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Interestingly, the cell surface binding of GFP+, a recombinant version of GFP exposing positively charged residues to mediate its HS-dependent cell surface binding and endocytosis 16 , was significantly decreased as well in C3orf58 -/- and SLC39A9 -/- cells (Fig
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The latter assertion has been confirmed by a series of studies showing that strategies directly preventing peroxynitrite generation or accelerating its degradation prevented the generation of nitrotyrosine in injured tubular cells, ameliorated renal histological damage, and reduced functional renal alterations (evaluated by the increase of plasma creatinine and urea, and the development of proteinuria) in KIR
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