IN THIS ISSUE .
June 18, 2009
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If Andy Warhol had been a biologist, he might have produced art like this. The colorful series of images shows the distribution of a protein called CHC22 clathrin in human muscle cells. A recent study found that CHC22 plays a key role in forming cellular compartments that store another specialized protein, which snatches glucose from the bloodstream to help regulate blood sugar levels. Studying CHC22 in more detail could help researchers better understand what goes wrong on a cellular level in type 2 diabetes. Copyright © Stéphane Vassilopoulos and Frances Brodsky at University of California, San Francisco.
NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development also supported this work.
Full story (No longer available)
Article abstract (from the May 29 issue of Science)
People who suffer from Huntington’s disease and similar neurodegenerative disorders have extra copies of a gene segment that makes mutant proteins. Biochemist David Corey and others at UT Southwestern Medical Center have designed molecules that specifically target the genetic repeats and may stop cells from making the harmful proteins. In the lab, some of the molecules drastically reduced and even eliminated the defective proteins. Some blocked only the mutant proteins while leaving normal versions alone. Moving from cell cultures to animals will help the researchers further explore the potential of their specially crafted molecule to treat these brain disorders.
NIH’s National Institute of Neurological Disorders and Stroke and National Institute of Biomedical Imaging and Bioengineering also funded this work.
Since its discovery in 1962, green fluorescent protein (GFP) has become an invaluable resource in biomedical imaging. But because of its short wavelength, the light that makes GFP glow doesn’t penetrate to the center of whole animals. So University of California, San Diego cell biologist Roger Tsien—who shared the 2008 Nobel Prize in chemistry for groundbreaking work with GFP—made infrared-fluorescent proteins (IFPs) that shine under longer-wavelength light, illuminating small animals such as mice. Although IFPs won’t be used in humans, Tsien and his team hope they will open a new window into the animal world.
In a mysterious phenomenon called atopic march, many young children who suffer from a severe form of eczema, or atopic dermatitis, later develop asthma. Now, biologist Raphael Kopan and others at the Washington University in St. Louis School of Medicine may have pinpointed the underlying cause. They gave lab mice a skin condition similar to eczema. They found that the damaged skin secreted a substance that traveled to the mice’s lungs, where it triggered asthmatic responses to allergens. If a comparable process is at work in humans, Kopan’s research could pave the way toward halting atopic march and helping other asthma sufferers.
Humans have evolved more complex brains and finer motor skills than chimpanzees. But where do such deviations lie in our DNA? Biostatistician Katherine Pollard at the Gladstone Institutes, University of California, San Francisco designed a computer program to sniff out the tiny differences between our DNA and chimps’ so she could then try to determine the role of those genetic segments. Among others, her program flagged unstudied snippets that may be involved in our brain function and the fetal development of our dexterous wrists and thumbs. Pollard and colleagues are studying these regions to better understand what makes us human.