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A protein's well-known cousin sheds light on its gout-linked relative
Date:4/8/2013

the protein's location and processing.

Knowing that the F508 deletion in CFTR creates instability in a certain part of the protein, the researchers introduced additional mutations intended to stabilize the wobbly region of the Q141K mutant ABCG2. As predicted, they found that this stabilization increased the amount of ABCG2 on the cell surface, suggesting again that ABCG2 had been saved from the recycling bin.

To confirm the involvement of the recycling process, the team fed the cells several small molecules known to help malformed proteins avoid degradation. One molecule, VRT-325, partially restores CFTR's activity. The same molecule was also able to increase the amount of mutant ABCG2 found in the cells and on their surfaces, and to decrease the amount of uric acid in the cells, bringing it within the normal range.

"Though there are many more lab tests needed before clinical trials can even be designed, our results represent an important step forward in both understanding how gout results from this mutation and finding a treatment," says Guggino.


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Contact: Catherine Kolf
ckolf@jhmi.edu
443-287-2251
Johns Hopkins Medicine
Source:Eurekalert

Page: 1 2 3

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