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Linsley, A., Snider, P., Zhou, H., Olaopa, M., Koushik, S.V., Lilly, B., Burch, J.B., Firulli, A.B., Conway, S.J. 2007. A YY1-containing upstream 37bp enhancer is critical for expression of the periostin adhesion factor in Schwann and outflow tract endocardial cushion cell lineages. Dev Biol. 2007 Jul 15;307(2):340-55.
Taylor, C.J., Motamed, K., and Lilly, B. 2006. Protein kinase C and downstream signaling pathways in a 3-dimensional model of phorbol ester-induced angiogenesis. Angiogenesis; 9(2): 39-51.
Corley KM, Taylor CJ, and Lilly B.
Hypoxia-inducible factor 1alpha modulates adhesion, migration, and FAK phosphorylation in vascular smooth muscle cells.
J Cell Biochem. 2005 Dec 1;96(5):971-85.
Najwer I, and Lilly B. Ca2+/calmodulin-dependent protein kinase IV activates cysteine-rich protein 1 through adjacent CRE and CArG elements.
Am J Physiol Cell Physiol. 2005 Oct;289(4):C785-93.
Lilly, B., Olson, E.N., and Beckerle, M.C. 2001. Identification of a CArG box-dependent enhancer within the CRP1 gene that directs expression in arterial but not venous or visceral smooth muscle cells. Dev. Biol. 240, 531-547.
Lilly, B., O'keefe, D.D., Thomas, J.B., and Botas, J. 1999. The LIM homeodomain protein dLim1 defines a subclass of neurons within the embryonic ventral nerve cord of Drosophila. Mech. Dev. 88, 195-205.
Stronach, B.E., Renfranz, P.J., Lilly, B. and Beckerle, M.C. 1999. Muscle LIM proteins are associated with sarcomeres and require dMEF2 for their expression during Drosophila myogenesis. Mol. Biol. Cell, 10, 2329-2342.
Harris, A.N., Ruiz-Lozano, P., Chen, Y.F., Sionit, P., Yu, Y.T., Lilly, B., Olson, E.N. and Chien, K.R. 1997. A novel A/T-rich element mediates ANF gene expression during cardiac myocyte hypertrophy. J. Mol. Cell. Cardiol. 29(2), 515-525.
Lilly, B., Zhao, B., Ranganayakulu, G., Paterson, B.M., Schulz, R. A. and Olson, E.N. 1995. The MADS domain transcription factor D-MEF2 is essential for muscle formation during Drosophila embryogenesis.Science 267, 688-693.
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Biographies
One important question that we are currently investigating is how smooth muscle precursors are summoned to the nascent vessel. Recruitment of smooth muscle cells is thought to be dependent upon paracrine signals emanating from the endothelial cell tube, however the mechanisms of these signaling events remain a mystery. We are utilizing a 3-D culture system to grow blood vessels in vitro as a means to examine the key molecules important for endothelial/smooth muscle cell interactions. 
Another area of research is aimed at addressing the mechanisms of smooth muscle differentiation. Differentiation is accompanied by the coordinate up-regulation of a select group of genes required for contraction. My lab is actively seeking to define the transcriptional mechanisms that govern selective gene expression in smooth muscle cells. Using smooth muscle-specific regulatory enhancers of the cysteine-rich protein 1 gene as tools, we directly test the response that individual components of signaling pathways have on gene expression. 
We employ a number of experimental approaches in our investigations. To study the behavior of cells in vitro, the lab utilizes both primary and established cell lines in combination with transfections, viral infections, and reporter assays. We apply a variety of molecular, cellular, and biochemical techniques to identify and analyze factors that we determine as being critical mediators of smooth muscle recruitment and differentiation. Finally, to examine the in vivo relevance of individual components for smooth muscle function, we use transgenic and knockout mice to address questions in an animal model.
