Medical school professors elected to National Academy of Sciences

Howard Chang of dermatology and of genetics, Richard Lewis of molecular and cellular physiology, and Peter Sarnow of microbiology and immunology were elected to the National Academy of Sciences.

Peter Sarnow, Howard Chang and Richard Lewis were eleced to the National Academy of Sciences.

Three faculty members at the School of Medicine are among the 120 newly elected members of the National Academy of Sciences.

Election to the academy recognizes distinguished and continuing achievements in original research. Nine new members were elected to the academy unversitywide. The medical school’s new members are:

Howard Chang, MD, PhD, the Virginia and D.K. Ludwig Professor of Cancer Genomics and of Genetics, is a professor of dermatology and of genetics and a Howard Hughes Medical Institute investigator. Chang’s research focuses on the role of epigenomics in the control of large groups of genes involved in cell cycle control, and on the study of long noncoding RNAs in biological development, cancer and aging. He is a member of Stanford Bio-X, the Stanford Maternal Child Health Research Institute, the Stanford Cancer Institute and the Wu Tsai Neurosciences Institute at Stanford

Richard Lewis, PhD, professor of molecular and cellular physiology, focuses on the molecular mechanisms of a class of ion channels called store-operated calcium channels. These channels are expressed in most cells, where they contribute to secretion, gene expression and cell differentiation. One type of store-operated calcium channel is essential for triggering T cells to proliferate and carry out immune functions. Mutations on the gene for this particular calcium-channel type results in a devastating condition called severe combined immunodeficiency. Lewis is a member of Stanford Bio-X and of the Wu Tsai Neurosciences Institute at Stanford.

Peter Sarnow, PhD, professor of microbiology and immunology, studies a microRNA known as miR-122. A small, noncoding strand of RNA, miR-122 is specific to the liver, where it’s essential to the replication of the liver-damaging hepatitis C virus’s RNA genome. Inhibiting miR-122 results in the rapid loss of viral RNA. Sarnow hopes to gain insights that lead to new treatments for hepatitis C. His lab also studies interactions between viral messenger RNA and the protein-making machinery of cells these viruses infect. Sarnow is a member Stanford Bio-X, the Stanford Maternal Child Health Research Institute and the Stanford Cancer Institute.



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