling pathway.
The role of cardiac MED13 in response to obesity
The second aspect focuses on MED1, a key component of the core Mediator complex that is generally inhibited by MED13. We have successfully developed the genetic and experimental tools necessary to study these questions in our lab giving us confidence that we can provide critical and novel knowledge to the cardiac transcription field