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Researchers Uncover Critical Player in Cell Communication

I outside the cell nucleus led us to suspect that this protein must be doing more than regulate gene expression,” says Desiderio.

Under normal conditions, calcium does not flow freely into and out of cells until a demand for it - such as a muscle contraction or nerve function -- triggers cells to take up the free floating element from their surroundings. Cells store calcium until still other signals occur to release it again.

“The finding was stunning to us because calcium is one of the most important messengers in cells,” says Desiderio, “and both it and TFII-I are in every cell. That affirmed our suspicion that TFII-I could be doing something important with calcium signaling.”

In one experiment, the Hopkins team knocked down the amount of TFII-I in lab-grown cells and looked for changes in calcium flow under a high-power microscope using a dye that glows when it comes in contact with calcium. A camera attached to the microscope recorded the brightness of the glow and fed that measure into a computer that calculates the amount of calcium.

Knocking down TFII-I and separately assaulting the cells with chemicals caused the cells to take up more calcium than usual.

The researchers realized that when they depleted the cells of TFII-I, the cell responded by installing more calcium channels in their surfaces that allow calcium and only calcium to enter the cell. “We think TFII-I must control calcium entry into the cell by somehow limiting the number of calcium channels at the cell’s surface,” says Desiderio.

“There’s good evidence suggesting that the frequency and intensity of this ebb and flow of calcium can determine a cell’s response to external cues,” says Desiderio. “TFII-I may be a universal player in communication between cells, in the brain, the immune system and elsewhere.”
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