Researchers at Johns Hopkins have figured out a key step in how 'free' calcium - the kind not contained in bones - is managed in the body. The finding could aid in the development of new treatments for a variety of neurological disorders that include Parkinson's disease, says the study published in the journal Nature Chemical Biology.

"Electrical signals carried by free-floating calcium ions are wildly important to keep the second-by-second functions of the body going," said David Yue, professor of biomedical engineering and neuroscience at The Johns Hopkins University.

According to Yue and his team, large proteins called calcium channels are the gatekeepers that determine when calcium enters cells. Embedded in cell membranes, these channels open and shut to regulate calcium flow into the cell.

"When calcium goes into cells, it sets off a cascade of vital activity, but just the right amount of calcium must enter - otherwise, problems arise," Yue added. To achieve this balance, two chemical regulators bind to calcium channels as a brake and accelerator for calcium entry.

Calmodulin, one type of calcium channel-binding protein, stops calcium from flowing through, while other proteins, known as calcium-binding proteins, accelerate calcium entry, the study said.

"Our experiments established that calmodulin and calcium-binding proteins work by binding to distinct parts of the calcium channel," explained Yue.

The researchers have been able to investigate how large molecules such as these function in living cells, the study said.


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