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February 17, 2010
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No, it's not Christmas in a beehive. Instead, each hexagon in this shifting honeycomb represents a gene. A computer program called GATE makes these movies by reading the data from an experiment and grouping genes that turn on (red) and off (green) at similar times. When researchers click on any part of the honeycomb, GATE connects them to databases brimming with more information about gene and protein activity. Such interaction helps biologists wrap their heads around the vast amount of data they and their colleagues have gathered. It also inspires new hypotheses in areas as diverse as stem cell differentiation and ecosystem evolution. Courtesy of the Ma'ayan Laboratory, Mount Sinai School of Medicine.
Severe muscle injuries—whether caused by an earthquake or excessive exercise—can hurt the kidneys. As muscles break down, they release contents that deposit in the kidneys, causing harmful oxidative damage that can lead to kidney failure. New work indicates that acetaminophen, an over-the-counter pain reliever, may stop the process—at least in rats. An international research team led by pharmacologist L. Jackson Roberts at Vanderbilt University showed that giving acetaminophen to rats before or after muscle injury prevented oxidative damage, thereby reducing kidney damage. The results, while promising in this animal model, will need to be confirmed in human clinical trials.
This work also was supported by NIH's National Institute of Allergy and Infectious Diseases and National Institute of Diabetes and Digestive and Kidney Diseases.
Many of today's medicines come from products found in nature. One such product, derived from a sponge in the Pacific Ocean, shows tantalizing promise against cancer, bacteria and fungi. But for 17 years, chemists worldwide have been unable to synthesize the molecule, known as palau'amine. By working around the clock, a team led by Phil Baran at The Scripps Research Institute has finally succeeded. In addition to making it possible to examine substances like palau'amine for their therapeutic potential, the team invented new chemical techniques that will empower the synthesis of related, challenging molecules.
Occasional errors in cell division can produce cells with too few or too many chromosomes, which can put a cell on the path toward becoming cancerous. Fortunately, cells usually sense the defect and stop dividing, putting the brakes on any possible cancer progression. Now, cell biologists Sarah Thompson and Duane Compton of Dartmouth Medical School figured out how. They found that a protein called p53 reins in cell division when the chromosome number deviates from normal. The findings help explain why abnormal chromosome number and loss of p53 often go hand in hand in the movement toward tumor formation.
In a common form of the muscle wasting disease, myotonic muscular dystrophy, a gene expressed in muscle cells carries an abnormally long segment of repeats. When the gene is transcribed into RNA, the repeat section draws in an RNA splicing protein called Mbnl1, hampering Mbnl1's ability to produce correctly spliced RNAs. Now, biochemists led by Manuel Ares of the University of California, Santa Cruz, have used a technology they pioneered to detect incorrect RNA splicing events in two mouse models of the muscular disease. The findings provide a broad picture of the mis-splicing events that underlie the disease and may lead to novel treatments and diagnostics.
This work also was supported by NIH's National Institute of Arthritis and Musculoskeletal and Skin Diseases.
Full story (no longer available)
Article abstract (from the February issue of Nature Structural & Molecular Biology)