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Officials last week revealed that the U.S. contribution to ITER could cost $3.9 billion by 2034—roughly four times the...
An experimental hepatitis B drug that looked safe in animal trials tragically killed five of 15 patients in 1993. Now,...
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A new report from the Intergovernmental Panel on Climate Change (IPCC) concludes that humanity has done little to slow...
Astronomers have discovered an Earth-sized planet in the habitable zone of a red dwarf—a star cooler than the sun—500...
Three years ago, Jennifer Francis of Rutgers University proposed that a warming Arctic was altering the behavior of the...
- 17 April 2014 12:48 pm , Vol. 344 , #6181
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Why Lazy Muscles Don't Get Wasted
14 July 2005 (All day)
Couch potatoes, take heart: Your body may be working overtime to keep you fit. A new study shows that a protein known as Runx1 springs into action to preserve your basic muscle structure even as your muscles shrink from lack of use.
People with sedentary jobs, senior citizens, and others with decreased activity can end up with smaller muscle fibers and reduced nerve supply to their muscles, giving them less strength. For most, this type of atrophy is reversible with exercise. Why muscle structure remains intact during disuse is a puzzle, and the mechanisms that regulate muscle wasting are poorly understood.
Delving into the mystery, Steven Burden, a molecular neurobiologist at New York University Medical School, and colleagues followed a clue--a protein known as Runx1. Runx1 has been found in abundance in atrophying muscle but is nearly absent in healthy muscle. Burden's team examined the effects of atrophy on two groups of inactive mice, one normal and another deprived of Runx1. Muscles shrank in both groups, but the normal mice showed few signs of permanent atrophy. The mice lacking Runx1, however, showed a striking amount of muscle wasting, the team reports 15 July in Genes and Development.
The researchers also examined healthy, active mice, with and without Runx1. Neither group showed signs of muscle wasting. "If everything else is working fine, you don't need Runx1," Burden says. "But if something else goes awry, suddenly it's needed." Exactly how Runx1 prevents muscle wasting remains unclear, but it appears to be multitasking: The researchers identified 29 genes that were affected by the protein, but some were activated and others repressed.
Burden's group has "uncovered an exciting new player," says Alfred Goldberg, a cell biologist at Harvard Medical School in Boston, Massachusetts. But he emphasizes that this study is just one part of the picture. A key question, he says, is whether Runx1 can also prevent muscle atrophy caused by diseases such as diabetes and cancer.