Journal of the American Society of Nephrology
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J Am Soc Nephrol 16: 3446-, 2005
© 2005 American Society of Nephrology

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 Correction to October Highlights
 
Xia X, et al.: The Endogenous CXXC Motif Governs the Cadmium Sensitivity of the Renal Na+/Glucose Co-Transporter. J Am Soc Nephrol 16: 1257–1265, 2005.

In Results, found on page 1259, the correct amounts of sialic acid liberation in the absence and presence of Triton X-100 was 85 ± 5 nmol/mg protein. The authors regret this error.


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 Correction to October Highlights
 
J Am Soc Nephrol 16: 2815–2816, 2005

Glomerulosclerosis—can proteomics help us understand it better?
We currently identify sclerotic glomeruli only by light and electron microscopy, but clearly there must be more subtle changes that precede these. Others have searched for such changes with molecular techniques such as DNA arrays with limited success. Xu et al. have employed a newer proteomic methodology to compare sclerotic to nonsclerotic and normal glomeruli in the remnant kidney model of secondary focal sclerosis. Not surprisingly, the sclerotic glomeruli differed substantially from normal ones. But of more interest, the nonsclerotic glomeruli in remnant kidneys were more like sclerotic than normal glomeruli, thus identifying early changes that likely predict, and may even cause, the development of sclerosis. A clue is provided by further studies of thymosin {beta}4, one of the upregulated proteins, that itself exerts a profibrotic effect by mediating angiotensin induction of PAI-1, which impairs breakdown of fibrin and extracellular matrix. These studies are important because they not only show the feasibility of applying proteomics to the detection and study of glomerular scarring, but also yield a new insight into what the mechanisms involved may be. See Wu et al., pages 2967–2875.



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