Abstract
Current drug discovery efforts for fibrotic diseases mostly target well-established receptors in pro-fibrotic signaling pathways. However, efficacy remains poor, perhaps due to the redundancy in the signaling pathways. Gene transcription mechanisms are critical control points for cell function as well as disease pathology. It has remained difficult to target gene transcription mechanisms with small molecule drugs due in part to the role of protein-protein interactions in transcription complexes. One such transcription mechanism that plays a critical role in cancer and fibrotic mechanisms is RhoA/C-GTPase regulation of the serum responsive transcription factor complex of serum response factor (SRF) and myocardin-related transcription factor (MRTF).
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