CardioGenomics: Christine Seidman

Christine Seidman
M.D.
Harvard Medical School

Biography
Christine Seidman is Professor of Medicine and Genetics at Harvard Medical School, Director of the Cardiovascular Genetics Service at Brigham and Women's Hospital, and Investigator of the Howard Hughes Medical Institute. As a clinical researcher, Dr. Seidman investigates the molecular etiology of human diseases, with a focus on congenital heart disease, familial hypertrophic cardiomyopathy, and familial dilated cardiomyopathy. Her research centers on defining the pathways involved in heart development and identifying gene mutations that lead to pathologic remodeling of the human heart.

e-mail:

Webcasts:

Dilated Cardiomyopathy: The Influence of Genotype on Phenotype
CardioGenomics Genetics and Genetic Epidemiology course, Boston, April 2003

Publications:

An abnormal Ca(2+) response in mutant sarcomere protein-mediated familial hypertrophic cardiomyopathy

Comparison of two murine models of familial hypertrophic cardiomyopathy

Consequences of pressure overload on sarcomere protein mutation-induced hypertrophic cardiomyopathy

Constitutively active AMP kinase mutations cause glycogen storage disease mimicking hypertrophic cardiomyopathy

Development of left ventricular hypertrophy in adults in hypertrophic cardiomyopathy caused by cardiac myosin-binding protein C gene mutations

Dilated cardiomyopathy and heart failure caused by a mutation in phospholamban

Dilated cardiomyopathy in homozygous myosin-binding protein-C mutant mice

Familial hypertrophic cardiomyopathy and atrial fibrillation caused by Arg663His beta-cardiac myosin heavy chain mutation

Homozygous mutation in cardiac troponin T: Implications for hypertrophic cardiomyopathy

Molecular epidemiology of hypertrophic cardiomyopathy

Mutations in sarcomere protein genes as a cause of dilated cardiomyopathy

Sarcomere Protein Gene Mutations in Hypertrophic Cardiomyopathy of the Elderly

Sarcomere protein gene mutations in hypertrophic cardiomyopathy of the elderly

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model

The genetic basis for cardiomyopathy: From mutation identification to mechanistic paradigms (Review)

Current Projects:

Sarcomere Gene Mutation Screening

Components

Cardiovascular Genetics Center