IN THIS ISSUE .
September 17, 2008
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Rather than march forward in an even line like normal cells, the cells (green) in this culture careen helter-skelter toward a "scratch" (black) that represents a wound. The cells lack an enzyme called APC2, which along with 65 other proteins altered cell migration in a laboratory model of wound healing. Information on the migration effects of more than 1,000 human genes has been made freely available via a user-friendly, interactive database. The database is a valuable model for data sharing and will spur research on cell migration. Courtesy of cell biologist Joan Brugge, Harvard Medical School.
Full story (link no longer available)
Brugge home page
Interactive database (link no longer available)
Article abstract (from the August 10 online issue of Nature Cell Biology) (link no longer available)
Getting severely injured people emergency medical care is key to their survival, but a new study says that not all people get equal access to it. When public health researcher David Chang of Johns Hopkins University examined 10 years of Maryland ambulance records and surveyed trauma health care workers, he uncovered a potential age bias in ambulance transport. He found that severely injured men and women older than 65 were 52 percent less likely to be taken by ambulance to a trauma center. The work suggests the need to better educate emergency personnel on the care and health of older people.
Studies have linked denser breast tissue to invasive forms of breast cancer, but researchers have been unable to tease apart the relationship—until now. Cancer biologist Alissa Weaver and her team at Vanderbilt University investigated how fingerlike protrusions on cancer cells poke holes through the extracellular matrix that surrounds them to invade other tissues. The researchers found that by increasing the density of the matrix, they increased its rigidity. This in turn produced chemical signals that promoted the protrusions' formation and activity, leading to more invasive cancer cells. The results suggest a possible mechanism for the association of tissue density and aggressive cancers.
Plants make molecules that kill bacteria, curb cancer, relax muscles, and relieve pain. Unfortunately, most of these molecules are hard to get in large quantities. That's no longer true for one important family of molecules, thanks to Caltech chemical engineer Christina Smolke and graduate student Kristy Hawkins. By inserting plant and human genes into baker's yeast, the scientists coaxed the fungi to mass-produce the therapeutic molecules. Along the way, they also discovered a new chemical function for a well-studied human drug-metabolizing enzyme. Continuing this research promises additional discoveries about enzymes and may reveal potential new drugs.
Full story (no longer available)
Smolke lab home page (no longer available)
Article abstract (from the September issue of Nature Chemical Biology)
Scientists have determined thousands of protein structures, but only a small number are of membrane proteins—molecules representing one-third of human proteins and more than half of all drug targets. Researchers led by biochemist Gerhard Wagner of Harvard Medical School now have solved the structure of VDAC-1, a pore-forming membrane protein that exports the cell's main energy source out of mitochondria. The work confirms that VDAC-1 interacts with proteins that inhibit programmed cell death, a natural and necessary process that can lead to disease. The detailed structure could guide research on this process as well as metabolism.
This work was supported by the NIH Roadmap for Medical Research.