This is the most recently article about Protein Mutation Unfolds.
Most diseases with a genetic basis involve a mutation in some gene that affects how much of its protein is made or how well that protein works. However, a growing body of research indicates that this scenario may not be universally true. Conn and Janovick explain that many diseases, including cystic fibrosis, Alzheimer's and diabetes, are products of improperly folded—but potentially functional—proteins. When the authors added a template for correct folding (which they call a pharmacoperone) to a cell with such a "mutant" protein, the cellular defect was fixed. This remedy suggests that the rescue of a person's own misfolded proteins may be an alternative to the broader physiological tinkering (and attendant side effects) caused by most of the current drugs used to treat these diseases.
| Figure 2. DNA in the nucleus contains information that specifies the sequence of each protein in the cell. RNA carries a copy of this information to the cytoplasmic compartment. With the help of ribosomes and other molecules, the RNA code is translated into a chain of amino acids that make up proteins; those that are destined for secretion or the membrane are created in the endoplasmic reticulum. At one time, scientists thought that the growing protein chain folded spontaneously, but they now know that chaperone proteins assist this process. |
| Tom Dunne |