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Nathan Tucker


Tucker NR, McLellan MA, Hu D, Ye J, Parsons VA, Mills RW, et al. Novel Mutation in FLNC (Filamin C) Causes Familial Restrictive Cardiomyopathy. Circ Cardiovasc Genet. 2017;10:e001780.

Tucker NR, Dolmatova E V., Lin H, Cooper RR, Ye J, Hucker WJ, et al. Diminished PRRX1 Expression Is Associated With Increased Risk of Atrial Fibrillation and Shortening of the Cardiac Action Potential. Circ Cardiovasc Genet. 2017;10:e001902.

Sinner MF, Tucker NR, Lunetta KL, Ozaki K, Smith JDG, Trompet S, et al. Integrating genetic, transcriptional, and functional analyses to identify 5 novel genes for atrial fibrillation. Circulation. 2014;130:1225–35.

Tucker NR, Mahida S, Ye J, Abraham EJ, Mina JA, Parsons VA, et al. Gain-of-function mutations in GATA6 lead to atrial fibrillation. Heart Rhythm. 2017;14:284–291.

Nathan Tucker, Ph.D.

Nathan Tucker is a project team lead in the Precision Cardiology Laboratory at the Broad Institute of MIT and Harvard, a joint effort between the Broad Institute and Bayer to identify novel mechanisms and potential therapeutic targets for cardiovascular disease. He currently heads efforts to employ low input transcriptomic and epigenomic approaches in human and model system cardiovascular tissues. He also serves as an Instructor of Medicine at Massachusetts General Hospital and Harvard Medical School.

Prior to joining the Broad Institute in 2016, he served as a postdoctoral research fellow at Massachusetts General Hospital where he focused on the genetic underpinnings of common and rare variant driven atrial fibrillation, mitral valve prolapse, and cardiomyopathies in the laboratory of Patrick Ellinor.

Nathan holds a Ph.D in cell biology and genetics from Washington State University.

Contact Nathan at

November 2019