Duke University Medical Center
DURHAM, N.C. - An immune system response that is critical to the first stages of fighting off viruses and harmful bacteria comes from an entirely different direction than most scientists had thought, according to a finding by researchers at the Duke University Medical Center.
Researchers have discovered that an important cellular "off-switch" that desensitizes receptors on the cell surface also regulates a second deactivation mechanism that had not been suspected before. Their finding that the off-switch, known as beta-arrestin, operates in two distinct ways may hint at a broader set of regulatory roles for the molecule.
A seemingly mild "insult" to the brain could sensitize neurons to attack by immune system proteins that are otherwise protective, researchers have found. The finding could explain why sufferers of Alzheimer's and other neurodegenerative diseases significantly worsen following such insults. The scientists believe that drugs to selectively inhibit the immune proteins could reduce the rate of neural damage in a wide range of neurodegenerative diseases. Such drugs could also protect other organs against damage from autoimmune diseases such as lupus and rheumatoid arthritis, in which the immune system attacks body tissues.
Brain cell membranes have established "doorways" that accept or reject molecules trying to pass into the cell, researchers have founbd. The discovery fundamentally changes how researchers think about the behavior of neurons. It had been long believed that surface molecules such as receptors are enveloped right where they rest in the fatty membrane, to be drawn into the cell's interior.
Researchers have detailed the functioning of an enzyme that is a central component of a signaling pathway important for about 30 percent of cancers. The findings about how the enzyme, called farnesyl transferase (FTase), works could help improve the FTase-inhibiting drugs that pharmaceutical companies are now testing to fight a broad spectrum of cancers.