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Joan Taylor, PhD, and is a UNC Lineberger Comprehensive Cancer Center member with research interest in understanding the signaling mechanisms whereby integrin-dependent signals regulate growth and development in the cardiovascular system.

Professor, Pathology & Lab Medicine
Associate Dean for Faculty Affairs and Leadership Development
UNC-Chapel Hill
Cancer Cell Biology

Area of Interest

As a basic scientist my research interests include defining the signaling networks that underlie the coordinated growth and development of the cardiovascular and musculoskeletal systems and mechanisms underlying the development of adult-onset diseases. We use a multi-disciplinary approach that includes the generation of animal models that mirror congenital cardiovascular and musculoskeletal defects in humans, and we identify affected signaling networks that govern the aforementioned processes (with a focus on signaling via the extracellular matrix) through cell biology, biochemical, proteomic, and genomic means. We also couple surgical models (transverse aortic banding, carotid ligation, left anterior descending coronary ligation/reperfusion, toxin injection) to genetically manipulated mice to better understand the pathogenesis of cardiovascular and skeletal muscle diseases. Finally, we continually identify clinical collaborators to facilitate our bench to bedside studies. Our current research largely focuses on the role(s) of the GRAF family of RhoGAPs of which we cloned the founding member GRAF1 in cardiovascular disease pathogenesis. Over the years we’ve shown that these proteins are critical for limiting RhoA dependent processes in smooth (GRAF2 and 3), skeletal (GRAF 1 and 2) and cardiac (GRAF1) muscle. For example, we were the first to show that GRAF3 (ArhGAP42) limits RhoA dependent maturation and contractility and is critical for BP maintenance in mice and patients and are currently exploring the chemical tractability of GRAF3 modulators as a new class of anti-hypertensive therapies. We also showed that GRAF1 and 2 are transiently upregulated in myoblasts during secondary myogenesis wherein they promote SKM differentiation, fusion, and injury repair and that GRAF1 depletion exacerbates cardiac and skeletal muscle degeneration in dystrophic mice suggesting and important role for this protein as a modifier of cardiomyopathies. Our latest findings show that GRAF1 mediates these processes, at least in part through serving as a novel regulator of a selective autophagy pathway that mediates clearance of dysfunction mitochondria. Given that numerous cancers, cardiometabolic and neuromuscular diseases are markedly accelerated by defects in mitochondrial quality control, defining the underlying mechanisms will be critical to lay the foundation for the development of future strategies to treat these debilitating diseases.

Find publications on PubMed

Headshot of Joan Taylor.