David Clapham's research focuses on the role of calcium as an intracellular messenger and on the signals that control channels that carry calcium between cells. The identification and characterization of these ion channels may make it possible to develop drugs that alleviate cardiac arrhythmias.
The amount of the calcium ion Ca2+ that is admitted to a cell has dramatic consequences for cell function. It determines the cell's motility, proliferation, transcription of genes, growth, secretion, and contraction. The amount of Ca2+ in cells is controlled more tightly than any other ion in the body. Too much, or too little, Ca2+ inside the cell causes cell death. Cell receptors and signaling pathways thus closely guard where, when, and how Ca2+ is admitted through ion channels.
The current focus of Clapham's research is to understand the underlying causes of cardiac arrhythmias, through defining the role of transient receptor potential (TRP) ion channels. In humans TRP channels mediate the transmission of and response to sensory stimuli, both throughout the body and at the level of a single cell.
About David Clapham
David Clapham received MD and PhD from Emory University. He completed his residency in Internal Medicine at Boston's Brigham and Women's Hospital and his postdoctoral fellowship at the Max Planck Institute in Goettingen, Germany.
Dr. Clapham is a Howard Hughes Medical Institute Investigator and a member of the National American Academy of Arts and Sciences. He is the recipient of numerous awards and prizes, including the Cole Award for Contributions to Membrane Biophysics of the Biophysical Society, the American Society for Clinical Investigation Award for Research and Contributions to the Biomedical Community, and the American Heart Association Basic Science Award.