Cells produce bad proteins all the time, and in large-enough numbers, these molecules can spell danger for the body. When misfolded or unfolded, proteins can't do their jobs. At worst, they harm cells by clumping into the sticky plaques that are the signatures for neurodegenerative disorders such as Alzheimer's disease.
A clear understanding of how most cells successfully manage protein repair and disposal has been elusive. But now, research has unmasked one of the molecular participants in the process. In the January Nature Cell Biology, scientists studying gene expression in failing hearts report the function of an important molecular player in the cell's quality-control system.
Called CHIP (carboxyl terminus of Hsc70-interacting protein), this molecule decides the fate of malformed proteins in heart muscle, says Cam Patterson of the University of North Carolina at Chapel Hill. CHIP judges whether to slate bad proteins for repair or destruction, he says.