George Khoury Lecture
Organized by NIH scientists to honor the memory of Dr. George Khoury, who was highly regarded as a superb scientist and caring mentor of the postdoctoral fellows in his laboratory. This annual lecture is part of the Wednesday Afternoon Lecture Series. Speakers are selected by a committee led by Dr. Eric Freed.
Thinking about cancer as an infectious disease
Infection causes 1 in 5 cancers worldwide. Many tumor suppressors, such as p53, have dual functions to prevent tumor cell growth and to inhibit viral replication. These molecules may have evolved from a primordial unicellular eukaryotic antiviral defense system that inhibited DNA synthesis and initiated programmed cell death in response to viral infection. Two cancer viruses found by our lab, Kaposi’s sarcoma herpesvirus and Merkel cell polyomavirus, provide examples of how virus targeting in a cell can be used to understand important circuits controlling tumor cell growth.
Hepatitis C and beyond: Never a dull moment
The Rice lab focuses on RNA viruses and is well known for its work on hepatitis C. Besides studies aimed at understanding basic viral replicative processes the lab also probes the interface between viruses and host intrinsic and innate immunity and small non-coding RNAs.
Intrinsic host defenses against HIV-1
The investigation of impeded viral replication in animal cells of particular types or species has uncovered great complexity in the interaction between retroviruses and their hosts. These studies have revealed that cells are equipped with a diverse set of proteins that can directly inhibit the replication of retroviruses, including HIV-1. Genes encoding antiretroviral proteins exhibit unusually high sequence variation, presumably because selection pressures exerted by ancient viral infections have caused them to evolve at an unusually rapid pace.
Chromatin structure and the control of gene expression
The Wu laboratory investigates the biochemical basis for histone H2A.Z exchange using the budding yeast model organism. They have identified the yeast SWR1 ATP-dependent chromatin remodeling complex as the responsible enzyme. In a purified system, SWR1 removes H2A-H2B dimers from nucleosomes and deposits free H2A.Z-H2B dimers in an ATP-dependent manner. Homologous enzymes have since been characterized in mammalian systems. How does SWR1 recognize promoters and enhancers genome-wide?
The page was last updated on Thursday, January 29, 2015 - 2:30pm
