Our laboratory focuses on understanding the causes of heart disease and on using knowledge of cardiac developmental pathways to devise novel therapeutic approaches for human cardiac disorders. Specifically, we study the molecular events regulating early and late developmental decisions that instruct progenitor cells to adopt a cardiac cell fate and subsequently fashion a functioning heart. We focus on transcriptional and post-transcriptional steps, particularly those involving microRNAs, during these steps. We also seek to identify the causes of human cardiovascular disease by applying modern genetic technologies for the study of complex traits such as congenital heart disease. By using a spectrum of approaches including mouse and human genetics, molecular and developmental biology, and biochemistry we hope to develop a broad understanding of the biology underlying cardiogenesis and cardiovascular disorders.
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Garg V, Kathiriya IS, Barnes R, Schluterman MK, King IN, Butler CA, Rothrock CR, Eapen RS, Hirayama-Yamada K, Joo K, Matsuoka R, Cohen JC, Srivastava D. (2003) GATA4 mutations cause human congenital heart defects and reveal an interaction with TBX5. Nature 424 : 443-447.
Bock-Marquette I, Saxena A, White MD, Dimaio JM, Srivastava D. (2004) Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair. Nature 432 : 466-472.
Garg V, Muth AN, Ransom JF, Schluterman MK, Barnes R, King IN, Grossfeld PD, Srivastava D. (2005) Mutations in NOTCH1 cause aortic valve disease. Nature 437 : 270-274.
Kwon C, Han Z, Olson EN, Srivastava D. (2005) MicroRNA1 influences cardiac differentiation in Drosophila and regulates Notch signaling. Proc. Natl. Acad. Sci. USA 102 : 18986-18991.
Srivastava D, Ivey KN. (2006) Potential of stem cell-based therapies for heart disease. Nature 441 : 1097-1099.
Srivastava D. Making or breaking the heart: From lineage determination to morphogenesis. Cell (in press).
information last updated July 2006
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Biomedical Sciences (BMS) Graduate Program
